@article {pmid39345742,
year = {2024},
author = {Liu, X and Wang, Z and Teng, C and Wang, Z},
title = {Changes in gut microbiota and metabolites of mice with intravenous graphene oxide-induced embryo toxicity.},
journal = {Toxicological research},
volume = {40},
number = {4},
pages = {571-584},
pmid = {39345742},
issn = {1976-8257},
abstract = {UNLABELLED: The expanding applications of graphene oxide (GO) nanomaterials have attracted interest in understanding their potential adverse effects on embryonic and fetal development. Numerous studies have revealed the importance of the maternal gut microbiota in pregnancy. In this study, we established a mouse GO exposure model to evaluate embryo toxicity induced by intravenous administration of GO during pregnancy. We also explored the roles of gut microbiota and fecal metabolites using a fecal microbiota transplantation (FMT) intervention model. We found that administration of GO at doses up to 1.25 mg/kg caused embryo toxicity, characterized by significantly increased incidences of fetal resorption, stillbirths, and decreased birth weight. In pregnant mice with embryo toxicity, the richness of the maternal gut microbiota was dramatically decreased, and components of the microbial community were disturbed. FMT alleviated the decrease in birth weight by remodeling the gut microbiota, especially via upregulation of the Firmicutes/Bacteroidetes ratio. We subsequently used untargeted metabolomics to identify characteristic fecal metabolites associated with GO exposure. These metabolites were closely correlated with the phyla Actinobacteria, Proteobacteria, and Cyanobacteria. Our findings offer new insights into the embryo toxic effects of GO exposure during pregnancy; they emphasize the roles of gut microbiota-metabolite interactions in adverse pregnancy outcomes induced by GO or other external exposures, as demonstrated through FMT intervention.

SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s43188-024-00242-3.},
}

@article {pmid39338992,
year = {2024},
author = {Lim, X and Ooi, L and Ding, U and Wu, HHL and Chinnadurai, R},
title = {Gut Microbiota in Patients Receiving Dialysis: A Review.},
journal = {Pathogens (Basel, Switzerland)},
volume = {13},
number = {9},
pages = {},
pmid = {39338992},
issn = {2076-0817},
abstract = {The human gut microbiota constitutes a complex community of microorganisms residing within the gastrointestinal tract, encompassing a vast array of species that play crucial roles in health and disease. The disease processes involved in chronic kidney disease (CKD) and end-stage kidney disease (ESKD) are now increasingly established to result in dysregulation of gut microbiota composition and function. Gut microbiota dysbiosis has been associated with poor clinical outcomes and all-cause mortality in patients with ESKD, particularly individuals receiving dialysis. Prior studies highlighted various factors that affect gut microbiota dysbiosis in CKD and ESKD. These include, but are not limited to, uraemic toxin accumulation, chronic inflammation, immune dysfunction, medications, and dietary restrictions and nutritional status. There is a lack of studies at present that focus on the evaluation of gut microbiota dysbiosis in the context of dialysis. Knowledge on gut microbiota changes in this context is important for determining their impact on dialysis-specific and overall outcomes for this patient cohort. More importantly, evaluating gut microbiota composition can provide information into potential targets for therapeutic intervention. Identification of specific microbial signatures may result in further development of personalised treatments to improve patient outcomes and mitigate complications during dialysis. Optimising gut microbiota through various therapeutic approaches, including dietary adjustments, probiotics, prebiotics, medications, and faecal transplantation, have previously demonstrated potential in multiple medical conditions. It remains to be seen whether these therapeutic approaches are effective within the dialysis setting. Our review aims to evaluate evidence relating to alterations in the gut microbiota of patients undergoing dialysis. A growing body of evidence pointing to the complex yet significant relationship which surrounds gut microbiota and kidney health emphasises the importance of gut microbial balance to improve outcomes for individuals receiving dialysis.},
}

@article {pmid39338430,
year = {2024},
author = {Fanizzi, F and D'Amico, F and Zanotelli Bombassaro, I and Zilli, A and Furfaro, F and Parigi, TL and Cicerone, C and Fiorino, G and Peyrin-Biroulet, L and Danese, S and Allocca, M},
title = {The Role of Fecal Microbiota Transplantation in IBD.},
journal = {Microorganisms},
volume = {12},
number = {9},
pages = {},
pmid = {39338430},
issn = {2076-2607},
abstract = {Gut microbiota dysbiosis has a critical role in the pathogenesis of inflammatory bowel diseases, prompting the exploration of novel therapeutic approaches like fecal microbiota transplantation, which involves the transfer of fecal microbiota from a healthy donor to a recipient with the aim of restoring a balanced microbial community and attenuating inflammation. Fecal microbiota transplantation may exert beneficial effects in inflammatory bowel disease through modulation of immune responses, restoration of mucosal barrier integrity, and alteration of microbial metabolites. It could alter disease course and prevent flares, although long-term durability and safety data are lacking. This review provides a summary of current evidence on fecal microbiota transplantation in inflammatory bowel disease management, focusing on its challenges, such as variability in donor selection criteria, standardization of transplant protocols, and long-term outcomes post-transplantation.},
}

@article {pmid39338312,
year = {2024},
author = {Qi, X and Sun, H and Liu, J and Cong, M and Zhang, X and Yan, Y and Xia, Z and Liu, T and Zhao, J},
title = {Phenylethanol Glycoside from Cistanche tubulosa Attenuates BSA-Induced Liver Fibrosis in Rats by Modulating the Gut Microbiota-Liver Axis.},
journal = {Pharmaceuticals (Basel, Switzerland)},
volume = {17},
number = {9},
pages = {},
pmid = {39338312},
issn = {1424-8247},
support = {2022D01D36//This work was financially supported by the Key project of Natural Science Foundation of Xinjiang Uygur Autonomous Region in China/ ; },
abstract = {This study aimed to investigate the effect of phenylethanol glycoside from Cistanche tubulosa (CPhGs) on the prevention of bovine serum albumin (BSA)-induced hepatic fibrosis in rats. Investigation of the mechanisms of the anti-hepatic fibrosis effect was focused on CPhGs' influence on the "gut-liver" regulation, including the gut microbiota, intestinal barrier, systemic lipopolysaccharide (LPS) concentration, and LPS-related signaling pathway. The results show that CPhGs restored the diversity of gut microbiota, increased the relative abundance of Bacteroidetes, and decreased the relative abundance of Firmicutes and Proteobacteria in the fibrotic rats. In addition, CPhGs promoted the enrichment of probiotics such as Blautia, Oscillospira, Ruminococcus, Odoribacter, Bacteroides, and Parabacteroides in intestines of these rats. Furthermore, CPhGs reduced histopathological injury in the intestine and restored the tight junctions of the intestine by increasing the expression of ZO-1, occludin, and E-cadherin. CPhGs efficiently reduced serum LPS and liver lipopolysaccharide-binding protein (LBP) levels and inhibited the LPS-TLR4/MyD88/NF-κB pathway, which is related to protein expression in the liver. Correlation analysis confirmed that these beneficial bacteria were negatively associated with pathological damage, while LPS and harmful bacteria were positively associated with liver injury. Our fecal microbiota transplantation (FMT) experiment confirmed that gut microbiota is an important part of disease progression and that CPhGs is useful for the prevention and treatment of hepatic fibrosis. Our data demonstrate that the anti-hepatic fibrosis mechanism of CPhGs was mediated by regulation of the "gut-liver" axis. These results can stimulate consideration for its use in clinical practices.},
}

@article {pmid39186389,
year = {2024},
author = {Cotto, C and Baker, K and Fallon, E and Rimon, S},
title = {Fecal Microbiota, Live-jslm (RBL; REBYOTA ®) for Prevention of Recurrent Clostridioides difficile Infection: What Gastroenterology Nurses Need to Know.},
journal = {Gastroenterology nursing : the official journal of the Society of Gastroenterology Nurses and Associates},
volume = {47},
number = {5},
pages = {378-382},
pmid = {39186389},
issn = {1538-9766},
mesh = {Humans ; *Clostridium Infections/prevention & control ; *Clostridioides difficile ; *Fecal Microbiota Transplantation ; Gastroenterology ; Feces/microbiology ; Recurrence ; Secondary Prevention/methods ; },
}

Humans
*Clostridium Infections/prevention & control
*Clostridioides difficile
*Fecal Microbiota Transplantation
Gastroenterology
Feces/microbiology
Recurrence
Secondary Prevention/methods

@article {pmid39337526,
year = {2024},
author = {Missiego-Beltrán, J and Beltrán-Velasco, AI},
title = {The Role of Microbial Metabolites in the Progression of Neurodegenerative Diseases-Therapeutic Approaches: A Comprehensive Review.},
journal = {International journal of molecular sciences},
volume = {25},
number = {18},
pages = {},
pmid = {39337526},
issn = {1422-0067},
mesh = {Humans ; *Neurodegenerative Diseases/metabolism/therapy/microbiology ; *Gastrointestinal Microbiome ; Animals ; *Probiotics/therapeutic use ; Prebiotics ; Fecal Microbiota Transplantation ; Disease Progression ; Blood-Brain Barrier/metabolism ; Oxidative Stress ; Fatty Acids, Volatile/metabolism ; },
abstract = {The objective of this review is to provide a comprehensive examination of the role of microbial metabolites in the progression of neurodegenerative diseases, as well as to investigate potential therapeutic interventions targeting the microbiota. A comprehensive literature search was conducted across the following databases: PubMed, Scopus, Web of Science, ScienceDirect, and Wiley. Key terms related to the gut microbiota, microbial metabolites, neurodegenerative diseases, and specific metabolic products were used. The review included both preclinical and clinical research articles published between 2000 and 2024. Short-chain fatty acids have been demonstrated to play a crucial role in modulating neuroinflammation, preserving the integrity of the blood-brain barrier, and influencing neuronal plasticity and protection. Furthermore, amino acids and their derivatives have been demonstrated to exert a significant influence on CNS function. These microbial metabolites impact CNS health by regulating intestinal permeability, modulating immune responses, and directly influencing neuroinflammation and oxidative stress, which are integral to neurodegenerative diseases. Therapeutic strategies, including prebiotics, probiotics, dietary modifications, and fecal microbiota transplantation have confirmed the potential to restore microbial balance and enhance the production of neuroprotective metabolites. Furthermore, novel drug developments based on microbial metabolites present promising therapeutic avenues. The gut microbiota and its metabolites represent a promising field of research with the potential to advance our understanding of and develop treatments for neurodegenerative diseases.},
}

Humans
*Neurodegenerative Diseases/metabolism/therapy/microbiology
*Gastrointestinal Microbiome
Animals
*Probiotics/therapeutic use
Prebiotics
Fecal Microbiota Transplantation
Disease Progression
Blood-Brain Barrier/metabolism
Oxidative Stress
Fatty Acids, Volatile/metabolism

@article {pmid39337098,
year = {2024},
author = {Tîrziu, AT and Susan, M and Susan, R and Sonia, T and Harich, OO and Tudora, A and Varga, NI and Tiberiu-Liviu, D and Avram, CR and Boru, C and Munteanu, M and Horhat, FG},
title = {From Gut to Eye: Exploring the Role of Microbiome Imbalance in Ocular Diseases.},
journal = {Journal of clinical medicine},
volume = {13},
number = {18},
pages = {},
pmid = {39337098},
issn = {2077-0383},
abstract = {Background: The gut microbiome plays a crucial role in human health, and recent research has highlighted its potential impact on ocular health through the gut-eye axis. Dysbiosis, or an imbalance in the gut microbiota, has been implicated in various ocular diseases. Methods: A comprehensive literature search was conducted using relevant keywords in major electronic databases, prioritizing recent peer-reviewed articles published in English. Results: The gut microbiota influences ocular health through immune modulation, maintenance of the blood-retinal barrier, and production of beneficial metabolites. Dysbiosis can disrupt these mechanisms, contributing to ocular inflammation, tissue damage, and disease progression in conditions such as uveitis, age-related macular degeneration, diabetic retinopathy, dry eye disease, and glaucoma. Therapeutic modulation of the gut microbiome through probiotics, prebiotics, synbiotics, and fecal microbiota transplantation shows promise in preclinical and preliminary human studies. Conclusions: The gut-eye axis represents a dynamic and complex interplay between the gut microbiome and ocular health. Targeting the gut microbiome through innovative therapeutic strategies holds potential for improving the prevention and management of various ocular diseases.},
}

@article {pmid39334498,
year = {2024},
author = {De Filippo, C and Chioccioli, S and Meriggi, N and Troise, AD and Vitali, F and Mejia Monroy, M and Özsezen, S and Tortora, K and Balvay, A and Maudet, C and Naud, N and Fouché, E and Buisson, C and Dupuy, J and Bézirard, V and Chevolleau, S and Tondereau, V and Theodorou, V and Maslo, C and Aubry, P and Etienne, C and Giovannelli, L and Longo, V and Scaloni, A and Cavalieri, D and Bouwman, J and Pierre, F and Gérard, P and Guéraud, F and Caderni, G},
title = {Gut microbiota drives colon cancer risk associated with diet: a comparative analysis of meat-based and pesco-vegetarian diets.},
journal = {Microbiome},
volume = {12},
number = {1},
pages = {180},
pmid = {39334498},
issn = {2049-2618},
support = {JTC-2017-7//Joint Programming Initiative a Healthy Diet for a Healthy Life-Intestinal Microbiomics (JPI HDHL-INTIMIC) Call for Joint Transnational Research Proposals on "Interrelation of the Intestinal Microbiome, Diet and Health"/ ; JTC-2017-7//Joint Programming Initiative a Healthy Diet for a Healthy Life-Intestinal Microbiomics (JPI HDHL-INTIMIC) Call for Joint Transnational Research Proposals on "Interrelation of the Intestinal Microbiome, Diet and Health"/ ; JTC-2017-7//Joint Programming Initiative a Healthy Diet for a Healthy Life-Intestinal Microbiomics (JPI HDHL-INTIMIC) Call for Joint Transnational Research Proposals on "Interrelation of the Intestinal Microbiome, Diet and Health"/ ; JTC-2017-7//Joint Programming Initiative a Healthy Diet for a Healthy Life-Intestinal Microbiomics (JPI HDHL-INTIMIC) Call for Joint Transnational Research Proposals on "Interrelation of the Intestinal Microbiome, Diet and Health"/ ; JTC-2017-7//Joint Programming Initiative a Healthy Diet for a Healthy Life-Intestinal Microbiomics (JPI HDHL-INTIMIC) Call for Joint Transnational Research Proposals on "Interrelation of the Intestinal Microbiome, Diet and Health"/ ; JTC-2017-7//Joint Programming Initiative a Healthy Diet for a Healthy Life-Intestinal Microbiomics (JPI HDHL-INTIMIC) Call for Joint Transnational Research Proposals on "Interrelation of the Intestinal Microbiome, Diet and Health"/ ; JTC-2017-7//Joint Programming Initiative a Healthy Diet for a Healthy Life-Intestinal Microbiomics (JPI HDHL-INTIMIC) Call for Joint Transnational Research Proposals on "Interrelation of the Intestinal Microbiome, Diet and Health"/ ; JTC-2017-7//Joint Programming Initiative a Healthy Diet for a Healthy Life-Intestinal Microbiomics (JPI HDHL-INTIMIC) Call for Joint Transnational Research Proposals on "Interrelation of the Intestinal Microbiome, Diet and Health"/ ; JTC-2017-7//Joint Programming Initiative a Healthy Diet for a Healthy Life-Intestinal Microbiomics (JPI HDHL-INTIMIC) Call for Joint Transnational Research Proposals on "Interrelation of the Intestinal Microbiome, Diet and Health"/ ; JTC-2017-7//Joint Programming Initiative a Healthy Diet for a Healthy Life-Intestinal Microbiomics (JPI HDHL-INTIMIC) Call for Joint Transnational Research Proposals on "Interrelation of the Intestinal Microbiome, Diet and Health"/ ; JTC-2017-7//Joint Programming Initiative a Healthy Diet for a Healthy Life-Intestinal Microbiomics (JPI HDHL-INTIMIC) Call for Joint Transnational Research Proposals on "Interrelation of the Intestinal Microbiome, Diet and Health"/ ; Expression of interest # 895//HDHL INTIMIC-Knowledge Platform on food, diet, intestinal microbiomics and human health/ ; Expression of interest # 895//HDHL INTIMIC-Knowledge Platform on food, diet, intestinal microbiomics and human health/ ; PE00000003//National Recovery and Resilience Plan (NRRP), Mission 4 Component 2 Investment 1.3 - Call for tender No. 341 of 15 March 2022 of Italian Ministry of University and Research funded by the European Union - NextGenerationEU; Project title "ON Foods - Research and innovation network on food and nutrition Sustainability, Safety and Security - Working ON Foods"/ ; PE00000003//National Recovery and Resilience Plan (NRRP), Mission 4 Component 2 Investment 1.3 - Call for tender No. 341 of 15 March 2022 of Italian Ministry of University and Research funded by the European Union - NextGenerationEU; Project title "ON Foods - Research and innovation network on food and nutrition Sustainability, Safety and Security - Working ON Foods"/ ; PE00000003//National Recovery and Resilience Plan (NRRP), Mission 4 Component 2 Investment 1.3 - Call for tender No. 341 of 15 March 2022 of Italian Ministry of University and Research funded by the European Union - NextGenerationEU; Project title "ON Foods - Research and innovation network on food and nutrition Sustainability, Safety and Security - Working ON Foods"/ ; ECS00000017//European Union - NextGenerationEU - National Recovery and Resilience Plan, Mission 4 Component 2 - Investment 1.5 - THE - Tuscany Health Ecosystem/ ; ECS00000017//European Union - NextGenerationEU - National Recovery and Resilience Plan, Mission 4 Component 2 - Investment 1.5 - THE - Tuscany Health Ecosystem/ ; G. Caderni//University of Florence (Fondo ex-60%), Italy/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome ; Rats ; *Colonic Neoplasms/microbiology/etiology ; *Diet, Vegetarian/adverse effects ; *Feces/microbiology ; *Fecal Microbiota Transplantation ; *RNA, Ribosomal, 16S/genetics ; Male ; Bacteria/classification/isolation & purification/genetics/metabolism ; Diet/adverse effects ; Azoxymethane ; Meat/adverse effects/microbiology ; Colorectal Neoplasms/microbiology/etiology ; Disease Models, Animal ; Humans ; },
abstract = {BACKGROUND: Colorectal cancer (CRC) risk is strongly affected by dietary habits with red and processed meat increasing risk, and foods rich in dietary fibres considered protective. Dietary habits also shape gut microbiota, but the role of the combination between diet, the gut microbiota, and the metabolite profile on CRC risk is still missing an unequivocal characterisation.

METHODS: To investigate how gut microbiota affects diet-associated CRC risk, we fed Apc-mutated PIRC rats and azoxymethane (AOM)-induced rats the following diets: a high-risk red/processed meat-based diet (MBD), a normalised risk diet (MBD with α-tocopherol, MBDT), a low-risk pesco-vegetarian diet (PVD), and control diet. We then conducted faecal microbiota transplantation (FMT) from PIRC rats to germ-free rats treated with AOM and fed a standard diet for 3 months. We analysed multiple tumour markers and assessed the variations in the faecal microbiota using 16S rRNA gene sequencing together with targeted- and untargeted-metabolomics analyses.

RESULTS: In both animal models, the PVD group exhibited significantly lower colon tumorigenesis than the MBD ones, consistent with various CRC biomarkers. Faecal microbiota and its metabolites also revealed significant diet-dependent profiles. Intriguingly, when faeces from PIRC rats fed these diets were transplanted into germ-free rats, those transplanted with MBD faeces developed a higher number of preneoplastic lesions together with distinctive diet-related bacterial and metabolic profiles. PVD determines a selection of nine taxonomic markers mainly belonging to Lachnospiraceae and Prevotellaceae families exclusively associated with at least two different animal models, and within these, four taxonomic markers were shared across all the three animal models. An inverse correlation between nonconjugated bile acids and bacterial genera mainly belonging to the Lachnospiraceae and Prevotellaceae families (representative of the PVD group) was present, suggesting a potential mechanism of action for the protective effect of these genera against CRC.

CONCLUSIONS: These results highlight the protective effects of PVD while reaffirming the carcinogenic properties of MBD diets. In germ-free rats, FMT induced changes reminiscent of dietary effects, including heightened preneoplastic lesions in MBD rats and the transmission of specific diet-related bacterial and metabolic profiles. Importantly, to the best of our knowledge, this is the first study showing that diet-associated cancer risk can be transferred with faeces, establishing gut microbiota as a determinant of diet-associated CRC risk. Therefore, this study marks the pioneering demonstration of faecal transfer as a means of conveying diet-related cancer risk, firmly establishing the gut microbiota as a pivotal factor in diet-associated CRC susceptibility. Video Abstract.},
}

Animals
*Gastrointestinal Microbiome
Rats
*Colonic Neoplasms/microbiology/etiology
*Diet, Vegetarian/adverse effects
*Feces/microbiology
*Fecal Microbiota Transplantation
*RNA, Ribosomal, 16S/genetics
Male
Bacteria/classification/isolation & purification/genetics/metabolism
Diet/adverse effects
Azoxymethane
Meat/adverse effects/microbiology
Colorectal Neoplasms/microbiology/etiology
Disease Models, Animal
Humans

@article {pmid39333864,
year = {2024},
author = {Huang, F and Deng, Y and Zhou, M and Tang, R and Zhang, P and Chen, R},
title = {Fecal microbiota transplantation from patients with polycystic ovary syndrome induces metabolic disorders and ovarian dysfunction in germ-free mice.},
journal = {BMC microbiology},
volume = {24},
number = {1},
pages = {364},
pmid = {39333864},
issn = {1471-2180},
support = {82201781//National Natural Science Foundation of China/ ; 81871141//National Natural Science Foundation of China/ ; 2022-PUMCH-B-123//National High-Level Hospital Clinical Research Funding/ ; 2018YFC1004801//National Key Research and Development Program/ ; 2020-I2M-CT-B-040//CAMS Innovation Fund for Medical Sciences (CIFMS)/ ; },
mesh = {*Polycystic Ovary Syndrome/microbiology/therapy ; Animals ; *Fecal Microbiota Transplantation ; Female ; Mice ; *Gastrointestinal Microbiome ; Humans ; *Dysbiosis/microbiology ; Feces/microbiology ; Metabolic Diseases/microbiology/etiology/therapy ; Bacteria/classification/isolation & purification/genetics ; Insulin Resistance ; Ovary/microbiology ; Germ-Free Life ; Disease Models, Animal ; Adult ; },
abstract = {BACKGROUND: Dysbiosis of the microbiome is a key hallmark of polycystic ovary syndrome (PCOS). However, the interaction between the host and microbiome and its relevance to the pathogenesis of PCOS remain unclear.

METHODS: To evaluate the role of the commensal gut microbiome in PCOS, we gavaged germ-free mice with the fecal microbiota from patients with PCOS or healthy individuals and evaluated the reproductive endocrine features of the recipient mice.

RESULTS: Mice transplanted with fecal microbiota from PCOS patients and those transplanted from healthy controls presented different bacterial profiles and reproductive endocrine features. The fecal microbiota of the mice in the PCOS group was enriched in Phocaeicola, Mediterraneibacter, Oscillospiraceae, Lawsonibacter and Rikenellaceae. Fecal microbiota transplantation (FMT) from PCOS patients induced increased disruption of ovarian functions, lipo-metabolic disturbance, insulin resistance and an obese-like phenotype in recipient mice.

CONCLUSION: Our findings suggest that the microbiome may govern the set point of PCOS-bearing individuals and that gut ecosystem manipulation may be a useful marker and target for the management of PCOS.},
}

*Polycystic Ovary Syndrome/microbiology/therapy
Animals
*Fecal Microbiota Transplantation
Female
Mice
*Gastrointestinal Microbiome
Humans
*Dysbiosis/microbiology
Feces/microbiology
Metabolic Diseases/microbiology/etiology/therapy
Bacteria/classification/isolation & purification/genetics
Insulin Resistance
Ovary/microbiology
Germ-Free Life
Disease Models, Animal
Adult

@article {pmid39333064,
year = {2024},
author = {Chen, X and Chen, X and Yan, D and Zhang, N and Fu, W and Wu, M and Ge, F and Wang, J and Li, X and Geng, M and Wang, J and Tang, D and Liu, J},
title = {GV-971 prevents severe acute pancreatitis by remodeling the microbiota-metabolic-immune axis.},
journal = {Nature communications},
volume = {15},
number = {1},
pages = {8278},
pmid = {39333064},
issn = {2041-1723},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; Male ; Mice ; *Pancreatitis/immunology/microbiology/metabolism ; *Mice, Inbred C57BL ; *Disease Models, Animal ; Macrophages/immunology/metabolism ; Fatty Acids, Volatile/metabolism ; Fecal Microbiota Transplantation ; Humans ; Metabolomics ; },
abstract = {Despite recent advances, severe acute pancreatitis (SAP) remains a lethal inflammation with limited treatment options. Here, we provide compelling evidence of GV-971 (sodium oligomannate), an anti-Alzheimer's medication, as being a protective agent in various male mouse SAP models. Microbiome sequencing, along with intestinal microbiota transplantation and mass cytometry technology, unveil that GV-971 reshapes the gut microbiota, increasing Faecalibacterium populations and modulating both peripheral and intestinal immune systems. A metabolomics analysis of cecal contents from GV-971-treated SAP mice further identifies short-chain fatty acids, including propionate and butyrate, as key metabolites in inhibiting macrophage M1 polarization and subsequent lethal inflammation by blocking the MAPK pathway. These findings suggest GV-971 as a promising therapeutic for SAP by targeting the microbiota metabolic immune axis.},
}

Animals
*Gastrointestinal Microbiome/drug effects
Male
Mice
*Pancreatitis/immunology/microbiology/metabolism
*Mice, Inbred C57BL
*Disease Models, Animal
Macrophages/immunology/metabolism
Fatty Acids, Volatile/metabolism
Fecal Microbiota Transplantation
Humans
Metabolomics

@article {pmid39331938,
year = {2024},
author = {Zhao, Y and Qiu, P and Shen, T},
title = {Gut microbiota and eye diseases: A review.},
journal = {Medicine},
volume = {103},
number = {39},
pages = {e39866},
pmid = {39331938},
issn = {1536-5964},
support = {NO.2023C03089//the Research and Development Plan of Zhejiang Science and Technology Department/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/physiology/immunology ; *Eye Diseases/microbiology/therapy/immunology ; Probiotics/therapeutic use ; Fecal Microbiota Transplantation ; Anti-Bacterial Agents/therapeutic use ; },
abstract = {Recent studies reveal that alterations in gut microbiota play a significant role in the progression of various diseases, including those affecting the eyes. The association between gut microbiota and eye health is an emerging focus of research. This review seeks to summarize the connection between the gut microbiome and specific eye conditions, such as ocular surface diseases, funduscopic disorders and immune-mediated eye diseases. Gut microbiota may influence these conditions by regulating the immune system or altering metabolites, thereby contributing to disease development. Strategies like probiotics, antibiotics, dietary modifications, and fecal transplants show promise in addressing these issues. This review examines how the gut microbiome may be linked to the pathogenesis of eye diseases, providing fresh therapeutic perspectives for ophthalmology.},
}

Humans
*Gastrointestinal Microbiome/physiology/immunology
*Eye Diseases/microbiology/therapy/immunology
Probiotics/therapeutic use
Fecal Microbiota Transplantation
Anti-Bacterial Agents/therapeutic use

@article {pmid39330818,
year = {2024},
author = {Hanifeh, M and Scarsella, E and Rojas, CA and Ganz, HH and Huhtinen, M and Laine, T and Spillmann, T},
title = {Oral Fecal Microbiota Transplantation in Dogs with Tylosin-Responsive Enteropathy-A Proof-of-Concept Study.},
journal = {Veterinary sciences},
volume = {11},
number = {9},
pages = {},
pmid = {39330818},
issn = {2306-7381},
support = {V3130001//Orion Corporation (Finland)/ ; },
abstract = {A clinical trial was conducted to evaluate the effect of fecal microbiota transplantation (FMT) on the canine chronic enteropathy clinical activity index (CCECAI), fecal consistency, and microbiome of dogs with tylosin-responsive enteropathy (TRE). The trial consisted of four phases: (1) screening with discontinuation of tylosin for 4 weeks, (2) inclusion with re-introduction of tylosin for 3-7 days, (3) treatment with FMT/placebo for 4 weeks, and (4) post-treatment with follow-up for 4 weeks after treatment cessation. The study found that the treatment efficacy of FMT (71.4%) was slightly higher than that of placebo (50%), but this difference was not statistically significant due to underpowering. The most abundant bacterial species detected in the fecal microbiomes of dogs with TRE before FMT or placebo treatment were Blautia hansenii, Ruminococcus gnavus, Escherichia coli, Clostridium dakarense, Clostridium perfringens, Bacteroides vulgatus, and Faecalimonas umbilicata. After FMT, the microbiomes exhibited increases in Clostridium dakarense, Clostridium paraputrificum, and Butyricicoccus pullicaecorum. The microbiome alpha diversity of TRE dogs was lower when on tylosin treatment compared to healthy dogs, but it increased after treatment in both the FMT and placebo groups. Comparisons with the stool donor showed that, on average, 30.4% of donor strains were engrafted in FMT recipients, with the most common strains being several Blautia sp., Ruminococcus gnavus, unclassified Lachnoclostridium, Collinsella intestinalis, and Fournierella massiliensis.},
}

@article {pmid39329364,
year = {2024},
author = {Rani, M and Akhilesh, and Chouhan, D and Uniyal, A and Tiwari, V},
title = {Fecal Microbiota Transplantation-Mediated Rebalancing of the Gut-Brain Axis Alleviates Cisplatin-Induced Neuropathic Pain.},
journal = {ACS chemical neuroscience},
volume = {},
number = {},
pages = {},
doi = {10.1021/acschemneuro.4c00267},
pmid = {39329364},
issn = {1948-7193},
abstract = {Chemotherapy-induced neuropathic pain (CINP) presents a significant challenge in cancer treatment, necessitating novel therapeutic approaches. The intricate relationship between CINP and the gut-brain axis indicates a crucial role for the gut microbiota in pain modulation during cancer therapy. In this study, we investigated the effect of gut microbiota and their modulation on CINP in rats. Cisplatin administration (20 mg/kg, ip) disrupted the integrity of the blood-spinal cord barrier, as evidenced by reduced expression of tight junction proteins occludin and claudin-5 and increased leakage of pro-inflammatory cytokines into the spinal cord. Fecal microbiota transplantation (FMT, 0.5 mL of P.O.) from healthy rats over 21 days restored barrier integrity, as confirmed by Evan's blue assay. FMT intervention halted the progression of cisplatin-induced pain, demonstrated through a battery of pain assays assessing mechanical, thermal, and cold allodynia alongside hyperalgesia measurements. Additionally, FMT treatment reduced oxidative stress and modulated neuro-inflammatory markers, resulting in a rebalanced cytokine profile with decreased levels of neuro-inflammatory cytokines (IL-6 and TNFα) and increased expression of the anti-inflammatory cytokine IL-10. Gut microbiota-mediated IL-1β/NF-κB signaling emerged as a critical factor in leukocyte recruitment and microglial activation, highlighting the gut-brain axis as a key regulatory nexus in managing cisplatin-induced neuropathic pain. These findings underscore the therapeutic potential of targeting gut microbiota modulation as a promising strategy for alleviating CINP and improving the well-being of cancer patients undergoing chemotherapy.},
}

@article {pmid39326141,
year = {2024},
author = {Hu, T and Zhu, Y and Zhou, X and Ye, M and Wang, X and Lu, C and Wang, Y},
title = {Baicalein ameliorates SEB-induced acute respiratory distress syndrome in a microbiota-dependent manner.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {135},
number = {},
pages = {156049},
doi = {10.1016/j.phymed.2024.156049},
pmid = {39326141},
issn = {1618-095X},
abstract = {BACKGROUND: Acute respiratory distress syndrome (ARDS) is characterized by sudden and extensive pulmonary inflammation, with a mortality rate of approximately 40 %. Presently, there is no effective treatment to prevent or reverse its severe consequences. Baicalein (BAI) is a natural vicinal trihydroxyflavone and has been identified as the core quality marker of Scutellariae baicalensis for its effect on lung inflammation. However, its oral bioavailability is limited. The majority of studies that investigate BAI's in vivo mechanisms use injection techniques. Currently, there is no clear understanding of the mechanisms by which low-bioavailable BAI functions orally.

PURPOSE: This study aimed to evaluate the efficiency of BAI in ARDS mice and its underlying mechanisms.

STUDY DESIGN AND METHODS: Behavioral experiments, histological analysis, immunofluorescence staining, flow cytometry of immune cells, qRT-PCR, and ELISA analysis were performed to evaluate the efficiency of BAI in ARDS mice. Lung tissues transcriptomic-based analyses were performed to detect the differentially expressed genes and biological pathways. Fecal samples were subjected to microbial 16S rRNA analysis and untargeted metabolomics analysis in order to identify the specific flora and metabolites associated with BAI. Furthermore, antibiotic cocktail treatment and fecal microbiota transplantation were used to elucidate the gut microbiota-mediated effects on ARDS.

RESULTS: In our study, we first find that oral administration of BAI effectively mitigates staphylococcal enterotoxin B-induced ARDS. BAI can alleviate gut dysbiosis and regulate the Toll-like signaling pathway and amino acid metabolism. The protective effects of BAI against ARDS are gut microbiota dependent. Modulation of gut microbiota increases the production of short-chain fatty acids and enhances lung barrier function, which is consistent with the therapeutic interventions with BAI. Notably, BAI greatly enriches the abundance of Prevotellaceae, a butyrate-producing bacterial family, exhibiting a positive correlation with key differentially expressed genes in the TLR4/MyD88 signaling cascades.

CONCLUSION: BAI emerges as a potential prebiotic agent to attenuate ARDS, and targeting specific microbial species may offer an innovative therapeutic approach to investigate other flavonoids with limited bioavailability.},
}

@article {pmid39276368,
year = {2024},
author = {Čížková, D and Payne, P and Bryjová, A and Ďureje, Ľ and Piálek, J and Kreisinger, J},
title = {Convergence of gut phage communities but not bacterial communities following wild mouse bacteriophage transplantation into captive house mice.},
journal = {The ISME journal},
volume = {18},
number = {1},
pages = {},
pmid = {39276368},
issn = {1751-7370},
support = {19-19307S//Czech Science Foundation/ ; e-INFRA CZ LM2018140//Ministry of Education, Youth, and Sports of the Czech Republic/ ; },
mesh = {Animals ; Mice ; *Gastrointestinal Microbiome ; *Bacteriophages/isolation & purification/genetics/physiology ; Bacteria/classification/virology/genetics/isolation & purification ; Animals, Wild/microbiology ; Specific Pathogen-Free Organisms ; Feces/microbiology/virology ; Female ; Virome ; },
abstract = {Bacteriophages are abundant components of vertebrate gut microbial communities, impacting bacteriome dynamics, evolution, and directly interacting with the superhost. However, knowledge about gut phageomes and their interaction with bacteriomes in vertebrates under natural conditions is limited to humans and non-human primates. Widely used specific-pathogen-free (SPF) mouse models of host-microbiota interactions have altered gut bacteriomes compared to wild mice, and data on phageomes from wild or other non-SPF mice are lacking. We demonstrate divergent gut phageomes and bacteriomes in wild and captive non-SPF mice, with wild mice phageomes exhibiting higher alpha-diversity and interindividual variability. In both groups, phageome and bacteriome structuring mirrored each other, correlating at the individual level. Re-analysis of previous data from phageomes of SPF mice revealed their enrichment in Suoliviridae crAss-like phages compared to our non-SPF mice. Disrupted bacteriomes in mouse models can be treated by transplanting healthy phageomes, but the effects of phageome transplants on healthy adult gut microbiota are still unknown. We show that experimental transplantation of phageomes from wild to captive mice did not cause major shifts in recipient phageomes. However, the convergence of recipient-to-donor phageomes confirmed that wild phages can integrate into recipient communities. The differences in the subset of integrated phages between the two recipient mouse strains illustrate the context-dependent effects of phage transplantation. The transplantation did not impact recipient gut bacteriomes. This resilience of healthy adult gut microbiomes to the intervention has implications for phage allotransplantation safety.},
}

Animals
Mice
*Gastrointestinal Microbiome
*Bacteriophages/isolation & purification/genetics/physiology
Bacteria/classification/virology/genetics/isolation & purification
Animals, Wild/microbiology
Specific Pathogen-Free Organisms
Feces/microbiology/virology
Female
Virome

@article {pmid39324491,
year = {2024},
author = {Pu, D and Yao, Y and Zhou, C and Liu, R and Wang, Z and Liu, Y and Wang, D and Wang, B and Wang, Y and Liu, Z and Zhang, Z and Feng, B},
title = {FMT rescues mice from DSS-induced colitis in a STING-dependent manner.},
journal = {Gut microbes},
volume = {16},
number = {1},
pages = {2397879},
doi = {10.1080/19490976.2024.2397879},
pmid = {39324491},
issn = {1949-0984},
mesh = {Animals ; *Colitis/therapy/chemically induced/immunology ; *Membrane Proteins/genetics/metabolism ; Mice ; *Dextran Sulfate/adverse effects ; *Gastrointestinal Microbiome ; *Fecal Microbiota Transplantation ; *Mice, Inbred C57BL ; Th17 Cells/immunology ; Disease Models, Animal ; Th1 Cells/immunology ; Colon/microbiology/immunology/pathology ; Macrophages/immunology ; Humans ; Th2 Cells/immunology ; },
abstract = {Fecal microbiota transplantation (FMT) is currently a promising therapy for inflammatory bowel disease (IBD). However, clinical studies have shown that there is an obvious individual difference in the efficacy of FMT. Therefore, it is a pressing issue to identify the factors that influence the efficacy of FMT and find ways to screen the most suitable patients for this therapy. In this work, we targeted the stimulator of interferon genes (STING), a DNA-sensing protein that regulates host-defense. By comparing the differential efficacy of FMT in mice with different expression level of STING, it is revealed that FMT therapy provides treatment for DSS-induced colitis in a STING-dependent manner. Mechanistically, FMT exerts a regulatory effect on the differentiation of intestinal Th17 cells and macrophages, splenic Th1 and Th2 cells, as well as Th1 cells of the mesenteric lymph nodes via STING, down-regulating the colonic M1/M2 and splenic Th1/Th2 cell ratios, thereby improving the imbalanced immune homeostasis in the inflamed intestine. Meanwhile, based on the 16SrDNA sequencing of mice fecal samples, STING was found to facilitate the donor strain colonization in recipients' gut, mainly Lactobacillales, thereby reshaping the gut microbiota disturbed by colitis. Consequently, we proposed that STING, as a key target of FMT therapy, is potentially a biomarker for screening the most suitable individuals for FMT to optimize treatment regimens and enhance clinical benefit.},
}

Animals
*Colitis/therapy/chemically induced/immunology
*Membrane Proteins/genetics/metabolism
Mice
*Dextran Sulfate/adverse effects
*Gastrointestinal Microbiome
*Fecal Microbiota Transplantation
*Mice, Inbred C57BL
Th17 Cells/immunology
Disease Models, Animal
Th1 Cells/immunology
Colon/microbiology/immunology/pathology
Macrophages/immunology
Humans
Th2 Cells/immunology

@article {pmid39323880,
year = {2024},
author = {Deng, L and Guo, X and Chen, J and Li, B and Liu, N and Xia, J and Ou, M and Hong, Z},
title = {Effect of intestinal microbiota transplantation on chronic hepatitis B virus infection associated liver disease.},
journal = {Frontiers in microbiology},
volume = {15},
number = {},
pages = {1458754},
pmid = {39323880},
issn = {1664-302X},
abstract = {BACKGROUND: Research on the effects of intestinal microbiota transplantation (IMT) on chronic HBV infection (CHB) progression associated liver disease (HBV-CLD) and alterations in the microbiota post-IMT are quite limited for the moment.

METHODS: By integrating microbiome with metabolome analyses, we aimed to the function of IMT and the alterations of gut microbiota in patients with HBV-CLD. First, this study included 20 patients with HBV-CLD and ten healthy controls. Then, 16 patients with CHB were given IMT with donor feces (heterologous) via oral capsule. Fecal samples from CHB patients were obtained before and after IMT, as well as healthy controls, for 16S rDNA sequencing and untargeted metabolomics analysis.

RESULTS: The proalbuminemia were significantly increased after IMT, and the HBsAg and TBA showed a significant decrease after IMT in the HBV-CLD patients. There was statistical difference in the Chaol indexes between between CHB patients and healthy controls, suggesting a lower abundance of the gut microbiota in HBV-CLD patients. In addition, there was statistical difference in the Shannon and Simpson indexes between prior to IMT and post-IMT, indicating that the impaired abundance of the gut microbiota had been improved after IMT. The host-microbiota-metabolite interplay, amino acid metabolism, nicotinate and nicotinamide metabolism, starch and sucrose metabolism, steroid biosynthesis, and vitamins metabolism, were significantly lower in HBV-CLD patients than healthy controls.

CONCLUSION: IMT may improve the therapeutic effects on patients HBV-CLD. Furthermore, IMT appears to improve amino acid metabolism by impaired abundance of the gut microbiota and therefore improve liver prealbumin synthesis.},
}

@article {pmid39323631,
year = {2024},
author = {Zhang, D and Cheng, H and Wu, J and Zhou, Y and Tang, F and Liu, J and Feng, W and Peng, C},
title = {The energy metabolism-promoting effect of aconite is associated with gut microbiota and bile acid receptor TGR5-UCP1 signaling.},
journal = {Frontiers in pharmacology},
volume = {15},
number = {},
pages = {1392385},
pmid = {39323631},
issn = {1663-9812},
abstract = {INTRODUCTION: As a widely used traditional Chinese medicine with hot property, aconite can significantly promote energy metabolism. However, it is unclear whether the gut microbiota and bile acids contribute to the energy metabolism-promoting properties of aconite. The aim of this experiment was to verify whether the energy metabolism-promoting effect of aconite aqueous extract (AA) is related to gut microbiota and bile acid (BA) metabolism.

METHODS: The effect of AA on energy metabolism in rats was detected based on body weight, body temperature, and adipose tissue by HE staining and immunohistochemistry. In addition, 16S rRNA high-throughput sequencing and targeted metabolomics were used to detect changes in gut microbiota and BA concentrations, respectively. Antibiotic treatment and fecal microbiota transplantation (FMT) were also performed to demonstrate the importance of gut microbiota.

RESULTS: Rats given AA experienced an increase in body temperature, a decrease in body weight, and an increase in BAT (brown adipose tissue) activity and browning of WAT (white adipose tissue). Sequencing analysis and targeted metabolomics indicated that AA modulated gut microbiota and BA metabolism. The energy metabolism promotion of AA was found to be mediated by gut microbiota, as demonstrated through antibiotic treatment and FMT. Moreover, the energy metabolism-promoting effect of aconite is associated with the bile acid receptor TGR5 (Takeda G-protein-coupled receptor 5)-UCP1 (uncoupling protein 1) signaling pathway.

CONCLUSION: The energy metabolism-promoting effect of aconite is associated with gut microbiota and bile acid receptor TGR5-UCP1 signaling.},
}

@article {pmid39322832,
year = {2024},
author = {Zeng, X and Ma, C and Fu, W and Xu, Y and Wang, R and Liu, D and Zhang, L and Hu, N and Li, D and Li, W},
title = {Changes in Type 1 Diabetes-Associated Gut Microbiota Aggravate Brain Ischemia Injury by Affecting Microglial Polarization Via the Butyrate-MyD88 Pathway in Mice.},
journal = {Molecular neurobiology},
volume = {},
number = {},
pages = {},
pmid = {39322832},
issn = {1559-1182},
support = {81701288//National Natural Science Foundation of China/ ; YQJH2023028//Program for Young Talents of Basic Research in Universities of Heilongjiang Province/ ; },
abstract = {People with type 1 diabetes (T1D) have a significantly elevated risk of stroke, but the mechanism through which T1D worsens ischemic stroke remains unclear. This study was aimed at investigating the roles of T1D-associated changes in the gut microbiota in aggravating ischemic stroke and the underlying mechanism. Fecal 16SrRNA sequencing indicated that T1D mice and mice with transplantation of T1D mouse gut microbiota had lower relative abundance of butyric acid producers, f_Erysipelotrichaceae and g_Allobaculum, and lower content of butyric acid in feces. After middle cerebral artery occlusion (MCAO), these mice had poorer neurological outcomes and more severe inflammation, but higher expression of myeloid differentiation factor 88 (MyD88) in the ischemic penumbra; moreover, the microglia were inclined to polarize toward the pro-inflammatory type. Administration of butyrate to T1D mice in the drinking water alleviated the neurological damage after MCAO. Butyrate influenced the response and polarization of BV2 and decreased the production of inflammatory cytokines via MyD88 after oxygen-glucose deprivation/reoxygenation. Knocking down MyD88 in the brain alleviated neurological outcomes and decreased the concentrations of inflammatory cytokines in the brain after stroke in mice with transplantation of T1D mouse gut microbiota. Poor neurological outcomes and aggravated inflammatory responses of T1D mice after ischemic stroke may be partly due to differences in microglial polarization mediated by the gut microbiota-butyrate-MyD88 pathway. These findings provide new ideas and potential intervention targets for alleviating neurological damage after ischemic stroke in T1D.},
}

@article {pmid39322747,
year = {2024},
author = {Zhang, SL and Wang, X and Cai, QQ and Chen, C and Zhang, ZY and Xu, YY and Yang, MX and Jia, QA and Wang, Y and Wang, ZM},
title = {Acarbose enhances the efficacy of immunotherapy against solid tumours by modulating the gut microbiota.},
journal = {Nature metabolism},
volume = {},
number = {},
pages = {},
pmid = {39322747},
issn = {2522-5812},
support = {82203048//National Natural Science Foundation of China (National Science Foundation of China)/ ; },
abstract = {The crucial role of gut microbiota in shaping immunotherapy outcomes has prompted investigations into potential modulators. Here we show that oral administration of acarbose significantly increases the anti-tumour response to anti-PD-1 therapy in female tumour-bearing mice. Acarbose modulates the gut microbiota composition and tryptophan metabolism, thereby contributing to changes in chemokine expression and increased T cell infiltration within tumours. We identify CD8[+] T cells as pivotal components determining the efficacy of the combined therapy. Further experiments reveal that acarbose promotes CD8[+] T cell recruitment through the CXCL10-CXCR3 pathway. Faecal microbiota transplantation and gut microbiota depletion assays indicate that the effects of acarbose are dependent on the gut microbiota. Specifically, acarbose enhances the efficacy of anti-PD-1 therapy via the tryptophan catabolite indoleacetate, which promotes CXCL10 expression and thus facilitates CD8[+] T cell recruitment, sensitizing tumours to anti-PD-1 therapy. The bacterial species Bifidobacterium infantis, which is enriched by acarbose, also improves response to anti-PD-1 therapy. Together, our study endorses the potential combination of acarbose and anti-PD-1 for cancer immunotherapy.},
}

@article {pmid39322314,
year = {2024},
author = {Van Hul, M and Cani, PD and Petifils, C and De Vos, WM and Tilg, H and El Omar, EM},
title = {What defines a healthy gut microbiome?.},
journal = {Gut},
volume = {},
number = {},
pages = {},
doi = {10.1136/gutjnl-2024-333378},
pmid = {39322314},
issn = {1468-3288},
abstract = {The understanding that changes in microbiome composition can influence chronic human diseases and the efficiency of therapies has driven efforts to develop microbiota-centred therapies such as first and next generation probiotics, prebiotics and postbiotics, microbiota editing and faecal microbiota transplantation. Central to microbiome research is understanding how disease impacts microbiome composition and vice versa, yet there is a problematic issue with the term 'dysbiosis', which broadly links microbial imbalances to various chronic illnesses without precision or definition. Another significant issue in microbiome discussions is defining 'healthy individuals' to ascertain what characterises a healthy microbiome. This involves questioning who represents the healthiest segment of our population-whether it is those free from illnesses, athletes at peak performance, individuals living healthily through regular exercise and good nutrition or even elderly adults or centenarians who have been tested by time and achieved remarkable healthy longevity.This review advocates for delineating 'what defines a healthy microbiome?' by considering a broader range of factors related to human health and environmental influences on the microbiota. A healthy microbiome is undoubtedly linked to gut health. Nevertheless, it is very difficult to pinpoint a universally accepted definition of 'gut health' due to the complexities of measuring gut functionality besides the microbiota composition. We must take into account individual variabilities, the influence of diet, lifestyle, host and environmental factors. Moreover, the challenge in distinguishing causation from correlation between gut microbiome and overall health is presented.The review also highlights the resource-heavy nature of comprehensive gut health assessments, which hinders their practicality and broad application. Finally, we call for continued research and a nuanced approach to better understand the intricate and evolving concept of gut health, emphasising the need for more precise and inclusive definitions and methodologies in studying the microbiome.},
}

@article {pmid39321881,
year = {2024},
author = {Bano, N and Khan, S and Ahamad, S and Kanshana, JS and Dar, NJ and Khan, S and Nazir, A and Bhat, SA},
title = {Microglia and Gut Microbiota: A Double-Edged Sword in Alzheimer's Disease.},
journal = {Ageing research reviews},
volume = {},
number = {},
pages = {102515},
doi = {10.1016/j.arr.2024.102515},
pmid = {39321881},
issn = {1872-9649},
abstract = {The strong association between gut microbiota (GM) and brain functions such as mood, behaviour, and cognition has been well documented. Gut-brain axis is a unique bidirectional communication system between the gut and brain, in which gut microbes play essential role in maintaining various molecular and cellular processes. GM interacts with the brain through various pathways and processes including, metabolites, vagus nerve, HPA axis, endocrine system, and immune system to maintain brain homeostasis. GM dysbiosis, or an imbalance in GM, is associated with several neurological disorders, including anxiety, depression, and Alzheimer's disease (AD). Conversely, AD is sustained by microglia-mediated neuroinflammation and neurodegeneration. Further, GM and their products also affect microglia-mediated neuroinflammation and neurodegeneration. Despite the evidence connecting GM dysbiosis and AD progression, the involvement of GM in modulating microglia-mediated neuroinflammation in AD remains elusive. Importantly, deciphering the mechanism/s by which GM regulates microglia-dependent neuroinflammation may be helpful in devising potential therapeutic strategies to mitigate AD. Herein, we review the current evidence regarding the involvement of GM dysbiosis in microglia activation and neuroinflammation in AD. We also discuss the possible mechanisms through which GM influences the functioning of microglia and its implications for therapeutic intervention. Further, we explore the potential of microbiota-targeted interventions, such as prebiotics, probiotics, faecal microbiota transplantation, etc., as a novel therapeutic strategy to mitigate neuroinflammation and AD progression. By understanding and exploring the gut-brain axis, we aspire to revolutionize the treatment of neurodegenerative disorders, many of which share a common theme of microglia-mediated neuroinflammation and neurodegeneration.},
}

@article {pmid39321863,
year = {2024},
author = {Liang, J and Xiong, Z and Lei, Q and Jiang, Z and Wei, J and Ouyang, F and Chen, Y and Zeng, J},
title = {Sleep dysfunction and gut dysbiosis related amino acids metabolism disorders in cynomolgus monkeys after middle cerebral artery occlusion.},
journal = {Experimental neurology},
volume = {},
number = {},
pages = {114970},
doi = {10.1016/j.expneurol.2024.114970},
pmid = {39321863},
issn = {1090-2430},
abstract = {INTRODUCTION: This study aimed to explore the characteristics of post-stroke sleep dysfunction and verify their association with gut dysbiosis and the related amino acid metabolism disorders. This was achieved by using fecal microbiota transplantation (FMT) in a non-human primate stroke model.

METHODS: Twenty adult male cynomolgus monkeys were divided into the sham (n = 4), middle cerebral artery occlusion (MCAO, n = 5), MCAO + FMT (n = 3), and donor (n = 8) groups. The MCAO+FMT group received FMT at post-MCAO week 4. Sleep parameters, gut microbiota, gamma-aminobutyric acid (GABA), and glutamine (Gln) in the cerebrospinal fluid (CSF) were measured at baseline and postoperative weeks 4, 8, and 12.

RESULTS: At postoperative weeks 4, 8, and 12, the MCAO group showed decreased sleep efficiency, measured as the percentage of sleep during the whole night (82.3 ± 3.2 % vs 91.3 ± 2.5 %, 79.0 ± 3.75 % vs 90.8 ± 3.2 %, and 69.5 ± 4.8 % vs 90.5 ± 2.7 %; all P < 0.05), lower relative abundance of Lactobacillus (all P < 0.05), and reduced GABA concentrations in the CSF (317.3 ± 30.6 nmol/L vs 437.7 ± 25.6 nmol/L, 303.1 ± 48.9 nmol/L vs 4 40.9 ± 37.8 nmol/L, and 337.9 ± 49.4 nmol/L vs 457.4 ± 39.2 nmol/L; all P < 0.05) compared with the sham group. Sleep efficiency at post-FMT weeks 4 and 8 (84.7 ± 1.1 % vs 79.0 ± 3.75 %, and 84.1 ± 2.0 % vs 69.5 ± 4.8 %; both P < 0.05) and GABA concentration in the CSF at post-FMT week 4 (403.1 ± 25.4 nmol/L vs 303.1 ± 48.9 nmol/L, P < 0.05) was higher in the MCAO+FMT group than in the MCAO group.

CONCLUSIONS: Post-stroke sleep dysfunction in monkeys is characterized by impaired sleep coherence, associated with decreased levels of probiotics such as Lactobacillus, GABA, and Gln in the CSF and can be ameliorated using FMT.},
}

@article {pmid39321508,
year = {2024},
author = {Phanchana, M and Pipatthana, M and Phetruen, T and Konpetch, P and Prangthip, P and Harnvoravongchai, P and Sripong, C and Singhakaew, S and Wongphayak, S and Chankhamhaengdecha, S and Janvilisri, T},
title = {Identification and preclinical evaluation of MMV676558 as a promising therapeutic candidate against Clostridioides difficile.},
journal = {Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie},
volume = {180},
number = {},
pages = {117469},
doi = {10.1016/j.biopha.2024.117469},
pmid = {39321508},
issn = {1950-6007},
abstract = {Clostridioides difficile, a gram-positive, toxin-producing, spore-forming anaerobe, is a major cause of antibiotic-associated diarrhoea. The bacterium's intrinsic drug resistance limits current treatment options to fidaxomicin and vancomycin for initial episodes, with anti-toxin B monoclonal antibody or faecal microbiota transplantation recommended for complicated or recurrent cases. This underscores the urgent need for novel therapeutics. In this study, we screened the MMV Pathogen Box at a 10 µM concentration against C. difficile R20291. Primary hits were evaluated for minimum inhibitory concentrations (MIC), killing kinetics, and biofilm inhibition. Bacterial cytological profiling (BCP) and transmission electron microscopy (TEM) were employed to study the mode of action. MMV676558 was further tested in a mouse model to assess survival, histopathology, and gut microbiota effects. We identified nineteen hits that inhibited over 50 % of C. difficile growth. MIC assays revealed three hits with MICs below 16 µg/mL: MMV676558, MMV688755, and MMV690027. These hits were effective against various C. difficile ribotypes. Killing kinetics were comparable or superior to vancomycin and fidaxomicin, and biofilm assays showed inhibitory effects. BCP and TEM analyses suggested membrane function disruption as the mode of action. Furthermore, MMV676558 demonstrated a protective effect in mice, with favourable histopathology and gut microbiota profiles. Given the urgent threat posed by C. difficile antibiotic resistance, discovering new treatments is a top priority. Our study identified three promising hits from the MMV Pathogen Box, with MMV676558 showing significant in vivo potential for further evaluation.},
}

@article {pmid39320321,
year = {2024},
author = {Berry, P and Khanna, S},
title = {Fecal microbiota spores, live-brpk (VOWST™/VOS) for prevention of recurrent Clostridioides difficile infection.},
journal = {Future microbiology},
volume = {},
number = {},
pages = {1-10},
doi = {10.1080/17460913.2024.2403892},
pmid = {39320321},
issn = {1746-0921},
abstract = {Clostridioides difficile infection (CDI) is a health crisis comprising a majority of healthcare-associated infections and is now being seen in the community. Persistent dysbiosis despite treatment with standard-of-care antibiotics increases risk of recurrent infections. Fecal microbiota transplantation has been an effective way of addressing dysbiosis, but the studies have lacked standardization, which makes outcome and safety data difficult to interpret. Standardized microbiome therapies have demonstrated efficacy and safety for recurrent CDI and have been approved to prevent recurrent infection. In this review, we discuss the data behind and the practice use of fecal microbiota spores, live-brpk (VOWST™ / VOS), a US FDA approved live biotherapeutic for the prevention of recurrent CDI.},
}

@article {pmid39320101,
year = {2024},
author = {Xue, H and Wang, Y and Mei, C and Han, L and Lu, M and Li, X and Chen, T and Wang, F and Tang, X},
title = {Gut microbiome and serum metabolome alterations associated with lactose intolerance (LI): a case‒control study and paired-sample study based on the American Gut Project (AGP).},
journal = {mSystems},
volume = {},
number = {},
pages = {e0083924},
doi = {10.1128/msystems.00839-24},
pmid = {39320101},
issn = {2379-5077},
abstract = {UNLABELLED: Lactose intolerance (LI) is a prevalent condition characterized by gastrointestinal symptoms that arise following lactose consumption. Recent evidence suggests that the gut microbiome may influence lactose levels in the gut. However, there is limited understanding regarding the alterations in microbiota and metabolism between individuals with LI and non-LI. This study conducted a paired-sample investigation utilizing data from the American Gut Project (AGP) and performed metagenomic and untargeted metabolomic analyses in a Chinese cohort to explore the interaction between the gut microbiome and serum metabolites. In addition, fecal microbiota transplantation (FMT) experiments were conducted to further examine the impact of the LI-associated gut microbiome on inflammatory outcomes. We identified 14 microbial genera that significantly differed between LI and controls from AGP data. Using a machine learning approach, group separation was predicted based on seven species and nine metabolites in the Chinese cohort. Notably, increased levels of Escherichia coli in the LI group were negatively correlated with several metabolites, including PC (22:6/0:0), indole, and Lyso PC, while reduced levels of Faecalibacterium prausnitzii and Eubacterium rectale were positively correlated with indole and furazolidone. FMT-LI rats displayed visceral hypersensitivity and an altered gut microbiota composition compared to FMT-HC rats. Metagenomic and metabolomic analyses revealed an enrichment of MAPK signaling in LI, which was confirmed by FMT-LI rats showing higher expression of ERK and RAS, along with increased concentrations of proinflammatory cytokines. This study provides valuable insights into the disrupted microbial and metabolic traits associated with LI, emphasizing potential microbiome-based approaches for its prevention and treatment.

IMPORTANCE: Lactose intolerance (LI) is a prevalent condition characterized by gastrointestinal symptoms after lactose consumption due to a deficiency of lactase. There is limited understanding regarding the microbiota and metabolic alterations between individuals with LI and non-LI. This study represents the first exploration to investigate metagenomic and metabolomic signatures among subjects with lactose intolerance as far as our knowledge. We identified 14 microbial genera in the Western cohort and 7 microbial species, along with 9 circulating metabolites in the Chinese cohort, which significantly differed in LI patients. Metagenomic and metabolomic analyses revealed an enrichment of MAPK signaling in LI patients. This finding was confirmed by FMT-LI rats, exhibiting increased expression of ERK and RAS, along with higher concentrations of pro-inflammatory cytokines. Our study provides insights into the disrupted functional and metabolic traits of the gut microbiome in LI, highlighting potential microbiome-based approaches for preventing and treating LI.},
}

@article {pmid39318889,
year = {2024},
author = {McGrath, E and Herson, MR and Kuehnert, MJ and Moniz, K and Szczepiorkowski, ZM and Pruett, TL},
title = {A WHO remit to improve global standards for medical products of human origin.},
journal = {Bulletin of the World Health Organization},
volume = {102},
number = {10},
pages = {707-714},
pmid = {39318889},
issn = {1564-0604},
mesh = {Humans ; *World Health Organization ; Global Health ; International Cooperation ; Biological Products/standards ; },
abstract = {In recent decades, considerable advances have been made in assuring the safety of blood transfusion and organ transplantation. However, with the increasing movement of medical products of human origin across international boundaries, there is a need to enhance global norms and governance. These products, which include blood, organs, tissues, cells, human milk and faecal microbiota, are today crucial for health care but they also pose unique risks due to their human origin, such as disease transmission and graft failure. Moreover, the demand for medical products of human origin often exceeds supply, leading to dependence on international supply chains, and emerging technologies like cell and gene therapy present further challenges because of their unproven efficacy and long-term risks. Current regulatory mechanisms, especially in low- and middle-income countries, are insufficient. The World Health Organization (WHO) has both the mandate and experience to lead the development of international quality and safety standards, consistent product nomenclature, and robust traceability and biovigilance systems. An international, multistakeholder approach is critical for addressing the complexities of how medical products of human origin are used globally and for ensuring their safety. This approach will require promoting uniform product descriptions, enhancing digital communication systems and leveraging existing resources to support countries in establishing regulations for these products. As illustrated by World Health Assembly resolution WHA77.4 on transplantation in 2024, WHO's ongoing efforts to ensure the safe, efficient and ethical use of medical products of human origin worldwide provide the opportunity to galvanize international cooperation on establishing norms.},
}

Humans
*World Health Organization
Global Health
International Cooperation
Biological Products/standards

@article {pmid39317918,
year = {2024},
author = {Ahmadi, S and Hasani, A and Khabbaz, A and Poortahmasbe, V and Hosseini, S and Yasdchi, M and Mehdizadehfar, E and Mousavi, Z and Hasani, R and Nabizadeh, E and Nezhadi, J},
title = {Dysbiosis and fecal microbiota transplant: Contemplating progress in health, neurodegeneration and longevity.},
journal = {Biogerontology},
volume = {},
number = {},
pages = {},
pmid = {39317918},
issn = {1573-6768},
abstract = {The gut-brain axis plays an important role in mental health. The intestinal epithelial surface is colonized by billions of commensal and transitory bacteria, known as the Gut Microbiota (GM). However, potential pathogens continuously stimulate intestinal immunity when they find the place. The last two decades have witnessed several studies revealing intestinal bacteria as a key factor in the health-disease balance of the gut, as well as disease-emergent in other parts of the body. Various neurological processes, such as cognition, learning, and memory, could be affected by dysbiosis in GM. Additionally, the aging process and longevity are related to systemic inflammation caused by dysbiosis. Commensal GM affects brain development, behavior, and healthy aging suggesting that building changes in GM might be a potential therapeutic method. The innovation in GM dysbiosis is intervention by Fecal Microbiota Transplantation (FMT), which has been confirmed as a therapy for recurrent Clostridium difficile infections and is promising for other clinical disorders, such as Parkinson's disease, Multiple Sclerosis (MS), Alzheimer's disease, and depression. Additionally, FMT may be possible to promote healthy aging, and extend longevity. This review aims to connect dysbiosis, neurological disorders, and aging and the potential of FMT as a therapeutic strategy to treat these disorders, and to enhance the quality of life in the elderly.},
}

@article {pmid39316685,
year = {2024},
author = {Ke, S and Gálvez, JAV and Sun, Z and Cao, Y and Pollock, NR and Chen, X and Kelly, CP and Liu, YY},
title = {Rational Design of Live Biotherapeutic Products for the Prevention of Clostridioides difficile Infection.},
journal = {The Journal of infectious diseases},
volume = {},
number = {},
pages = {},
doi = {10.1093/infdis/jiae470},
pmid = {39316685},
issn = {1537-6613},
abstract = {Clostridioides difficile infection (CDI) is a major cause of healthcare- and antibiotic-associated diarrhea. While fecal microbiota transplantation (FMT) shows promise for recurrent CDI, its mechanisms and long-term safety are not fully understood. Live biotherapeutic products (LBPs) using pre-defined bacterial consortia offer an alternative option, but the rational designing LBPs remains challenging. Here, we employ a computational pipeline and three metagenomic datasets to identify microbial strains for LBPs targeting CDI. We constructed the CDI-related microbial genome catalog, comprising 3,741 non-redundant metagenome-assembled genomes (nrMAGs) and identified multiple potential protective nrMAGs, including strains from Dorea formicigenerans, Oscillibacter welbionis, and Faecalibacterium prausnitzii. Importantly, some of these protective nrMAGs were found to play an important role in FMT success, and most top protective nrMAGs can be validated by various previous findings. Our results demonstrate a framework for selecting microbial strains targeting CDI, paving the way for the computational design of LBPs against other enteric infections.},
}

@article {pmid39315788,
year = {2024},
author = {Wang, Y and Bing, H and Jiang, C and Wang, J and Wang, X and Xia, Z and Chu, Q},
title = {Gut microbiota dysbiosis and neurological function recovery after intracerebral hemorrhage: an analysis of clinical samples.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0117824},
doi = {10.1128/spectrum.01178-24},
pmid = {39315788},
issn = {2165-0497},
abstract = {We aimed to investigate the microbial community composition in patients with intracerebral hemorrhage (ICH) and its effect on prognosis. We designed two clinical cohort studies to explore the gut dysbiosis after ICH and their relationship with neurological function prognosis. First, fecal samples from patients with ICH at three time points: T1 (within 24 h of admission), T2 (3 days after surgery), and T3 (7 days after surgery), and healthy volunteers were subjected to 16S rRNA sequencing using Illumina high-throughput sequencing technology. When differential gut microbiota was identified, the correlation between clinical indicators and microbiotas was analyzed. Subsequently, the patients with ICH were categorized into GOOD and POOR groups based on their Glasgow Outcome Scale Extended (GOS-E) score, and the disparities in gut microbiota between the two groups were assessed. Univariate and multivariate logistic regression analyses were performed to identify independent risk factors. The composition and diversity of the gut microbiota in patients with ICH were different from those in the control group and changed dynamically with the extension of the course of cerebral hemorrhage. The abundances of Enterococcaceae, Clostridiales incertae sedis XI, and Peptoniphilaceae were significantly increased in patients with ICH, whereas Bacteroidaceae, Ruminococcaceae, Lachnospiraceae, and Veillonellaceae were significantly reduced. The relative abundance of Enterococcus gradually increased with the extension of the duration of ICH after surgery, and the abundance of Bacteroides gradually decreased. The abundance of Enterococcus before surgery was found to be negatively associated with patient neurological function prognosis. The original ICH score and Lachnospiraceae status were independent risk factors for predicting the prognosis of neurological function in patients with ICH (P < 0.05). Changes in the gut microbiota diversity in patients with ICH were related to prognosis. Lachnospiraceae may have a protective effect on prognosis.IMPORTANCEAcute central nervous system injuries like hemorrhagic stroke are major global health issues. While surgical hematoma removal can alleviate brain damage, severe cases still have a high 1-month mortality rate of up to 40%. Gut microbiota significantly impacts health, and treatments like fecal microbiota transplantation (FMT) and probiotics can improve brain damage by correcting gut microbiota imbalances caused by ischemic stroke. However, few clinical studies have explored this relationship in hemorrhagic stroke. This study investigated the impact of cerebral hemorrhage on the composition of gut microbiota, and we found that Lachnospiraceae were the independent risk factors for poor prognosis in intracerebral hemorrhage (ICH). The findings offer potential insights for the application of FMT in patients with ICH, and it may improve the prognosis of patients.},
}

@article {pmid38925098,
year = {2024},
author = {Barron, M and Fernando, DG and Atkinson, SN and Kirby, J and Kindel, TL},
title = {Sleeve Gastrectomy Protects Against Hypertension in Rats due to Changes in the Gut Microbiome.},
journal = {The Journal of surgical research},
volume = {301},
number = {},
pages = {118-126},
doi = {10.1016/j.jss.2024.05.044},
pmid = {38925098},
issn = {1095-8673},
mesh = {Animals ; *Gastrointestinal Microbiome ; *Gastrectomy/adverse effects ; Male ; *Hypertension/microbiology/etiology/therapy ; *Rats, Zucker ; *Fecal Microbiota Transplantation ; Rats ; *Obesity/microbiology/surgery ; Blood Pressure ; Disease Models, Animal ; Feces/microbiology ; },
abstract = {INTRODUCTION: Sleeve gastrectomy (SG), results in improvement in hypertension. We have previously published that rodent SG improves hypertension independent of weight loss associated with unique shifts in the gut microbiome. We tested if the gut microbiome directly improves blood pressure by performing fecal material transfer (FMT) from post-SG rats to surgery-naïve animals.

METHODS: We performed SG or Sham surgery in male, Zucker rats (n = 6-7) with obesity. Stool was collected postop from surgical donors for treatment of recipient rats. Three nonsurgical groups received daily, oral consumption of SG stool, sham stool, or vehicle alone (Nutella) for 10 wk (n = 7-8). FMT treatment was assessed for effects on body weight, food intake, oral glucose tolerance, and blood pressure. Genomic deoxyribonucleic acid of stool from donor and recipient groups were sequenced by 16S ribosomal ribonucleic acid and analyzed for diversity, abundance, and importance.

RESULTS: Ten weeks of SG-FMT treatment significantly lowered systolic blood pressures in surgery-naïve, recipient rats compared to vehicle treatment alone (126.8 ± 13.3 mmHg versus 151.8 ± 12.2 mmHg, P = 0.001). SG-FMT treatment also significantly altered beta diversity metrics compared to Sham-FMT and vehicle treatment. In random forest analysis, amplicon sequence variant level significantly predicted FMT group, P = 0.01.

CONCLUSIONS: We have found a direct link between gut microbial changes after SG and regulation of blood pressure. Future mechanistic studies are required to learn what specific gut microbial changes are required to induce improvements in obesity-associated hypertension and translation to clinical, metabolic surgery.},
}

Animals
*Gastrointestinal Microbiome
*Gastrectomy/adverse effects
Male
*Hypertension/microbiology/etiology/therapy
*Rats, Zucker
*Fecal Microbiota Transplantation
Rats
*Obesity/microbiology/surgery
Blood Pressure
Disease Models, Animal
Feces/microbiology

@article {pmid39315776,
year = {2024},
author = {Li, S and Liu, M and Han, Y and Liu, C and Cao, S and Cui, Y and Zhu, X and Wang, Z and Liu, B and Shi, Y},
title = {Gut microbiota-derived gamma-aminobutyric acid improves host appetite by inhibiting satiety hormone secretion.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0101524},
doi = {10.1128/msystems.01015-24},
pmid = {39315776},
issn = {2379-5077},
abstract = {Globally, appetite disorders have become an increasingly prominent public health issue. While short-term appetite loss may seem relatively harmless, prolonged instances can lead to serious physical and mental damage. In recent years, numerous studies have highlighted the significant role of the "microbiota-gut-brain" axis in the regulation of feeding behavior in organisms, suggesting that targeting the gut microbiota may be a novel therapeutic strategy for appetite disorders. However, the molecular mechanisms through which the gut microbiota mediates the increase in host appetite and the causal relationship between the two remain unclear. Based on this, we conducted 16S rRNA sequencing to analyze the gut microbiota of rabbits with high and low feed intake, followed by fecal microbiota transplantation (FMT) and metabolite gavage experiments to elucidate the underlying mechanisms. Our research indicates that the high feed intake group exhibited significant enrichment of the g__Bacteroides and gamma-aminobutyric acid (GABA), and intragastric administration of GABA effectively promoted the host's feeding behavior. The underlying mechanism involves GABA derived from the gut microbiota inhibiting the secretion of satiety hormones to enhance the host's feeding behavior. Furthermore, the results of FMT suggest that differences in gut microbiota composition may be a contributing factor to varying levels of feed intake in the host. In conclusion, these findings emphasize the role of the gut microbiota-derived GABA, in increasing host feed intake, offering a new target for the treatment of appetite disorders from the perspective of gut microbiota.IMPORTANCEThe incidence of anorexia is rapidly increasing and has become a global burden. Gut microbiota can participate in the regulation of host feeding behavior, yet the molecular mechanisms through which the gut microbiota mediates the increase in host appetite and the causal relationship between them remain unclear. In this study, we utilized 16S rRNA sequencing to investigate the composition of the gut microbiota in rabbits with varying levels of feed intake and employed fecal microbiota transplantation and gastric infusion experiments with gamma-aminobutyric acid (GABA) to elucidate the potential mechanisms involved. GABA derived from the gut microbiota can effectively enhance the host's feeding behavior by inhibiting the secretion of satiety hormones. This discovery underscores the pivotal role of the gut microbiota in modulating host appetite, offering novel research avenues and therapeutic targets for appetite disorders.},
}

@article {pmid39315595,
year = {2024},
author = {Sun, B and Wang, Y and Bai, J and Li, X and Ma, L and Man, S},
title = {Litchi Procyanidins Ameliorate DSS-Induced Colitis through Gut Microbiota-Dependent Regulation of Treg/Th17 Balance.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.4c05577},
pmid = {39315595},
issn = {1520-5118},
abstract = {Ulcerative colitis (UC) is a common chronic, relapsing inflammatory bowel condition. Procyanidins (PC) are known for their antiangiogenic, anti-inflammatory, antioxidant, and antimetastatic properties. However, there is comparatively limited information on how PC interacts with UC. In this study, 5 mg/10 mL/kg body weight of PC was administered to mice with dextran sulfate sodium (DSS)-induced colitis mice. PC treatment prolonged the survival period of mice, ameliorated UC symptoms, reduced damage to the intestinal mucosal barrier, and increased the protein expression of ZO-1 and occludin in the DSS-treated mice. Importantly, PC treatment significantly reduced gene expression related to Th17 cell differentiation, including STAT3, SMAD3, TGF-β, and JAK1. The results of the flow cytometry analysis indicated significant increase in the number of Treg cells and a concomitant decrease in the proportion of Th17 cells in the colon following PC treatment. Additionally, PC increased the abundance of gut microbiota such as Bacteroidota, Oscillospiraceae, Muribaculaceae, and Desulfovibrionaceae, as well as the concentrations of acetate acid, propionate acid, and butyrate acid in the feces. PC also activated short-chain fatty acid receptors, such as G-protein coupled receptor 43 in the colon, which promoted the proliferation of Treg cells. The depletion of gut microbiota and subsequent transplantation of fecal microbiota demonstrated that PC's effects on gut microbiota were effective in improving UC and restoring intestinal Th17/Treg homeostasis in a microbiota-dependent manner. This suggests that PC could be a promising functional food for the prevention and treatment of UC in the future.},
}

@article {pmid39315196,
year = {2024},
author = {Luo, C and Yang, Y and Jiang, C and Lv, A and Zuo, W and Ye, Y and Ke, J},
title = {Influenza and the gut microbiota: A hidden therapeutic link.},
journal = {Heliyon},
volume = {10},
number = {18},
pages = {e37661},
pmid = {39315196},
issn = {2405-8440},
abstract = {BACKGROUND: The extensive community of gut microbiota significantly influences various biological functions throughout the body, making its characterization a focal point in biomedicine research. Over the past few decades, studies have revealed a potential link between specific gut bacteria, their associated metabolic pathways, and influenza. Bacterial metabolites can communicate directly or indirectly with organs beyond the gut via the intestinal barrier, thereby impacting the physiological functions of the host. As the microbiota increasingly emerges as a 'gut signature' in influenza, gaining a deeper understanding of its role may offer new insights into its pathophysiological relevance and open avenues for novel therapeutic targets. In this Review, we explore the differences in gut microbiota between healthy individuals and those with influenza, the relationship between gut microbiota metabolites and influenza, and potential strategies for preventing and treating influenza through the regulation of gut microbiota and its metabolites, including fecal microbiota transplantation and microecological preparations.

METHODS: We utilized PubMed and Web of Science as our search databases, employing keywords such as "influenza," "gut microbiota," "traditional Chinese medicine," "metabolites," "prebiotics," "probiotics," and "machine learning" to retrieve studies examining the potential therapeutic connections between the modulation of gut microbiota and its metabolites in the treatment of influenza. The search encompassed literature from the inception of the databases up to December 2023.

RESULTS: Fecal microbiota transplantation (FMT), microbial preparations (probiotics and prebiotics), and traditional Chinese medicine have unique advantages in regulating intestinal microbiota and its metabolites to improve influenza outcomes. The primary mechanism involves increasing beneficial intestinal bacteria such as Bacteroidetes and Bifidobacterium while reducing harmful bacteria such as Proteobacteria. These interventions act directly or indirectly on metabolites such as short-chain fatty acids (SCFAs), amino acids (AAs), bile acids, and monoamines to alleviate lung inflammation, reduce viral load, and exert anti-influenza virus effects.

CONCLUSION: The gut microbiota and its metabolites have direct or indirect therapeutic effects on influenza, presenting broad research potential for providing new directions in influenza research and offering references for clinical prevention and treatment. Future research should focus on identifying key strains, specific metabolites, and immune regulation mechanisms within the gut microbiota to accurately target microbiota interventions and prevent respiratory viral infections such as influenza.},
}

@article {pmid39314882,
year = {2024},
author = {Larsen, OFA and Brummer, RJM},
title = {Perspective: on the future of fecal microbiota transplantation.},
journal = {Frontiers in microbiology},
volume = {15},
number = {},
pages = {1449133},
pmid = {39314882},
issn = {1664-302X},
abstract = {Fecal Microbiota Transplantation (FMT) has shown to possess impressive potential benefit for a wide range of clinical indications. Due to its inherent safety issues and efficacy constraints, the use of personalized FMT analogs could be a promising avenue. The development of such analogs will require a detailed understanding of their functionality, encompassing not only microbe-host interactions of the microbial taxa that are involved, but also of the ecological dimensions of the analogs and an overview of the gastrointestinal sites where these relevant microbial interactions take place. Moreover, characterization of taxa that have been lost due to diminished exposure to beneficial microbes, as a consequence of Western lifestyle, may lead to creation of future FMT analogs with the capacity to restore functionalities that we have lost.},
}

@article {pmid39314425,
year = {2024},
author = {de Araujo, A and Sree Kumar, H and Yang, T and Plata, AA and Dirr, EW and Bearss, N and Baekey, DM and Miller, DS and Donertas-Ayaz, B and Ahmari, N and Singh, A and Kalinoski, AL and Garrett, TJ and Martyniuk, CJ and de Lartigue, G and Zubcevic, J},
title = {Intestinal serotonergic vagal signaling as a mediator of microbiota-induced hypertension.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2024.07.17.603451},
pmid = {39314425},
issn = {2692-8205},
abstract = {Hypertension is a pervasive global health challenge, impacting over a billion individuals worldwide. Despite strides in therapeutic strategies, a significant proportion of patients remain resistant to the currently available therapies. While conventional treatments predominantly focus on cardiac, renal, and cerebral targets, emerging research underscores the pivotal role of the gut and its microbiota. Yet, the precise mechanisms governing interactions between the gut microbiota and the host blood pressure remain unclear. Here we describe a neural host-microbiota interaction that is mediated by the intestinal serotonin (5-HT) signaling via vagal 5HT3a receptors and which is crucial for maintenance of blood pressure homeostasis. Notably, a marked decrease in both intestinal 5-HT and vagal 5HT3aR signaling is observed in hypertensive rats, and in rats subjected to fecal microbiota transplantation from hypertensive rats. Leveraging an intersectional genetic strategy in a Cre rat line, we demonstrate that intestinal 5HT3aR vagal signaling is a crucial link between the gut microbiota and blood pressure homeostasis and that recovery of 5-HT signaling in colon innervating vagal neurons can alleviate hypertension. This paradigm-shifting finding enhances our comprehension of hypertensive pathophysiology and unveils a promising new therapeutic target for combating resistant hypertension associated with gut dysbiosis.},
}

@article {pmid39311394,
year = {2024},
author = {Ben Salem, I and Khemiri, H and Drechsel, O and Arbi, M and Böttcher, S and Mekki, N and Ben Fraj, I and Souiai, O and Yahyaoui, M and Ben Farhat, E and Meddeb, Z and Touzi, H and Ben Mustapha, I and BenKahla, A and Ouederni, M and Barbouche, MR and Diedrich, S and Triki, H and Haddad-Boubaker, S},
title = {Reversion of neurovirulent mutations, recombination and high intra-host diversity in vaccine-derived poliovirus excreted by patients with primary immune deficiency.},
journal = {Journal of medical virology},
volume = {96},
number = {9},
pages = {e29918},
doi = {10.1002/jmv.29918},
pmid = {39311394},
issn = {1096-9071},
support = {811034//European project PHINDaccess: Strengthening Omics data analysis capacities in pathogen-host interaction/ ; LR20IPT10//Tunisian Ministry of Higher Education and Scientifc Research/ ; },
mesh = {Humans ; *Poliovirus/genetics/classification/isolation & purification/immunology ; *Poliovirus Vaccine, Oral/genetics/adverse effects ; *Recombination, Genetic ; *Mutation ; *Poliomyelitis/virology/prevention & control ; *Feces/virology ; Male ; Female ; *Virus Shedding ; Genome, Viral/genetics ; Genetic Variation ; Primary Immunodeficiency Diseases/genetics ; Child, Preschool ; Evolution, Molecular ; Child ; Infant ; Virulence/genetics ; Phylogeny ; },
abstract = {Patients with Primary immunodeficiency (PIDs) may be infected by Polioviruses (PVs), especially when vaccinated with live Oral Polio Vaccine before diagnosis. They may establish long-term shedding of divergent strains and may act as reservoirs of PV transmission. This study delved into the effect of the genetic evolution of complete PV genomes, from MHC class II-deficient patients, on the excretion duration and clinical outcomes. Stool samples from three PID patients underwent analysis for PV detection through inoculation on cell culture and real-time PCR, followed by VP1 partial sequencing and full genome sequencing using the Illumina technology. Our findings revealed a low number of mutations for one patient who cleared the virus, while two exhibited a high intra-host diversity favoring the establishment of severe outcomes. Neurovirulence-reverse mutations were detected in two patients, possibly leading to paralysis development. Furthermore, a recombination event, between type 3 Vaccine-Derived Poliovirus and Sabin-like1 (VDPV3/SL1), occurred in one patient. Our findings have suggested an association between intra-host diversity, recombination, prolonged excretion of the virus, and emergence of highly pathogenic strains. Further studies on intra-host diversity are crucial for a better understanding of the virus evolution as well as for the success of the Global Polio Eradication Initiative.},
}

Humans
*Poliovirus/genetics/classification/isolation & purification/immunology
*Poliovirus Vaccine, Oral/genetics/adverse effects
*Recombination, Genetic
*Mutation
*Poliomyelitis/virology/prevention & control
*Feces/virology
Male
Female
*Virus Shedding
Genome, Viral/genetics
Genetic Variation
Primary Immunodeficiency Diseases/genetics
Child, Preschool
Evolution, Molecular
Child
Infant
Virulence/genetics
Phylogeny

@article {pmid39309854,
year = {2024},
author = {Wu, M and Chen, X and Lu, Q and Yao, X},
title = {Fecal microbiota transplantation for the treatment of chronic inflammatory skin diseases.},
journal = {Heliyon},
volume = {10},
number = {18},
pages = {e37432},
pmid = {39309854},
issn = {2405-8440},
abstract = {The regulation of immune functions and the maintenance of homeostasis in the internal environment are both integral to human gut microbiota (GM). If GM is disturbed, it can result in a range of autoimmune diseases, including chronic inflammatory skin conditions. Chronic inflammatory skin diseases driven by T or B-cell-mediated immune reactions are complex, including the most prevalent diseases and some rare diseases. Expanding knowledge of GM dysbiosis in chronic inflammatory skin diseases has emerged. The GM has some causal roles in the pathogenesis of these skin conditions. Targeting microbiota treatment, particularly fecal microbiota transplantation (FMT), is considered to be a promising strategy. FMT was commonly used in intestinal diseases by reshaping and balancing GM, serving as a reasonable administration in these skin inflammatory diseases. This paper summarizes the existing knowledge of GM dysbiosis in chronic inflammatory skin diseases and the research data on FMT treatment for such conditions.},
}

@article {pmid39306158,
year = {2024},
author = {Peng, G and Wang, S and Zhang, H and Xie, F and Jiao, L and Yuan, Y and Ma, C and Wu, H and Meng, Z},
title = {Tremella aurantialba polysaccharides alleviates ulcerative colitis in mice by improving intestinal barrier via modulating gut microbiota and inhibiting ferroptosis.},
journal = {International journal of biological macromolecules},
volume = {},
number = {},
pages = {135835},
doi = {10.1016/j.ijbiomac.2024.135835},
pmid = {39306158},
issn = {1879-0003},
abstract = {We aimed to investigate the effect of a polysaccharide from Tremella aurantialba on ulcerative colitis (UC), which targets ferroptosis in epithelial cells. TA 2-1 (127 kDa) was isolated from T. aurantialba and consisted of Man, Xyl, GlcA, Glc, Fuc and Rha with a molar ratio of 59.2: 23.2: 13.9: 1.6: 1.7: 0.4, exhibited a 1, 3-Man structure with branch chains of T-Xylp, 1,3-Xylp, 1,4-GlcAp, and T-Manp at its O-2 position. TA 2-1 (100 mg/mL) inhibited the cell viability of ferroptosis (19.8 %) in RLS3-induced Caco2 cells and significantly ameliorated symptoms in the colons of mice with dextran sodium sulfate (DSS)-induced UC. TA 2-1 remarkably repaired the intestinal barrier by upregulating claudin-1 and zonula occludens-1 levels. Further analysis found TA 2-1 significantly suppressed lipid peroxidation by regulating ferroptosis-related proteins in UC mice, suggesting that its protective effects are partially mediated by inhibiting ferroptosis. Further analysis of the gut microbiota and fecal microbiota transplantation revealed TA 2-1 might relieve UC symptoms or inhibit ferroptosis by modulating the gut microbiota's composition or metabolites. Results suggest the protective effects of TA 2-1 on the intestinal barrier by inhibiting ferroptosis of epithelial cells, at least by regulating the gut microbiota, highlighting the potential of TA 2-1 in UC treatment.},
}

@article {pmid39306049,
year = {2024},
author = {Shan, L and Fan, H and Guo, J and Zhou, H and Li, F and Jiang, Z and Wu, D and Feng, X and Mo, R and Liu, Y and Zhang, T and Zhou, Y},
title = {Impairment of oocyte quality caused by gut microbiota dysbiosis in obesity.},
journal = {Genomics},
volume = {116},
number = {5},
pages = {110941},
doi = {10.1016/j.ygeno.2024.110941},
pmid = {39306049},
issn = {1089-8646},
abstract = {Obesity poses risks to oocyte maturation and embryonic development in mice and humans, linked to gut microbiota dysbiosis and altered host metabolomes. However, it is unclear whether symbiotic gut microbes have a pivotal role in oocyte quality. In mouse models of fecal microbiota transplantation, we demonstrated aberrant meiotic apparatus and impaired maternal mRNA in oocytes, which is coincident with the poor developmental competence of embryos. Using metabolomics profiling, we discovered that the cytosine and cytidine metabolism was disturbed, which could account for the fertility defects observed in the high-fat diet (HFD) recipient mice. Additionally, cytosine and cytidine are closely related with gut microbiota dysbiosis, which is accompanied by a notable reduction of abundance of Christensenellaceae R-7 group in the HFD mice. In summary, our findings provided evidence that modifying the gut microbiota may be of value in the treatment of infertile female individuals with obesity.},
}

@article {pmid38367140,
year = {2024},
author = {Tao, Y and Luo, CJ and Zhang, BH and Shen, XY and Zhao, RK and Ma, BY and Shen, N and Luo, CY and Wang, JM and Xia, YJ and Xie, L and Chen, J and Mo, X},
title = {Diagnostic performance of a multiplexed gastrointestinal PCR panel for identifying diarrheal pathogens in children undergoing hematopoietic stem cell transplant.},
journal = {World journal of pediatrics : WJP},
volume = {20},
number = {9},
pages = {966-975},
pmid = {38367140},
issn = {1867-0687},
support = {20dz2260900//Shanghai Key Laboratory of Clinical Molecular Diagnostics for Pediatrics/ ; 20dz2261100//Shanghai Key Laboratory of Emergency Prevention Diagnosis and Treatment of Respiratory Infectious Diseases/ ; 22ZR1440300//Natural Science Foundation of Shanghai/ ; 81971890//National Natural Science Foundation of China/ ; PKJ2020-Y01//Science and Technology Innovation Plan Of Shanghai Science and Technology CommissionScience and Technology Development Fund of Shanghai Pudong New Area/ ; 20Y11903600//Scientific and Technology Commission of Shanghai Municipality/ ; 2022XD054//Shanghai Municipal Health Commission/ ; 22SG13//Shanghai Municipal Education Commission/ ; },
mesh = {Humans ; *Hematopoietic Stem Cell Transplantation/adverse effects ; Male ; Female ; *Diarrhea/microbiology/diagnosis/etiology ; Child ; Child, Preschool ; Prospective Studies ; Adolescent ; Multiplex Polymerase Chain Reaction ; Feces/microbiology/virology ; Infant ; Graft vs Host Disease/diagnosis ; },
abstract = {BACKGROUND: Diarrhea is a common complication of hematopoietic stem cell transplantation (HSCT) and is associated with substantial morbidity, but its etiology is often unknown. Etiologies of diarrhea in this population include infectious causes, chemotherapy- or medication-induced mucosal injury and graft-versus-host disease (GVHD). Distinguishing these potential causes of diarrhea is challenging since diarrheal symptoms are often multifactorial, and the etiologies often overlap in transplant patients. The objectives of this study were to evaluate whether the FilmArray gastrointestinal (GI) panel would increase diagnostic yield and the degree to which pre-transplantation colonization predicts post-transplantation infection.

METHODS: From November 2019 to February 2021, a total of 158 patients undergoing HSCT were prospectively included in the study. Stool specimens were obtained from all HSCT recipients prior to conditioning therapy, 28 ± 7 days after transplantation and at any new episode of diarrhea. All stool samples were tested by the FilmArray GI panel and other clinical microbiological assays.

RESULTS: The primary cause of post-transplantation diarrhea was infection (57/84, 67.86%), followed by medication (38/84, 45.24%) and GVHD (21/84, 25.00%). Ninety-five of 158 patients were colonized with at least one gastrointestinal pathogen before conditioning therapy, and the incidence of infectious diarrhea was significantly higher in colonized patients (47/95, 49.47%) than in non-colonized patients (10/63, 15.87%) (P < 0.001). Fourteen of 19 (73.68%) patients who were initially colonized with norovirus pre-transplantation developed a post-transplantation norovirus infection. Twenty-four of 62 (38.71%) patients colonized with Clostridium difficile developed a diarrheal infection. In addition, FilmArray GI panel testing improved the diagnostic yield by almost twofold in our study (55/92, 59.78% vs. 30/92, 32.61%).

CONCLUSIONS: Our data show that more than half of pediatric patients who were admitted for HSCT were colonized with various gastrointestinal pathogens, and more than one-third of these pathogens were associated with post-transplantation diarrhea. In addition, the FilmArray GI panel can increase the detection rate of diarrheal pathogens in pediatric HSCT patients, but the panel needs to be optimized for pathogen species, and further studies assessing its clinical impact and cost-effectiveness in this specific patient population are also needed.},
}

Humans
*Hematopoietic Stem Cell Transplantation/adverse effects
Male
Female
*Diarrhea/microbiology/diagnosis/etiology
Child
Child, Preschool
Prospective Studies
Adolescent
Multiplex Polymerase Chain Reaction
Feces/microbiology/virology
Infant
Graft vs Host Disease/diagnosis

@article {pmid39305117,
year = {2024},
author = {Walrath, T and Najarro, KM and Giesy, LE and Khair, S and Orlicky, DJ and McMahan, RH and Kovacs, EJ},
title = {Reducing the excessive inflammation after burn injury in aged mice by maintaining a healthier intestinal microbiome.},
journal = {FASEB journal : official publication of the Federation of American Societies for Experimental Biology},
volume = {38},
number = {18},
pages = {e70065},
doi = {10.1096/fj.202401020R},
pmid = {39305117},
issn = {1530-6860},
support = {R01 AG018859/AG/NIA NIH HHS/United States ; R35 GM131831/GM/NIGMS NIH HHS/United States ; T32 GM136444/GM/NIGMS NIH HHS/United States ; T32 AG000279/AG/NIA NIH HHS/United States ; F32 AG082443/AG/NIA NIH HHS/United States ; I01BX004335//U.S. Department of Veterans Affairs (VA)/ ; },
mesh = {Animals ; *Burns/microbiology ; *Gastrointestinal Microbiome ; Mice ; *Inflammation/microbiology ; Mice, Inbred C57BL ; Male ; Aging ; Feces/microbiology ; Lung/microbiology/metabolism/pathology ; Fecal Microbiota Transplantation ; Bacteroidetes ; Ileum/microbiology/metabolism ; },
abstract = {One in six people are projected to be 65 years or older by 2050. As the population ages, better treatments for injuries that disproportionately impact the aged population will be needed. Clinical studies show that people aged 65 and older experience higher rates of morbidity and mortality after burn injury, including a greater incidence of pulmonary complications when compared to younger burn injured adults, which we and others believe is mediated, in part, by inflammation originating in the intestines. Herein, we use our clinically relevant model of scald burn injury in young and aged mice to determine whether cohousing aged mice with young mice or giving aged mice oral gavage of fecal material from young mice is sufficient to alter the microbiome of the aged mice and protect them from inflammation in the ileum and the lungs. Aged burn injured mice have less DNA expression of Bacteroidetes in the feces and an unhealthy Firmicutes/Bacteroidetes ratio. Both Bacteroidetes and the ratio of these two phyla are restored in aged burn injured by prior cohousing for a month with younger mice but not fecal transfer from young mice. This shift in the microbiome coincides with heightened expression of danger-associated molecular patterns (DAMP), and pro-inflammatory cytokine interleukin-6 (il6) in the ileum and lung of aged, burn injured mice, and heightened antimicrobial peptide camp in the lung. Cohousing reverses DAMP expression in the ileum and lung, and cathelicidin-related antimicrobial peptide protein (camp) in the lung, while fecal transfer heightened DAMPs while reducing camp in the lung, and also increased IL-6 protein in the lungs. These results highlight the importance of the intestinal microbiome in mediating inflammation within the gut-lung axis, giving insights into potential future treatments in the clinic.},
}

Animals
*Burns/microbiology
*Gastrointestinal Microbiome
Mice
*Inflammation/microbiology
Mice, Inbred C57BL
Male
Aging
Feces/microbiology
Lung/microbiology/metabolism/pathology
Fecal Microbiota Transplantation
Bacteroidetes
Ileum/microbiology/metabolism

@article {pmid39303815,
year = {2024},
author = {Xie, X and Li, W and Xiong, Z and Xu, J and Liao, T and Sun, L and Xu, H and Zhang, M and Zhou, J and Xiong, W and Fu, Z and Li, Z and Han, Q and Cui, D and Anthony, DC},
title = {Metformin reprograms tryptophan metabolism via gut Microbiome-Derived bile acid metabolites to ameliorate Depression-Like behaviors in mice.},
journal = {Brain, behavior, and immunity},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.bbi.2024.09.014},
pmid = {39303815},
issn = {1090-2139},
abstract = {As an adjunct therapy, metformin enhances the efficacy of conventional antidepressant medications. However, its mode of action remains unclear. Here, metformin was found to ameliorate depression-like behaviors in mice exposed to chronic restraint stress (CRS) by normalizing the dysbiotic gut microbiome. Fecal transplants from metformin-treated mice ameliorated depressive behaviors in stressed mice. Microbiome profiling revealed that Akkermansia muciniphila (A. muciniphila), in particular, was markedly increased in the gut by metformin and that oral administration of this species alone was sufficient to reverse CRS-induced depressive behaviors and normalize aberrant stress-induced 5-hydroxytryptamine (5-HT) metabolism in the brain and gut. Untargeted metabolomic profiling further identified the bile acid metabolites taurocholate and deoxycholic acid as direct A. muciniphila-derived molecules that are, individually, sufficient to rescue the CRS-induced impaired 5-HT metabolism and depression-like behaviors. Thus, we report metformin reprograms 5-HT metabolism via microbiome-brain interactions to mitigate depressive syndromes, providing novel insights into gut microbiota-derived bile acids as potential therapeutic candidates for depressive mood disorders from bench to bedside.},
}

@article {pmid39303724,
year = {2024},
author = {Wang, X and Fang, Y and Liang, W and Wong, CC and Qin, H and Gao, Y and Liang, M and Song, L and Zhang, Y and Fan, M and Liu, C and Lau, HC and Xu, L and Li, X and Song, W and Wang, J and Wang, N and Yang, T and Mo, M and Zhang, X and Fang, J and Liao, B and Sung, JJY and Yu, J},
title = {Fusobacterium nucleatum facilitates anti-PD-1 therapy in microsatellite stable colorectal cancer.},
journal = {Cancer cell},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ccell.2024.08.019},
pmid = {39303724},
issn = {1878-3686},
abstract = {Microsatellite stable (MSS) colorectal cancers (CRCs) are often resistant to anti-programmed death-1 (PD-1) therapy. Here, we show that a CRC pathogen, Fusobacterium nucleatum (Fn), paradoxically sensitizes MSS CRC to anti-PD-1. Fecal microbiota transplantation (FMT) from patients with Fn-high MSS CRC to germ-free mice bearing MSS CRC confers sensitivity to anti-PD-1 compared to FMT from Fn-low counterparts. Single Fn administration also potentiates anti-PD-1 efficacy in murine allografts and CD34[+]-humanized mice bearing MSS CRC. Mechanistically, we demonstrate that intratumoral Fn generates abundant butyric acid, which inhibits histone deacetylase (HDAC) 3/8 in CD8[+] T cells, inducing Tbx21 promoter H3K27 acetylation and expression. TBX21 transcriptionally represses PD-1, alleviating CD8[+] T cell exhaustion and promoting effector function. Supporting this notion, knockout of a butyric acid-producing gene in Fn abolishes its anti-PD-1 boosting effect. In patients with MSS CRC, high intratumoral Fn predicts favorable response to anti-PD-1 therapy, indicating Fn as a potential biomarker of immunotherapy response in MSS CRC.},
}

@article {pmid39303605,
year = {2024},
author = {Zhao, Y and Sokol, H and Cao, Q and Zhang, H and Yan, Y and Xie, L and Wang, H},
title = {Systemic inflammatory response to daily exposure to microcystin-LR and the underlying gut microbial mechanisms.},
journal = {Journal of hazardous materials},
volume = {480},
number = {},
pages = {135855},
doi = {10.1016/j.jhazmat.2024.135855},
pmid = {39303605},
issn = {1873-3336},
abstract = {Cyanobacterial toxins have raised global concerns due to potential chronic disease implications from daily drinking water exposure, which remain largely unknown despite extensive research on their acute effects. To understand the mechanisms underlying microcystin-LR (MC-LR)-induced inflammation-associated diseases. Mice were exposed to MC-LR for one year at concentrations comparable to human environmental exposure levels. Comprehensive pathological observation and multi-omics approaches based on 16S rRNA gene sequencing, untargeted metabolomics, transcriptomics and proteomics were conducted across various organs. Daily exposure to MC-LR induced intestinal microbial dysbiosis and colitis-like changes. It also caused systemic chronic inflammation marked by elevated serum levels of inflammatory cytokines, inflammation-associated pathological changes, and identification of infection-related genes/proteins within the gut-brain-spleen-liver axis. Furthermore, multi-omics analysis across organs suggested that Muribaculaceae may promote a systemic infection-inflammatory response, relying on kynurenine metabolites signaling in peripheral tissues. In contrast, Lachnospiraceae may act an opposing role, dependent on intestinal indole derivatives via the neuroimmunomodulation pathway. A fecal microbiota transplantation experiment confirmed that alterations in Muribaculaceae and Lachnospiraceae resulting from exposure to MC-LR triggered the local and systemic chronic inflammation in mice. This study light on the potential strategies employed by gut microbial community in regulating MC-induced inflammation-associated chronic diseases under repeated exposure through drinking water.},
}

@article {pmid39301964,
year = {2024},
author = {Bohm, MS and Ramesh, AV and Pierre, JF and Cook, KL and Murphy, EA and Makowski, L},
title = {Fecal microbiome transfer an investigative tool and treatment strategy in cancer.},
journal = {American journal of physiology. Gastrointestinal and liver physiology},
volume = {},
number = {},
pages = {},
doi = {10.1152/ajpgi.00171.2024},
pmid = {39301964},
issn = {1522-1547},
support = {R01CA253329//HHS | NIH | National Cancer Institute (NCI)/ ; U01CA272541//HHS | NIH | National Cancer Institute (NCI)/ ; U01CA272977//HHS | NIH | National Cancer Institute (NCI)/ ; R01CA246809//HHS | NIH | National Cancer Institute (NCI)/ ; BC210715//U.S. Department of Defense (DOD)/ ; },
abstract = {The gut microbiome plays a critical role in the development, progression, and treatment of cancer. As interest in microbiome-immune-cancer interactions expands, the prevalence of fecal microbial transplant (FMT) models has increased proportionally. However, current literature does not provide adequate details or consistent approaches to allow for necessary rigor and experimental reproducibility. In this review, we evaluate key studies utilizing FMT to investigate the relationship between the gut microbiome and various types of cancer. Additionally, we will discuss the common pitfalls of these experiments and methods for improved standardization and validation as the field utilizes FMT with greater frequency. Last, this review focuses on the impacts of the gut and extra-intestinal microbes, pre-biotics, pro-biotics, and post-biotics in cancer risk and response to therapy across a variety of tumor types.},
}

@article {pmid39301264,
year = {2024},
author = {Zhao, Y and Ma, S and Liang, L and Cao, S and Fan, Z and He, D and Shi, X and Zhang, Y and Liu, B and Zhai, M and Wu, S and Kuang, F and Zhang, H},
title = {Gut Microbiota-Metabolite-Brain Axis Reconstitution Reverses Sevoflurane-Induced Social and Synaptic Deficits in Neonatal Mice.},
journal = {Research (Washington, D.C.)},
volume = {7},
number = {},
pages = {0482},
pmid = {39301264},
issn = {2639-5274},
abstract = {Background: The mechanisms underlying social dysfunction caused by repeated sevoflurane in early life remain unclear. Whether the gut microbiota-metabolite-brain axis is involved in the mechanism of sevoflurane developmental neurotoxicity still lacks report. Methods: Mice received 3% sevoflurane at postnatal day (PND) 6, 7, and 8 for 2 h per day. Metagenomic sequencing and untargeted metabolomic analysis were applied to investigate the effects of sevoflurane on gut microbiota and metabolism. The animal social behavior and the synaptic development were analyzed during PND 35. Subsequently, fecal microbiota transplantation (FMT) from the control group and bile acid administration were performed to see the expected rescuing effect on socially related behaviors that were impaired by repeated sevoflurane exposure in the mice. Results: In the 3-chamber test, sevoflurane-exposed mice spent less time with stranger mice compared with the control group. The density of both the apical and basal spine decreased in mice exposed to sevoflurane. In addition, repeated sevoflurane exposure led to a notable alteration in the gut microbiota and metabolite synthesis, particularly bile acid. FMT reduced the production of intestinal bile acid and attenuated the effect of sevoflurane exposure on social function and synaptic development. Cholestyramine treatment mimics the protective effects of FMT. Conclusions: The gut microbiota-metabolite-brain axis underlies social dysfunction caused by sevoflurane exposure in early age, and bile acid regulation may be a promising intervention to this impairment.},
}

@article {pmid39302074,
year = {2024},
author = {Duan, T and Alim, A and Tian, H and Li, T},
title = {Roundup-Induced Gut Dysbiosis, Irrelevant to Aromatic Amino Acid Deficiency, Impairs the Gut Function in Rats.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.4c04045},
pmid = {39302074},
issn = {1520-5118},
abstract = {Glyphosate, the most popular herbicide globally, has long been considered safe for mammals. However, whether glyphosate can disturb gut microbiota via inhibiting aromatic amino acid (AAA) synthesis has been under debate recently. Here, we evaluated the impacts of chronic exposure to Roundup on gut health with the addition of AAA and explored the mechanism behind Roundup-induced gut dysfunction by performing fecal microbiota transplantation. 500 mg/kg·bw of Roundup, independent of AAA deficiency, caused severe damage to gut function, as characterized by gut microbial dysbiosis, oxidative stress damage, intestinal inflammation, and histopathological injury, particularly in female rats. Notably, similar to Roundup, Roundup-shaped gut microbiome evidently damaged serum, cecum, and colon profiling of oxidative stress biomarkers (malonaldehyde (MDA), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), glutathione (GSH), and H2O2). Moreover, it induced 0.65-, 3.29-, and 2.36-fold increases in colonic IL-1β, IL-6, and TNF-α levels, and 0.34-fold decreases in the IL-10 level. Upon transplanting healthy fecal microbiota to Roundup-treated rats, they exhibited a healthier gut microenvironment with mitigated inflammation, oxidative damage, and intestinal injury. Overall, our findings provide new insights into the safety of Roundup, highlight the crucial role of gut microbiota in Roundup-induced gut dysfunction, and pave the way for developing gut-microbiota-based strategies to address Roundup-related safety issues.},
}

@article {pmid39300177,
year = {2024},
author = {Hunthai, S and Usawachintachit, M and Taweevisit, M and Srisa-Art, M and Anegkamol, W and Tosukhowong, P and Rattanachaisit, P and Chuaypen, N and Dissayabutra, T},
title = {Unraveling the role of gut microbiota by fecal microbiota transplantation in rat model of kidney stone disease.},
journal = {Scientific reports},
volume = {14},
number = {1},
pages = {21924},
pmid = {39300177},
issn = {2045-2322},
support = {B36G660010//the Program Management Unit for Human Resources and Institutional Development, Research, and Innovation (PMU-B)/ ; RA65/045//Ratchadapiseksompotch Fund, Faculty of Medicine, Chulalongkorn University, grant number/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome ; *Fecal Microbiota Transplantation ; *Kidney Calculi/microbiology/metabolism/therapy ; Humans ; Rats ; Male ; *Rats, Wistar ; Dysbiosis/microbiology ; Disease Models, Animal ; Feces/microbiology ; Female ; Adult ; Middle Aged ; },
abstract = {Emerging research on the microbiome highlights the significant role of gut health in the development of kidney stones, indicating that an imbalance in gut bacteria or dysbiosis can influence the formation of stones by altering oxalate metabolism and urinary metabolite profiles. In particular, the overabundance of specific bacteria such as Enterococcus and Oxalobacter spp., which are known to affect oxalate absorption, is observed in patients with urolithiasis. This study investigates the effects of gut dysbiosis on urolithiasis through fecal microbiota transplantation (FMT) from patients to rats and its impact on urinary mineral excretion and stone formation. Fecal samples from eight patients with calcium oxalate stones and ten healthy volunteers were collected to assess the gut microbiome. These samples were then transplanted to antibiotic-pretreated Wistar rats for a duration of four weeks. After transplantation, we evaluated changes in the fecal gut microbiome profile, urinary mineral excretion rates, and expression levels of intestinal zonula occluden-1 (ZO-1), SLC26A6 and renal NF-κB. In humans, patients with urolithiasis exhibited increased urinary calcium and oxalate levels, along with decreased citrate excretion and increased urinary supersaturation index. The fecal microbiota showed a notable abundance of Bacteroidota. In rodents, urolithiasis-FMT rats showed urinary disturbances similar to patients, including elevated pH, oxalate level, and supersaturation index, despite negative renal pathology. In addition, a slight elevation in the expression of renal NF-κB, a significant intestinal SLC26A6, and a reduction in ZO-1 expression were observed. The gut microbiome of urolithiasis-FMT rats showed an increased abundance of Bacteroidota, particularly Muribaculaceae, compared to their healthy FMT counterparts. In conclusion, the consistent overabundance of Bacteroidota in both urolithiasis patients and urolithiasis-FMT rats is related to altered intestinal barrier function, hyperoxaluria, and renal inflammation. These findings suggest that gut dysbiosis, characterized by an overgrowth of Bacteroidota, plays a crucial role in the pathogenesis of calcium oxalate urolithiasis, underscoring the potential of targeting the gut microbiota as a therapeutic strategy.},
}

Animals
*Gastrointestinal Microbiome
*Fecal Microbiota Transplantation
*Kidney Calculi/microbiology/metabolism/therapy
Humans
Rats
Male
*Rats, Wistar
Dysbiosis/microbiology
Disease Models, Animal
Feces/microbiology
Female
Adult
Middle Aged

@article {pmid39300146,
year = {2024},
author = {Juhász, B and Horváth, K and Kuti, D and Shen, J and Feuchtinger, A and Zhang, C and Bata-Vidács, I and Nagy, I and Kukolya, J and Witting, M and Baranyi, M and Ferenczi, S and Walch, A and Sun, N and Kovács, KJ},
title = {Dipeptide metabolite, glutamyl-glutamate mediates microbe-host interaction to boost spermatogenesis.},
journal = {Scientific reports},
volume = {14},
number = {1},
pages = {21864},
pmid = {39300146},
issn = {2045-2322},
support = {SFB 824 C04//Deutsche Forschungsgemeinschaft/ ; 124424//Hungarian National Research, Development and Innovation Office/ ; -1.2.1-NKP-2017-00002//National Brain Research Program 2017/ ; RRF-2.3.1-21-2022-00011//National Laboratory of Translational Neuroscience/ ; },
mesh = {Animals ; Male ; Mice ; *Spermatogenesis ; *Dipeptides/metabolism ; *Testis/metabolism/microbiology ; Sperm Count ; Fecal Microbiota Transplantation ; Testosterone/metabolism ; Host Microbial Interactions ; Metabolomics/methods ; Gastrointestinal Microbiome ; Fertility ; },
abstract = {The decrease in sperm count and infertility is a global issue that remains unresolved. By screening environmental bacterial isolates, we have found that a novel lactic acid bacterium, Lactiplantibacillus plantarum SNI3, increased testis size, testosterone levels, sperm count, sexual activity and fertility in mice that have consumed the bacteria for four weeks. The abundance of L. plantarum in the colon microbiome was positively associated with sperm count. Fecal microbiota transplantation (FMT) from L. plantarum SNI3-dosed mice improved testicular functions in microbiome-attenuated recipient animals. To identify mediators that confer pro-reproductive effects on the host, untargeted in situ mass spectrometry metabolomics was performed on testis samples of L. plantarum SNI3-treated and control mice. Enrichment pathway analysis revealed several perturbed metabolic pathways in the testis of treated mice. Within the testis, a dipeptide, glutamyl-glutamate (GluGlu) was the most upregulated metabolite following L. plantarum SNI3 administration. To validate the pro-reproductive feature of GluGlu, systemic and local injections of the dipeptide have been performed. γ-GluGlu increased sperm count but had no effect on testosterone. These findings highlight the role of γ-GluGlu in mediating spermatogenetic effects of L. plantarum on the male mouse host and -following relevant human clinical trials- may provide future tools for treating certain forms of male infertility.},
}

Animals
Male
Mice
*Spermatogenesis
*Dipeptides/metabolism
*Testis/metabolism/microbiology
Sperm Count
Fecal Microbiota Transplantation
Testosterone/metabolism
Host Microbial Interactions
Metabolomics/methods
Gastrointestinal Microbiome
Fertility

@article {pmid39299827,
year = {2024},
author = {Sanabani, SS},
title = {Impact of Gut Microbiota on Lymphoma: New Frontiers in Cancer Research.},
journal = {Clinical lymphoma, myeloma & leukemia},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.clml.2024.08.008},
pmid = {39299827},
issn = {2152-2669},
abstract = {The gut microbiome (GMB), which is made up of various microorganisms, plays a crucial role in maintaining the health of the host. Disruptions in this delicate ecosystem, known as microbial dysbiosis, have been linked to various diseases, including hematologic malignancies such as lymphoma. This review article explores the complex relationship between the GMB and the development of lymphoma and highlights its implications for diagnostic and therapeutic approaches. It discusses how GMB influences lymphoma development directly through the presence of certain microorganisms and indirectly through changes in the immune system. The clinical relevance of GMB is highlighted and its potential utility for diagnosis, predicting treatment outcomes and developing personalized therapeutic strategies for lymphoma patients is demonstrated. The review also looks at microbiome-targeted interventions such as fecal microbiome transplantation and dietary modification, which have shown promise for treating microbial dysbiosis and improving patient outcomes. In addition, it highlights the analytical challenges and the need for further research to fully elucidate the mechanistic functions of the GMB in the context of lymphoma. This review emphasizes the critical role of GMB in lymphomagenesis and its potential for the development of diagnostic and therapeutic strategies.},
}

@article {pmid37204182,
year = {2024},
author = {Wu, X and Tian, X and Cao, G and Wang, Z and Wu, X and Gu, Y and Yan, T},
title = {Distinct profiles of bile acid metabolism caused by gut microbiota in kidney transplantation recipients revealed by 16S rRNA gene sequencing.},
journal = {Archives of physiology and biochemistry},
volume = {130},
number = {5},
pages = {581-590},
doi = {10.1080/13813455.2023.2212331},
pmid = {37204182},
issn = {1744-4160},
mesh = {*Kidney Transplantation/adverse effects ; *Gastrointestinal Microbiome ; Humans ; *Bile Acids and Salts/metabolism ; *RNA, Ribosomal, 16S/genetics ; Male ; Female ; Adult ; Middle Aged ; Phylogeny ; Feces/microbiology ; },
abstract = {The present study sought to characterise the gut microbiota of subjects with kidney transplantation and healthy control to identify the distinct gut microbiota and analyse their potential function. We found that gut microbiota abundance had significant differences in subjects between the two groups. Line Discriminant Analysis (LDA) Effect Size (LEfSe) analysis showed that the bacterial taxa were differentially represented between the two groups, and the potential biomarkers at different taxonomic levels in kidney transplant recipients were Streptococcus, Enterococcaceae, and Ruminococcus. Phylogenetic investigation of communities by reconstruction of unobserved states (PICRUSt) Functional Inference analyses suggested that the difference in gut microbiota between the two groups was correlated with bile acid metabolism. In conclusion, gut microbiota abundance is different between the two groups, which is related to bile acid metabolism, and may influence the metabolic homeostasis of allograft recipients.},
}

*Kidney Transplantation/adverse effects
*Gastrointestinal Microbiome
Humans
*Bile Acids and Salts/metabolism
*RNA, Ribosomal, 16S/genetics
Male
Female
Adult
Middle Aged
Phylogeny
Feces/microbiology

@article {pmid39299249,
year = {2024},
author = {Aubert, O and Irvine, WFE and Aminoff, D and de Blaauw, I and Cascio, S and Cretolle, C and Iacobelli, BD and Mantzios, K and Midrio, P and Miserez, M and Sarnacki, S and Schmiedeke, E and Schwarzer, N and Sloots, C and Stenström, P and Lacher, M and Gosemann, JH},
title = {European Reference Network eUROGEN Guidelines on the Management of Anorectal Malformations, Part II: Treatment.},
journal = {European journal of pediatric surgery : official journal of Austrian Association of Pediatric Surgery ... [et al] = Zeitschrift fur Kinderchirurgie},
volume = {},
number = {},
pages = {},
doi = {10.1055/s-0044-1791257},
pmid = {39299249},
issn = {1439-359X},
abstract = {INTRODUCTION: Anorectal malformations (ARMs) are rare birth defects affecting the anorectum and oftentimes the genitourinary region. The management of ARM patients is complex and requires highly specialized surgical and medical care. The European Reference Network eUROGEN for rare and complex urogenital conditions aimed to develop comprehensive guidelines for the management of ARM applicable on a European level.

METHODS:  The Dutch Quality Standard for ARM served as the basis for the development of guidelines. Literature was searched in Medline, Embase, and Cochrane. The ADAPTE method was utilized to incorporate the newest available evidence. A panel of 15 experts from seven European countries assessed currency, acceptability, and applicability of recommendations. Recommendations from the Dutch Quality Standard were adapted, adopted, or rejected and recommendations were formed considering the current evidence, expert opinion, and the European context.

RESULTS:  Surgical and medical treatment of ARM, postoperative instructions, toilet training, and management of fecal and urinary incontinence were addressed. Seven new studies were identified. The panel adapted 23 recommendations, adopted 3, and developed 8 de novo. The overall level of newly found evidence was considered low.

CONCLUSION:  Treatment of ARM patients requires a multidisciplinary team and expertise about anatomical and surgical aspects of the disease, as well as long-term follow-up. This guideline offers recommendations for surgical and medical treatment of ARM and associated complications, according to the best available evidence and applicable on a European level.},
}

@article {pmid39298907,
year = {2024},
author = {Kaul, R and Paul, P and Harfouche, M and Ayyan, M and Laws, S and Chaari, A},
title = {The effect of microbiome-modulating therapeutics on glucose homeostasis in metabolic syndrome: A systematic review, meta-analysis, and meta-regression of clinical trials.},
journal = {Diabetes & metabolic syndrome},
volume = {18},
number = {8},
pages = {103118},
doi = {10.1016/j.dsx.2024.103118},
pmid = {39298907},
issn = {1878-0334},
abstract = {BACKGROUND: Metabolic syndrome (MetS) is a chronic disorder featuring overweight/obesity, high blood pressure, and dysfunction of lipid and carbohydrate metabolism. Microbiome-modulating probiotics, prebiotics, synbiotics and fecal microbiota transplant (FMT) are promising adjunct therapies for improving parameters of glucose homeostasis and insulinemia.

METHODS: We conducted a comprehensive systematic review, meta-analyses, and meta-regressions to investigate the effect of the abovementioned microbiome therapies on various biomarkers after screening clinical trials published through April 2023. We pooled data using random effects meta-analyses, reporting them as mean differences (MDs) with 95 % confidence intervals (CIs), and conducting univariate linear model meta-regressions.

RESULTS: Data from 21 trial comparisons across 19 studies (n = 911) revealed that, compared to placebo/control, microbiome-modulating therapies were associated with statistically significant changes in fasting plasma glucose (MD: 4.03 mg/dL [95%CI: 6.93; -1.13]; p effect = 0.006, I[2] = 89.8 %), and fasting insulin (MD: 2.56 μU/mL [95%CI: 4.28; -0.84]; p effect = 0.004, I[2] = 87.9 %), but not insulin resistance or sensitivity indices and HbA1c. Age, baseline BMI, baseline biomarker value, pro/synbiotic dosage, trial duration, nutraceutical type, and WHO region were factors affecting the efficacy of these interventions at producing changes in biomarkers, signaling the potential role of personalized precision medicine adjunct therapy for deranged glucose homeostasis in patients with MetS. Nevertheless, presence of heterogeneity calls for further investigation before their clinical application.

CONCLUSIONS: Probiotics, prebiotics, synbiotics and FMT supplementation improved fasting glucose and insulin in patients with MetS. Further large-scale and high-quality trials are required before potential clinical applications.},
}

@article {pmid39298815,
year = {2024},
author = {Wang, XZ and Huang, JL and Zhang, J and Li, QH and Zhang, PP and Wu, C and Jia, YY and Su, H and Sun, X},
title = {Fecal microbiota transplantation as a new way for OVA-induced atopic dermatitis of juvenile mice.},
journal = {International immunopharmacology},
volume = {142},
number = {Pt B},
pages = {113183},
doi = {10.1016/j.intimp.2024.113183},
pmid = {39298815},
issn = {1878-1705},
abstract = {Children all over the world suffer from atopic dermatitis (AD), a prevalent condition that impairs their health. Corticosteroids, which have long-term negative effects, are frequently used to treat AD. There has been a growing body of research on the gut microbiota's function in AD. Nevertheless, the function and underlying mechanisms of fecal microbiota transplantation (FMT) in AD children remain to be established. Therefore, in order to assess the preventive effects of FMT treatment on AD and investigate the mechanisms, we constructed an ovalbumin (OVA)-induced juvenile mouse AD model in this investigation. This study explored the role and mechanism of FMT treatment in AD through 16S RNA sequencing, pathological histological staining, molecular biology, and Flow cytometry. Results demonstrated that the FMT treatment improved the gut microbiota's diversity and composition, bringing it back to a level similar to that of a close donor. Following FMT treatment, OVA-specific antibodies were inhibited, immunoglobulin (Ig) E production was decreased, the quantity of mast cells and eosinophils was decreased, and specific inflammatory markers in the skin and serum were decreased. Further mechanistic studies revealed that FMT treatment induced CD103[+] DCs and programmed cell death ligand 1 (PD-L1)/programmed cell death 1 (PD-1) expression in skin-draining lymph nodes and promoted Treg production to induce immune tolerance and suppress skin inflammation. Meanwhile, changes in the gut microbiota were substantially correlated with Th2 cytokines, OVA-specific antibodies, and PD-L1/PD-1. In conclusion, FMT regulates the Th1/Th2 immunological balance and the gut microbiota. It may also inhibit AD-induced allergy responses through the PD-L1/PD-1 pathway, and providing a unique idea and possibly a fresh approach to the treatment of AD.},
}

@article {pmid39295732,
year = {2024},
author = {Wang, S and Yuan, Z and Gao, X and Wu, J and Ren, Y and Yu, X and Li, J and Wei, W},
title = {Global research trends on the links between gut microbiota and radiotherapy: a bibliometric analysis (2004-2023).},
journal = {Frontiers in cellular and infection microbiology},
volume = {14},
number = {},
pages = {1414196},
pmid = {39295732},
issn = {2235-2988},
mesh = {*Gastrointestinal Microbiome ; *Bibliometrics ; Humans ; *Radiotherapy ; China ; },
abstract = {BACKGROUND: There is a crosstalk between gut microbiota and radiotherapy. The aim of this study is to use bibliometric analysis to explore the research status and development trends of research on gut microbiota and radiotherapy.

METHODS: A literature search regarding publications on gut microbiota and radiotherapy from 2004 to 2023 was retrieved. CiteSpace and VOSviewer were used to conduct the bibliometric analysis. The growth rate of publications, leading countries and institutions, preferred journals, top authors and co-cited authors, top co-cited references, keywords and citation were analyzed in this study.

RESULTS: A total of 2821 papers were extracted. The number of papers has increased rapidly over the past decade, especially after 2017. The USA and China had the most publications and made great contributions to this field. The Chinese Academy of Sciences stood out as the institution with the highest number of publications, followed by the Chinese Academy of Medical Sciences & Peking Union Medical College. The most influential authors were Fan Saijun and Li Yuan. PLoS One had the most publications and the most total citations. Highly cited papers and high-frequency keywords illustrated the current status and trends. Furthermore, analysis of keyword with burst revealed that immunotherapy, acid, intestinal barrier, therapy, immunotherapy, fecal microbiota transplantation, etc, are at the forefront of research in this area.

CONCLUSION: This study provides an overview of research on gut microbiota and radiotherapy, highlighting influential contributors, impactful publications, and emerging trends. Our finding suggests avenues for further exploration to improve clinical outcomes.},
}

*Gastrointestinal Microbiome
*Bibliometrics
Humans
*Radiotherapy
China

@article {pmid39295910,
year = {2023},
author = {Sehn Hilgert, S and Dias, DPM},
title = {The intestinal microbiota as an ally in the treatment of Alzheimer's disease.},
journal = {Gut microbiome (Cambridge, England)},
volume = {4},
number = {},
pages = {e9},
pmid = {39295910},
issn = {2632-2897},
abstract = {The evolution of the understanding of the intestinal microbiota and its influence on our organism leverages it as a potential protagonist in therapies aimed at diseases that affect not only the intestine but also neural pathways and the central nervous system itself. This study, developed from a thorough systematic review, sought to demonstrate the influence of the intervention on the intestinal microbiota in subjects with Alzheimer's disease. Clinical trials using different classes of probiotics have depicted noteworthy remission of symptoms, whose measurement was performed based on screenings and scores applied before, during, and after the period of probiotics use, allowing the observation of changes in functionality and symptomatology of patients. On the other hand, faecal microbiota transplantation requires further validation through clinical trials, even though it has already been reported in case studies as promising from the symptomatology point of view. The current compilation of studies made it possible to demonstrate the potential influence of the intestinal microbiota on Alzheimer's pathology. However, new clinical studies with a larger number of participants are needed to obtain further clarification on pathophysiological correlations.},
}

@article {pmid39295774,
year = {2022},
author = {Iribarren, C and Maasfeh, L and Öhman, L and Simrén, M},
title = {Modulating the gut microenvironment as a treatment strategy for irritable bowel syndrome: a narrative review.},
journal = {Gut microbiome (Cambridge, England)},
volume = {3},
number = {},
pages = {e7},
pmid = {39295774},
issn = {2632-2897},
abstract = {Irritable bowel syndrome (IBS) is a disorder of gut-brain interaction with a complex pathophysiology. Growing evidence suggests that alterations of the gut microenvironment, including microbiota composition and function, may be involved in symptom generation. Therefore, attempts to modulate the gut microenvironment have provided promising results as an indirect approach for IBS management. Antibiotics, probiotics, prebiotics, food and faecal microbiota transplantation are the main strategies for alleviating IBS symptom severity by modulating gut microbiota composition and function (eg. metabolism), gut barrier integrity and immune activity, although with varying efficacy. In this narrative review, we aim to provide an overview of the current approaches targeting the gut microenvironment in order to indirectly manage IBS symptoms.},
}

@article {pmid39293564,
year = {2024},
author = {Zhang, M and Yin, YS and May, KS and Wang, S and Purcell, H and Zhang, XS and Blaser, MJ and den Hartigh, LJ},
title = {The role of intestinal microbiota in physiologic and body compositional changes that accompany CLA-mediated weight loss in obese mice.},
journal = {Molecular metabolism},
volume = {},
number = {},
pages = {102029},
doi = {10.1016/j.molmet.2024.102029},
pmid = {39293564},
issn = {2212-8778},
abstract = {BACKGROUND: Obesity continues to be a major problem, despite known treatment strategies such as lifestyle modifications, pharmaceuticals, and surgical options, necessitating the development of novel weight loss approaches. The naturally occurring fatty acid, 10,12 conjugated linoleic acid (10,12 CLA), promotes weight loss by increasing fat oxidation and browning of white adipose tissue, leading to increased energy expenditure in obese mice. Coincident with weight loss, 10,12 CLA also alters the murine gut microbiota by enriching for microbes that produce short chain fatty acids (SCFAs), with concurrent elevations in fecal butyrate and plasma acetate.

METHODS: To determine if the observed microbiota changes are required for 10,12 CLA-mediated weight loss, adult male mice with diet-induced obesity were given broad-spectrum antibiotics (ABX) to perturb the microbiota prior to and during 10,12 CLA-mediated weight loss. Conversely, to determine whether gut microbes were sufficient to induce weight loss, conventionally-raised and germ-free mice were transplanted with cecal contents from mice that had undergone weight loss by 10,12 CLA supplementation.

RESULTS/CONCLUSION: While body weight was minimally modulated by ABX-mediated perturbation of gut bacterial populations, adult male mice given ABX were more resistant to the increased energy expenditure and fat loss that are induced by 10,12 CLA supplementation. Transplanting cecal contents from donor mice losing weight due to oral 10,12 CLA consumption into conventional or germ-free mice led to improved glucose metabolism with increased butyrate production. These data suggest a critical role for the microbiota in diet-modulated changes in energy balance and glucose metabolism, and distinguish the metabolic effects of orally delivered 10,12 CLA from cecal transplantation of the resulting microbiota.},
}

@article {pmid39293366,
year = {2024},
author = {Chen, S and Xue, X and Zhang, H and Huang, X and Lin, X and He, J and Chen, L and Luo, S and Gao, J},
title = {Jianwei Shoutai Pills alleviates miscarriage by modulating gut microbial production of BAs and NLRP3-inflammasome at the maternal-fetal interface of rats.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {135},
number = {},
pages = {156000},
doi = {10.1016/j.phymed.2024.156000},
pmid = {39293366},
issn = {1618-095X},
abstract = {BACKGROUND: Miscarriage has the characteristics of recurrent attacks and complex etiology, so it is gradually attracted the wide attention of scholars in the fields of reproduction. Potential association between gut microbiome (GM) and pregnancy disorders has been investigated. Jianwei Shoutai pills (JWP), as a representative formula, have been proven to have protective effect in both clinical and experimental research in miscarriage. However, the specific mechanism of JWP in miscarriage through GM remains unclear.

PURPOSE: To investigate the underlying mechanism of JWP against miscarriage through the gut-uterus axis.

METHODS: The effects of JWP on an RU486-induced rat model of miscarriage were evaluated by embryo resorption rate, vaginal bleeding rate, and appearance of the uterus and embryo. We used 16S rRNA sequencing to measure the extent of the effect of JWP on GM of rats with miscarriage. Bile acid (BA) content of the feces of rats treated with JWP was evaluated by high performance liquid chromatography-tandem mass spectrometry (HPLC-MS). The activation of bile acid-associated receptor, Farnesoid X receptor (FXR), was evaluated by immunofluorescence. The expression level of NLRP3 inflammasome-associated protein was detected by Western blot or Elisa. Fecal microbiota transplantation (FMT) was used to confirm that GM was essential for the therapeutic effect of JWP in miscarriage.

RESULTS: JWP significantly ameliorated miscarriage symptoms and embryo resorption rate caused by RU486-induced miscarriage as well as restored the abnormal activation of NLRP3-inflammasome at the maternal-fetal interface. Furthermore, JWP can significantly regulated GM dysbiosis and closely associated with BA metabolism by KEGG pathway prediction analysis. Several BA content were significantly restored by HPLC-MS. The expression of NLRP3 inflammasome-associated protein at maternal-fetal interface was reversed by JWP. Combined with FMT, JWP could regulate activation of NLRP3 at the maternal-fetal interface by BAs produced by GM.

CONCLUSION: JWP restored abnormal activation of the NLRP3-inflammasome in an RU486-induced miscarriage rat model, and corrected the BA disorder by regulating imbalance of the GM.},
}

@article {pmid39292598,
year = {2024},
author = {Goldsmith, J and Tomkovich, S and Auniņš, JG and McGovern, BH and Mahoney, JC and Hasson, BR and McChalicher, CWJ and Ege, DS},
title = {End-to-end donor screening and manufacturing controls: complementary quality-based strategies to minimize patient risk for donor-derived microbiome therapeutics.},
journal = {Gut microbes},
volume = {16},
number = {1},
pages = {2402550},
doi = {10.1080/19490976.2024.2402550},
pmid = {39292598},
issn = {1949-0984},
mesh = {Humans ; *Fecal Microbiota Transplantation ; *Gastrointestinal Microbiome/drug effects ; *Feces/microbiology ; *Donor Selection ; Enema ; },
abstract = {Advances in microbiome therapeutics have been motivated by a deeper understanding of the role that the gastrointestinal microbiome plays in human health and disease. The FDA approval of two stool-derived live biotherapeutic products (LBPs), REBYOTA® 150 mL enema (fecal microbiota, live-jslm; formerly RBX2660) and VOWST® oral capsules (fecal microbiota spores, live-brpk; formerly SER-109), for the prevention of recurrent CDI in adults following antibiotic treatment for recurrent CDI provides promise and insights for the development of LBPs for other diseases associated with microbiome dysfunction. Donor-derived products carry risk of disease transmission that must be mitigated through a robust donor screening program and downstream manufacturing controls. Most published recommendations for donor screening practices are prescriptive and do not include a systematic, risk-based approach for donor stool-derived products. A general framework for an end-to-end donor screening program is needed using risk management strategies for donor-derived microbiome therapeutic using a matrixed approach, combining the elements of donor screening with manufacturing controls that are designed to minimize risk to patients. A donor screening paradigm that incorporates medical history, physical examination, laboratory testing, and donor sample inspection are only the first steps in reducing risk of transmission of infectious agents. Manufacturing controls are the cornerstone of risk mitigation when screening unwittingly fails. Failure Mode and Effects Analysis (FMEA) can be used as a tool to assess for residual risk that requires further donor or manufacturing controls. Together, a well-reasoned donor program and manufacturing controls are complementary strategies that must be revisited and reexamined frequently with constant vigilance to mitigate risk to patients. In the spirit of full disclosure and informed consent, physicians should discuss any limitations in the donor screening and manufacturing processes with their patients prior to treatment with microbiome-based therapeutics.},
}

Humans
*Fecal Microbiota Transplantation
*Gastrointestinal Microbiome/drug effects
*Feces/microbiology
*Donor Selection
Enema

@article {pmid39290901,
year = {2024},
author = {Polak, K and Muszyński, T and Frątczak, A and Meznerics, F and Bánvölgyi, A and Kiss, N and Miziołek, B and Bergler-Czop, B},
title = {Study of gut microbiome alterations in plaque psoriasis patients compared to healthy individuals.},
journal = {Postepy dermatologii i alergologii},
volume = {41},
number = {4},
pages = {378-387},
pmid = {39290901},
issn = {1642-395X},
abstract = {INTRODUCTION: Many studies have shown significant alterations in the gut microbiome of patients with psoriasis compared to healthy controls.

AIM: The primary objective of the current research was to explore the impact of gut microbiome composition on the progression and severity of plaque psoriasis.

MATERIAL AND METHODS: A total of 20 patients with moderate-to-severe psoriasis and 20 healthy individuals were recruited and provided a stool sample to assess the gut microbiome. After the samples were prepared according to the NGS library preparation workflow, they were sequenced using the Illumina platform and the report was generated that underwent statistical analysis.

RESULTS: The microbiome profiles of psoriasis patients exhibited significant differences compared to healthy controls as evidenced by the statistical analysis of various bacterial genera, with the median abundance significantly lower in psoriasis patients compared to healthy controls (p = 0.033). The analysis of the Firmicutes-to-Bacteroidetes ratio, a commonly evaluated marker of dysbiosis, did not reach statistical significance (p = 0.239). However, there was a noticeable trend towards a higher median ratio in psoriasis patients compared to healthy controls. The ratio did not show significant associations with PASI or BSA but trends towards significance with DLQI (B = -12.11, p = 0.095).

CONCLUSIONS: Overall, the above findings underscore the importance of the gut microbiome in psoriasis and suggest that modulation of specific bacterial genera, especially that with significant differences, could be a potential strategy for therapeutic intervention. Targeting these depleted genera through microbiome-based interventions, such as probiotic supplementation or faecal microbiota transplantation, could potentially help to restore gut homeostasis and alleviate the inflammatory burden in psoriasis.},
}

@article {pmid39289768,
year = {2024},
author = {Lo, SW and Hung, TH and Lin, YT and Lee, CS and Chen, CY and Fang, CJ and Lai, PC},
title = {Clinical efficacy and safety of faecal microbiota transplantation in the treatment of irritable bowel syndrome: a systematic review, meta-analysis and trial sequential analysis.},
journal = {European journal of medical research},
volume = {29},
number = {1},
pages = {464},
pmid = {39289768},
issn = {2047-783X},
support = {NCKUH-11304017//National Cheng Kung University Hospital/ ; },
mesh = {*Irritable Bowel Syndrome/therapy ; Humans ; *Fecal Microbiota Transplantation/methods ; Treatment Outcome ; Quality of Life ; Randomized Controlled Trials as Topic ; },
abstract = {BACKGROUND: The aim of this study is to evaluate the efficacy and safety of faecal microbiota transplantation (FMT) for the treatment of irritable bowel syndrome (IBS).

METHODS: We searched four databases for randomised controlled trials (RCTs) that compared FMT with a control intervention in patients with IBS. The revised Cochrane risk-of-bias (RoB) tool was chosen for appraisal. Meta-analysis with trial sequential analysis (TSA) was conducted. Grading of Recommendations Assessment Development and Evaluation (GRADE) methodology was used to assess the certainty of evidence (CoE).

RESULTS: We included 12 RCTs with a total of 615 participants. Meta-analyses showed no significant difference between the FMT and control groups in terms of clinical responses (relative risk [RR] = 1.44, 95% confidence interval [CI] 0.88-2.33) and changes in IBS Severity Scoring System (IBS-SSS) scores (standardised mean difference [SMD] =  - 0.31, 95% CI  - 0.72 to 0.09) and IBS Quality of Life (IBS-QOL) scores (SMD = 0.30, 95% CI  - 0.09 to 0.69). Subgroup analysis revealed that in studies with low RoB and using endoscopy, nasojejunal tube and rectal enema delivery, FMT led to a significant improvement in clinical responses and changes in IBS-SSS and IBS-QOL scores. TSA suggested that the current evidence is inconclusive and that the CoE is very low.

CONCLUSION: This study suggests that patients with IBS may benefit from FMT especially when it is administered via endoscopy, nasojejunal tube or rectal enema. However, the certainty of evidence is very low. Further research is needed to confirm the efficacy and safety of FMT for IBS treatment.

TRIAL REGISTRATION: PROSPERO registration number CRD42020211002.},
}

*Irritable Bowel Syndrome/therapy
Humans
*Fecal Microbiota Transplantation/methods
Treatment Outcome
Quality of Life
Randomized Controlled Trials as Topic

@article {pmid39288846,
year = {2024},
author = {Chen, Q and Cheng, W and Zhang, J and Chi, C and Lin, M and He, C and Liao, Z and Gong, F},
title = {Fibroblast Growth Factor 21 Improves Insulin Sensitivity by Modulating the Bile Acid-Gut Microbiota Axis in Type Ⅱ Diabetic Mice.},
journal = {Free radical biology & medicine},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.freeradbiomed.2024.09.017},
pmid = {39288846},
issn = {1873-4596},
abstract = {BACKGROUND: Fibroblast growth factor 21 (FGF21) is an important regulator of glycolipid metabolism. However, whether the gut microbiota is related to the anti-diabetic and obesity effects of FGF21 remains unclear.

METHODS: Our research used KO/KO db/db male mice and streptozotocin (STZ)-induced to simulate the construction of two type II diabetic mellitus (T2DM) models, and detected impaired glucose tolerance in the model by using the ipGTT and ITT assays, and collected feces from the model mice for sequencing of the intestinal flora and the content of short-chain fatty acids. H＆E staining was used to detect changes in intestinal tissue, the serum levels of LPS and GLP-1 were detected by ELISA.

RESULTS: In this study, we found that FGF21 significantly improved insulin sensitivity, attenuated intestinal lesions, and decreased serum lipopolysaccharide (LPS) concentrations in T2DM mice. Moreover, FGF21 reshaped the gut microbiota and altered their metabolic pathways in T2DM mice, promoting the production of short-chain fatty acids (SCFAs) and the secretion of glucagon-like peptide 1 (GLP-1). Fecal transplantation experiments further confirmed that feces from FGF21-treated diabetic mice demonstrated similar effects as FGF21 in terms of anti-diabetic activity and regulation of gut microbiota dysbiosis. Additionally, the antibiotic depletion of gut microbiota abolished the beneficial effects of FGF21, including increased GLP-1 secretion and fecal SCFA concentration. Additionally, the FGF21 effects of ameliorating intestinal damage and suppressing plasma LPS secretion were suppressed. All these findings suggest that FGF21 prevents intestinal lesions by modifying the gut microbiota composition. Furthermore, FGF21 affected bile acid synthesis by inhibiting CYP7A1, the key enzyme of bile acid synthesis.

CONCLUSSION: Therefore, FGF21 enriched beneficial bacteria by preventing bile acid synthesis and stimulating the secretion of the intestinal hormone GLP-1 via the increased production of gut microbiota metabolites, thereby exerting its anti-diabetic effects.},
}

@article {pmid39287858,
year = {2024},
author = {Engin, ED},
title = {Microbiota and Lipotoxicity.},
journal = {Advances in experimental medicine and biology},
volume = {1460},
number = {},
pages = {357-372},
pmid = {39287858},
issn = {0065-2598},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Dysbiosis ; *Metabolic Syndrome/microbiology/metabolism ; *Obesity/microbiology/metabolism ; Animals ; Lipid Metabolism ; Inflammation/metabolism/microbiology ; Adipose Tissue/metabolism/immunology ; },
abstract = {Gut microbiota is an indispensable commensal partner of human superorganism. The wealth of genetic repertoire provided by these microorganisms extends host's substrate processing capability. Energy and nutrient harvesting machinery primarily depends on the proper function of these organisms. However, the dynamic composition of microbiota changes with age, lifestyle, stress factors, infections, medications, and host pathophysiological conditions. Host immune system is primarily responsible for shaping up the microbial community and sustaining the symbiotic state. This involves controlling the delicate balance between agility toward pathobionts and tolerance toward symbionts. When things go wrong with this crosstalk, dysbiosis may arise.Metabolic syndrome is a multisystemic, low-grade chronic inflammatory disease that involves dyslipidemia, glucose intolerance, insulin resistance, and central obesity. Excess caloric intake with high-sugar and high-fat diet promote high energy harvesting and lipogenesis. The secretion of adipokines accompanies lipid spillover from fat cells, which contribute to insulin resistance and the expansion of adipose tissue in ectopic sites. Proinflammatory cytokines from adipose tissue macrophages increase the extent of adipose dysfunction.The inflammatory nature of obesity and metabolic syndrome recall the connection between dysbiosis and immune dysfunction. A remarkable association exits between obesity, inflammatory bowel disease, gluten-sensitive enteropathy, and dysbiosis. These conditions compromise the gut mucosa barrier and allow lipopolysaccharide to enter circulation. Unresolved chronic inflammation caused by one condition may overlap or trigger the other(s). Experimental studies and therapeutic trials of fecal microbiota transplantation promise limited improvement in some of these conditions.Typically, metabolic syndrome is considered as a consequence of overnutrition and the vicious cycle of lipogenesis, lipid accumulation, and chronic low-level inflammation. Because of the complex nature of this disorder, it remains inconclusive whether dysbiosis is a cause or consequence of obesity and metabolic syndrome.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Dysbiosis
*Metabolic Syndrome/microbiology/metabolism
*Obesity/microbiology/metabolism
Animals
Lipid Metabolism
Inflammation/metabolism/microbiology
Adipose Tissue/metabolism/immunology

@article {pmid39287045,
year = {2024},
author = {Li, N and Han, X and Ruan, M and Huang, F and Yang, L and Xu, T and Wang, H and Wu, H and Shi, S and Wang, Y and Wu, X and Wang, S},
title = {Prebiotic inulin controls Th17 cells mediated central nervous system autoimmunity through modulating the gut microbiota and short chain fatty acids.},
journal = {Gut microbes},
volume = {16},
number = {1},
pages = {2402547},
pmid = {39287045},
issn = {1949-0984},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Inulin/administration & dosage/pharmacology ; *Encephalomyelitis, Autoimmune, Experimental/immunology/drug therapy/microbiology ; *Th17 Cells/immunology ; Mice ; *Prebiotics/administration & dosage ; *Mice, Inbred C57BL ; Female ; *Fatty Acids, Volatile/metabolism ; *Autoimmunity/drug effects ; *Multiple Sclerosis/immunology/drug therapy/microbiology ; Central Nervous System/immunology ; Bacteria/classification/isolation & purification ; },
abstract = {Multiple sclerosis (MS) is an autoimmune disease characterized by inflammatory demyelination occurring in the central nervous system (CNS). Inulin is a common prebiotic that can improve metabolic disorders by modulating the gut microbiota. However, its capacity to affect CNS autoimmunity is poorly recognized. Experimental autoimmune encephalomyelitis (EAE) is a classical mouse model of MS. Herein, we found that oral administration of inulin ameliorated the severity EAE in mice, accompanied by reductions in inflammatory cell infiltration and demyelination in the CNS. These reductions were associated with decreased proportion and numbers of Th17 cells in brain and spleen. Consistent with the findings, the serum concentrations of IL-17, IL-6, and TNF-α were reduced in inulin treated EAE mice. Moreover, the proliferation of auto-reactive lymphocytes, against MOG35-55 antigen, was attenuated ex vivo. Mechanistically, inulin treatment altered the composition of gut microbiota. It increased Lactobacillus and Dubosiella whereas decreased g_Prevotellaceae_NK3B31_group at the genus level, alongside with elevated concentration of butyric acid in fecal content and serum. In vitro, butyrate, but not inulin, could inhibit the activation of MOG35-55 stimulated lymphocytes. Furthermore, fecal microbiota transplantation assay confirmed that fecal contents of inulin-treated normal mice had an ameliorative effect on EAE mice. In contrast, antibiotic cocktail (ABX) treatment diminished the therapeutic effect of inulin in EAE mice as well as the reduction of Th17 cells, while supplementation with Lactobacillus reuteri restored the amelioration effect. These results confirmed that the attenuation of inulin on Th17 cells and inflammatory demyelination in EAE mice was dependent on its modulation on gut microbiota and metabolites. Our findings provide a potential therapeutic regimen for prebiotic inulin supplementation in patients with multiple sclerosis.},
}

Animals
*Gastrointestinal Microbiome/drug effects
*Inulin/administration & dosage/pharmacology
*Encephalomyelitis, Autoimmune, Experimental/immunology/drug therapy/microbiology
*Th17 Cells/immunology
Mice
*Prebiotics/administration & dosage
*Mice, Inbred C57BL
Female
*Fatty Acids, Volatile/metabolism
*Autoimmunity/drug effects
*Multiple Sclerosis/immunology/drug therapy/microbiology
Central Nervous System/immunology
Bacteria/classification/isolation & purification

@article {pmid39285046,
year = {2024},
author = {Wang, Z and Gong, M and Fang, Y and Yuan, H and Zhang, C},
title = {Reconstruction characteristics of gut microbiota from patients with type 1 diabetes affect the phenotypic reproducibility of glucose metabolism in mice.},
journal = {Science China. Life sciences},
volume = {},
number = {},
pages = {},
pmid = {39285046},
issn = {1869-1889},
abstract = {The human microbiota-associated (HMA) mice model, especially the germ-free (GF)-humanized mice, has been widely used to probe the causal relationships between gut microbiota and human diseases such as type 1 diabetes (T1D). However, most studies have not clarified the extent to which the reconstruction of the human donor microbiota in recipient mice correlates with corresponding phenotypic reproducibility. In this study, we transplanted fecal microbiota from five patients with T1D and four healthy people into GF mice, and microbiota from each donor were transplanted into 10 mice. Mice with similar microbiota structure to the donor exhibited better phenotypic reproducibility. The characteristics of the microbial community assembly of donors also influenced the phenotypic reproducibility in mice, and individuals with a higher proportion of stochastic processes showed more severe disorders. Microbes enriched in patients with T1D had a stronger colonization potential in mice with impaired glucose metabolism, and microbiota functional features related to T1D were better reproduced in these mice. This indicates that assembly traits and colonization efficacy of microbiota influence phenotypic reproducibility in GF-humanized mice. Our findings provide important insights for using HMA mice models to explore links between gut microbiota and human diseases.},
}

@article {pmid39283061,
year = {2024},
author = {McBurney, MI and Cho, CE},
title = {Understanding the role of the human gut microbiome in overweight and obesity.},
journal = {Annals of the New York Academy of Sciences},
volume = {},
number = {},
pages = {},
doi = {10.1111/nyas.15215},
pmid = {39283061},
issn = {1749-6632},
abstract = {The gut microbiome may be related to the prevalence of overweight and obesity, but high interindividual variability of the human microbiome complicates our understanding. Obesity often occurs concomitantly with micronutrient deficiencies that impair energy metabolism. Microbiota composition is affected by diet. Host-microbiota interactions are bidirectional. We propose three pathways whereby these interactions may modulate the gut microbiome and obesity: (1) ingested compounds or derivatives affecting small intestinal transit, endogenous secretions, digestion, absorption, microbiome balance, and gut barrier function directly affect host metabolism; (2) substrate availability affecting colonic microbial composition and contact with the gut barrier; and (3) microbial end products affecting host metabolism. The quantity/concentration, duration, and/or frequency (circadian rhythm) of changes in these pathways can alter the gut microbiome, disrupt the gut barrier, alter host immunity, and increase the risk of and progression to overweight and obesity. Host-specific characteristics (e.g., genetic variations) may further affect individual sensitivity and/or resilience to diet- and microbiome-associated perturbations in the colonic environment. In this narrative review, the effects of selected interventions, including fecal microbiota transplantation, dietary calorie restriction, dietary fibers and prebiotics, probiotics and synbiotics, vitamins, minerals, and fatty acids, on the gut microbiome, body weight, and/or adiposity are summarized to help identify mechanisms of action and research opportunities.},
}

@article {pmid39282548,
year = {2024},
author = {Salvati, F and Catania, F and Murri, R and Fantoni, M and Torti, C},
title = {Clostridioides difficile infection: an update.},
journal = {Le infezioni in medicina},
volume = {32},
number = {3},
pages = {280-291},
pmid = {39282548},
issn = {2532-8689},
abstract = {Clostridioides difficile (C. difficile) is a Gram-positive, spore-forming anaerobic bacterium emerged as a leading cause of diarrhea globally. CDI's (Clostridioides difficile infection) impact on healthcare systems is concerning due to high treatment cost and increased hospitalisation time. The incidence of CDI has been influenced by hypervirulent strains such as the 027 ribotype, responsible for significant outbreaks in North America and Europe. CDI's epidemiology has evolved, showing increased community-acquired cases alongside traditional hospital-acquired infections. Mortality rates remain high, with recurrent infections further elevating the risk. Transmission of C. difficile primarily occurs via spores, which survive in healthcare settings and play a pivotal role in transmission. Not only health workers, but also the food chain could have a significant impact on the transmission of infection, although no confirmed foodborne cases have been documented. Pathogenicity of C. difficile involves spore germination and toxin production. Toxins A and B can cause cellular damage and inflammatory responses in the host, leading to colitis. Clinical picture can range from mild diarrhea to fulminant colitis with toxic megacolon, and bowel perforation. Risk factors for CDI include antibiotic exposure, advanced age, hospitalization, and use of proton pump inhibitors. Patients who experience abdominal surgery or patients with inflammatory bowel disease (IBD) are particularly susceptible due to their compromised gut microbiota. Management of CDI has evolved, with fidaxomicin emerging as a superior treatment option over vancomycin for initial and recurrent infections due to its reduction of recurrence rate. Faecal microbiota transplantation (FMT) is effective for recurrent CDI, restoring gut eubiosis. Bezlotoxumab, a monoclonal antibody against C. difficile toxin B, has shown promise in reducing recurrence rates. Severe cases of CDI may require surgical intervention, particularly in instances of toxic megacolon or bowel perforation. In conclusion, CDI remains a significant clinical entity. Further research are needed to improve patients' outcome and reduce the burden on healthcare systems.},
}

@article {pmid39282183,
year = {2024},
author = {Mishra, V and Mishra, Y},
title = {Role of Gut Microbiome in Cancer Treatment.},
journal = {Indian journal of microbiology},
volume = {64},
number = {3},
pages = {1310-1325},
pmid = {39282183},
issn = {0046-8991},
abstract = {The gut microbiota influences the effectiveness and side effects of cancer treatments, particularly immunotherapy and associated immune-related complications. This important involvement of the microbiome is supported by the patients receiving antibiotics responding poorly to immunotherapy. Relatively few research has examined the underlying processes, and until recently, data regarding the detection of the microbial organisms that trigger these effects were inconsistent. Since then, a deeper comprehension of the processes of action and taxonomic classification of the relevant species has been attained. It's been demonstrated that certain bacterial species can enhance the body's reaction to immune checkpoint inhibitors through the release of distinct metabolites or products. Nonetheless, in certain patients who are not responding, Gram-negative bacteria may have a dominating suppressive impact. Patients' propensity to react to immunotherapy can be somewhat accurately predicted by machine learning techniques based on their microbiome makeup. Consequently, there has been an increase in interest in modifying the microbiome makeup to enhance patient reaction to medication. Clinical proof-of-concept studies demonstrate that dietary modifications or fecal microbiota transplantation (FMT) might be used therapeutically to increase the efficacy of immunotherapy in cancer patients. Current developments and new approaches for microbiota-based cancer treatments have been emphasized. In conclusion, preclinical research on animals and human clinical trials has made tremendous progress in our understanding of the function of the gut microbiome in health and illness. These investigations have shed light on the effects of food, FMT, probiotics, prebiotics, and microbiome-disease connections. However, there are still a lot of issues and restrictions that must be resolved before this research can be used in real-world clinical settings.},
}

@article {pmid39282181,
year = {2024},
author = {Kamath, HS and Shukla, R and Shah, U and Patel, S and Das, S and Chordia, A and Satish, P and Ghosh, D},
title = {Role of Gut Microbiota in Predisposition to Colon Cancer: A Narrative Review.},
journal = {Indian journal of microbiology},
volume = {64},
number = {3},
pages = {1-13},
pmid = {39282181},
issn = {0046-8991},
abstract = {Globally, colorectal cancer (CRC) is a leading cause of cancer-related mortality. Dietary habits, inflammation, hereditary characteristics, and gut microbiota are some of its causes. The gut microbiota, a diverse population of bacteria living in the digestive system, has an impact on a variety of parameters, including inflammation, DNA damage, and immune response. The gut microbiome has a significant role in colon cancer susceptibility. Many studies have highlighted dysbiosis, an imbalance in the gut microbiota's makeup, as a major factor in colon cancer susceptibility. Dysbiosis has the potential to produce toxic metabolites and pro-inflammatory substances, which can hasten the growth of tumours. The ability of the gut microbiota to affect the host's immune system can also influence whether cancer develops or not. By better comprehending these complex interactions between colon cancer predisposition and gut flora, new preventive and therapeutic techniques might be developed. Targeting the gut microbiome with dietary modifications, probiotics, or faecal microbiota transplantation may offer cutting-edge approaches to reducing the risk of colon cancer and improving patient outcomes. The complex connection between the makeup of the gut microbiota and the emergence of colorectal cancer is explored in this narrative review.},
}

@article {pmid39281978,
year = {2024},
author = {Zhang, S and Lu, G and Wang, W and Li, Q and Wang, R and Zhang, Z and Wu, X and Liang, C and Liu, Y and Li, P and Wen, Q and Cui, B and Zhang, F},
title = {A predictive machine-learning model for clinical decision-making in washed microbiota transplantation on ulcerative colitis.},
journal = {Computational and structural biotechnology journal},
volume = {24},
number = {},
pages = {583-592},
pmid = {39281978},
issn = {2001-0370},
abstract = {Machine learning based on clinical data and treatment protocols for better clinical decision-making is a current research hotspot. This study aimed to build a machine learning model on washed microbiota transplantation (WMT) for ulcerative colitis (UC), providing patients and clinicians with a new evaluation system to optimize clinical decision-making. Methods Patients with UC who underwent WMT via mid-gut or colonic delivery route at an affiliated hospital of Nanjing Medical University from April 2013 to June 2022 were recruited. Model ensembles based on the clinical indicators were constructed by machine-learning to predict the clinical response of WMT after one month. Results A total of 366 patients were enrolled in this study, with 210 patients allocated for training and internal validation, and 156 patients for external validation. The low level of indirect bilirubin, activated antithrombin III, defecation frequency and cholinesterase and the elderly and high level of creatine kinase, HCO3 [-] and thrombin time were related to the clinical response of WMT at one month. Besides, the voting ensembles exhibited an area under curve (AUC) of 0.769 ± 0.019 [accuracy, 0.754; F1-score, 0.845] in the internal validation; the AUC of the external validation was 0.614 ± 0.017 [accuracy, 0.801; F1-score, 0.887]. Additionally, the model was available at https://wmtpredict.streamlit.app. Conclusions This study pioneered the development of a machine learning model to predict the one-month clinical response of WMT on UC. The findings demonstrate the potential value of machine learning applications in the field of WMT, opening new avenues for personalized treatment strategies in gastrointestinal disorders. Trial registration clinical trials, NCT01790061. Registered 09 February 2013 - Retrospectively registered, https://clinicaltrials.gov/study/NCT01790061.},
}

@article {pmid39281262,
year = {2024},
author = {Nagesh, VK and Tran, HH and Elias, D and Kianifar Aguilar, I and Sethi, T and Menon, A and Mansour, C and Furman, F and Tsotsos, K and Subar, T and Auda, A and Sidiqui, A and Lamar, J and Wadhwani, N and Dey, S and Lo, A and Atoot, A and Weissman, S and Sifuentes, H and Bangolo, AI},
title = {Therapeutics involved in managing initial and recurrent Clostridium difficile infection: An updated literature review.},
journal = {World journal of gastrointestinal pharmacology and therapeutics},
volume = {15},
number = {5},
pages = {95467},
pmid = {39281262},
issn = {2150-5349},
abstract = {Clostridium difficile infection (CDI) has been increasing due to the effect of recurrent hospitalizations. The use of antibiotics has been shown to alter the gut microbiome and lead to CDIs. The treatment is limited to three major antibiotics; however, the incidence of recurrent CDIs has been increasing and drug resistance is a major concern. This aspect is a growing concern in modern medicine especially in the elderly population, critical care patients, and immunocompromised individuals who are at high risk of developing CDIs. Clostridium difficile can lead to various complications including septic shock and fulminant colitis that could prove to be lethal in these patients. Newer modalities of treatment have been developed including bezlotoxumab, a monoclonal antibody and fecal microbiota transplant. There have been studies showing asymptomatic carriers and drug resistance posing a major threat to the healthcare system. Newer treatment options are being studied to treat and prevent CDIs. This review will provide an insight into the current treatment modalities, prevention and newer modalities of treatment and challenges faced in the treatment of CDIs.},
}

@article {pmid39280427,
year = {2024},
author = {Lima Barrientos, J and Rojas Huerta, A and Perez Mendoza, A and Abreu Lopez, BA and Salolin Vargas, VP and Garcia Gonzalez, OY and Saldaña Ruiz, MA and Diarte, E and Torijano Sarria, AJ},
title = {The Relationship Between Gut Microbiome and Ophthalmologic Diseases: A Comprehensive Review.},
journal = {Cureus},
volume = {16},
number = {8},
pages = {e66808},
pmid = {39280427},
issn = {2168-8184},
abstract = {The gut microbiome has been studied in recent years due to its association with various pathological pathways involved in different diseases, caused by its structure, function, and diversity alteration. The knowledge of this mechanism has generated interest in the investigation of its relationship with ophthalmologic diseases. Recent studies infer the existence of a gut-eye microbiota axis, influenced by the intestinal barrier, the blood-retina barrier, and the immune privilege of the eye. A common denominator among ophthalmologic diseases that have been related to this axis is inflammation, which is perpetuated by dysbiosis, causing an alteration of the intestinal barrier leading to increased permeability and, in turn, the release of components such as lipopolysaccharides (LPS), trimethylamine oxide (TMAO), and bacterial translocation. Some theories explain that depending on how the microbiome is composed, a different type of T cells will be activated, while others say that some bacteria can pre-activate T cells that mimic ocular structures and intestinal permeability that allow leakage of metabolites into the circulation. In addition, therapies such as probiotics, diet, and fecal microbiota transplantation (FMT) have been shown to favor the presence of a balanced population of microorganisms that limit inflammation and, in turn, generate a beneficial effect in these eye pathologies. This review aims to analyze how the intestinal microbiome influences various ocular pathologies based on microbial composition and pathological mechanisms, which may provide a better understanding of the diseases and their therapeutic potential.},
}

@article {pmid39280360,
year = {2024},
author = {Patibandla, S and Bhatt, N and Lief, S and Beauti, SM and Ansari, AZ},
title = {Gut Microbiota Modulation in the Management of Chronic Obstructive Pulmonary Disease: A Literature Review.},
journal = {Cureus},
volume = {16},
number = {8},
pages = {e66875},
pmid = {39280360},
issn = {2168-8184},
abstract = {Chronic obstructive pulmonary disease (COPD) represents a significant global health burden, characterized by progressive airflow limitation and exacerbations that significantly impact patient morbidity and mortality. Recent research has investigated the interplay between the gut and the lungs, known as the gut-lung axis, highlighting the role of the gut microbiome in COPD pathogenesis. Dysbiosis, characterized by microbial imbalance, has implications for COPD, influencing disease progression and susceptibility to exacerbations. This comprehensive review integrates current scientific literature on gut microbiota modulation as a therapeutic avenue for COPD management. Through a thorough discussion of studies investigating probiotics, prebiotics, synbiotics, antibiotics, dietary fiber, and fecal microbiota transplantation, this review summarizes the influence of these interventions on COPD via the gut-lung axis through the modulation of systemic inflammation, mucosal immunity, and metabolic processes. The interventions highlighted here show potential in preventing COPD exacerbations, preserving lung function, and improving patient quality of life. By compiling the latest scientific evidence, this review provides a comprehensive framework for physicians and researchers to deduce the effectiveness of gut microbiome modulation as an adjunctive therapeutic strategy in COPD management.},
}

@article {pmid39280189,
year = {2024},
author = {Jeyaraman, M and Mariappan, T and Jeyaraman, N and Muthu, S and Ramasubramanian, S and Santos, GS and da Fonseca, LF and Lana, JF},
title = {Gut microbiome: A revolution in type II diabetes mellitus.},
journal = {World journal of diabetes},
volume = {15},
number = {9},
pages = {1874-1888},
pmid = {39280189},
issn = {1948-9358},
abstract = {Type II diabetes mellitus (T2DM) has experienced a dramatic increase globally across countries of various income levels over the past three decades. The persistent prevalence of T2DM is attributed to a complex interplay of genetic and environmental factors. While numerous pharmaceutical therapies have been developed, there remains an urgent need for innovative treatment approaches that offer effectiveness without significant adverse effects. In this context, the exploration of the gut microbiome presents a promising avenue. Research has increasingly shown that the gut microbiome of individuals with T2DM exhibits distinct differences compared to healthy individuals, suggesting its potential role in the disease's pathogenesis and progression. This emerging field offers diverse applications, particularly in modifying the gut environment through the administration of prebiotics, probiotics, and fecal microbiome transfer. These inter-ventions aim to restore a healthy microbiome balance, which could potentially alleviate or even reverse the metabolic dysfunctions associated with T2DM. Although current results from clinical trials have not yet shown dramatic effects on diabetes management, the groundwork has been laid for deeper investigation. Ongoing and future clinical trials are critical to advancing our understanding of the microbiome's impact on diabetes. By further elucidating the mechanisms through which microbiome alterations influence insulin resistance and glucose metabolism, researchers can develop more targeted interventions. The potential to harness the gut microbiome in developing new therapeutic strategies offers a compelling prospect to transform the treatment landscape of T2DM, potentially reducing the disease's burden significantly with approaches that are less reliant on traditional pharmaceuticals and more focused on holistic, systemic health improvements.},
}

@article {pmid39278946,
year = {2024},
author = {Messaoudene, M and Ferreira, S and Saint-Lu, N and Ponce, M and Truntzer, C and Boidot, R and Le Bescop, C and Loppinet, T and Corbel, T and Féger, C and Bertrand, K and Elkrief, A and Isaksen, M and Vitry, F and Sablier-Gallis, F and Andremont, A and Bod, L and Ghiringhelli, F and de Gunzburg, J and Routy, B},
title = {The DAV132 colon-targeted adsorbent does not interfere with plasma concentrations of antibiotics but prevents antibiotic-related dysbiosis: a randomized phase I trial in healthy volunteers.},
journal = {Nature communications},
volume = {15},
number = {1},
pages = {8083},
pmid = {39278946},
issn = {2041-1723},
mesh = {Humans ; *Anti-Bacterial Agents/pharmacology/administration & dosage/adverse effects ; *Healthy Volunteers ; Animals ; *Dysbiosis/microbiology/chemically induced ; Female ; Mice ; Adult ; Male ; *Gastrointestinal Microbiome/drug effects ; *Colon/microbiology/drug effects ; *Feces/microbiology/chemistry ; Middle Aged ; Fecal Microbiota Transplantation ; Young Adult ; Immune Checkpoint Inhibitors ; },
abstract = {The deleterious impact of antibiotics (ATB) on the microbiome negatively influences immune checkpoint inhibitors (ICI) response in patients with cancer. We conducted a randomized phase I study (EudraCT:2019-A00240-57) with 148 healthy volunteers (HV) to test two doses of DAV132, a colon-targeted adsorbent, alongside intravenous ceftazidime-avibactam (CZA), piperacillin-tazobactam (PTZ) or ceftriaxone (CRO) and a group without ATB. The primary objective of the study was to assess the effect of DAV132 on ATB plasma concentrations and both doses of DAV132 did not alter ATB levels. Secondary objectives included safety, darkening of the feces, and fecal ATB concentrations. DAV132 was well tolerated, with no severe toxicity and similar darkening at both DAV132 doses. DAV132 led to significant decrease in CZA or PTZ feces concentration. When co-administered with CZA or PTZ, DAV132 preserved microbiome diversity, accelerated recovery to baseline composition and protected key commensals. Fecal microbiota transplantation (FMT) in preclinical cancer models in female mice from HV treated with CZA or PTZ alone inhibited anti-PD-1 response, while transplanted samples from HV treated with ATB + DAV132 circumvented resistance to anti-PD-1. This effect was linked to activated CD8[+] T cell populations in the tumor microenvironment. DAV132 represents a promising strategy for overcoming ATB-related dysbiosis and further studies are warranted to evaluate its efficacy in cancer patients.},
}

Humans
*Anti-Bacterial Agents/pharmacology/administration & dosage/adverse effects
*Healthy Volunteers
Animals
*Dysbiosis/microbiology/chemically induced
Female
Mice
Adult
Male
*Gastrointestinal Microbiome/drug effects
*Colon/microbiology/drug effects
*Feces/microbiology/chemistry
Middle Aged
Fecal Microbiota Transplantation
Young Adult
Immune Checkpoint Inhibitors

@article {pmid39277768,
year = {2024},
author = {Ma, X and Park, HS and Shin, YJ and Kim, JK and Hong, JK and Han, SW and Yoon, IY and Kim, DH},
title = {The extracellular vesicle of depressive patient-derived Escherichia fergusonii induces vagus nerve-mediated neuroinflammation in mice.},
journal = {Journal of neuroinflammation},
volume = {21},
number = {1},
pages = {224},
pmid = {39277768},
issn = {1742-2094},
support = {RS-2024-00344277//the Korea Dementia Research Project/ ; 2017R1A5A2014768//National Research Foundation of Korea/ ; },
mesh = {Animals ; Mice ; *Vagus Nerve/metabolism ; *Extracellular Vesicles/metabolism ; Humans ; Male ; *Neuroinflammatory Diseases/metabolism ; *Depression/metabolism/etiology ; Mice, Inbred C57BL ; Vagotomy ; },
abstract = {BACKGROUND: Gut microbiota dysbiosis is closely associated with psychiatric disorders such as depression and anxiety (DA). In our preliminary study, fecal microbiota transplantation from volunteers with psychological stress and subclinical symptoms of depression (Vsd) induced DA-like behaviors in mice. Escherichia fergusonii (Esf) was found to be more abundant in the feces of Vsd compared to healthy volunteers. Therefore, we investigated the effect of Esf on DA-like behavior and neuroinflammation in mice with and without celiac vagotomy.

METHODS AND RESULTS: Orally gavaged Esf increased DA-like behaviors, tumor necrosis factor (TNF)-α, and toll-like receptor-4 (TLR4) expression, and NF-κB[+]Iba1[+] and lipopolysaccharide (LPS)[+]Iba1[+] cell populations, while decreasing serotonin, 5-HT1A receptor, and brain-derived neurotrophic factor (BDNF) expression in the hippocampus and prefrontal cortex. However, celiac vagotomy attenuated Esf-induced DA-like behavior and neuroinflammation. Orally gavaged extracellular vesicle (EV) from Vsd feces (vfEV) or Esf culture (esEV) induced DA-like behavior and inflammation in hippocampus, prefrontal cortex and colon. However, celiac vagotomy attenuated vfEV- or esEV-induced DA-like behaviors and inflammation in the brain alone, while vfEV- or esEV-induced blood LPS and TNF-α levels, colonic TNF-α expression and NF-κB-positive cell number, and fecal LPS level were not. Although orally gavaged fluorescence isothiocyanate-labeled esEV was translocated into the blood and hippocampus, celiac vagotomy decreased its translocation into the hippocampus alone.

CONCLUSIONS: esEVs may be translocated into the brain via the vagus nerve and bloodstream, subsequently inducing TNF-α expression and suppressing serotonin, its receptor, and BDNF expression through the activation of TLR4-mediated NF-κB signaling, thereby contributing to DA pathogenesis.},
}

Animals
Mice
*Vagus Nerve/metabolism
*Extracellular Vesicles/metabolism
Humans
Male
*Neuroinflammatory Diseases/metabolism
*Depression/metabolism/etiology
Mice, Inbred C57BL
Vagotomy

@article {pmid39277177,
year = {2024},
author = {Meng, Q and Zhang, S and Zhang, C and Liu, B and Zhu, W and Wu, L and Zhang, Q and Li, Y and Wang, X and Bian, H},
title = {Disordered gut microbiota in postmenopausal stage amplifies intestinal tight junction damage to accelerate atherosclerosis.},
journal = {Beneficial microbes},
volume = {},
number = {},
pages = {1-23},
doi = {10.1163/18762891-bja00036},
pmid = {39277177},
issn = {1876-2891},
abstract = {The causes and characteristics of gut microbiota abnormalities and whether microbiota manipulation can prevent atherosclerosis in the postmenopausal stage remain to be determined. Aortic oestrogen receptor expression, histological changes and gut microbiota in women before and after menopause were detected. Serum oestrogen levels, systemic inflammation, intestinal oestrogen receptor expression and histological changes, atherosclerosis, and gut microbiota in low density lipoprotein deletion (LDLR-∕-) female mice before and after ovariectomy were tested. This study examined aortic oestrogen receptor expression, histological changes, and gut microbiota in women before and after menopause, and tested serum oestrogen levels, systemic inflammation, intestinal oestrogen receptor expression, histological changes, atherosclerosis, and gut microbiota in low-density lipoprotein receptor knockout (LDLR-∕-) female mice before and after ovariectomy. We demonstrated that the downregulation of oestrogen and oestrogen receptors after menopause promotes gut microbiota disturbance in both women and female mice. We found that gut microbiota disturbance amplifies the intestinal barrier damage and aggravates systemic inflammation, thereby promoting atherosclerosis in female mice. Faecal microbiota transplantation and antibiotics inhibit the proinflammatory properties of gut microbiota and prevent atherosclerosis by reducing intestinal barrier damage in postmenopausal mice. Together, our study highlights the causes of gut microbiota disturbances and the role of microbiota manipulation in preventing atherosclerosis in postmenopausal stage.},
}

@article {pmid39276451,
year = {2024},
author = {Tian, Y and Tian, R and He, J and Guo, Y and Yan, P and Chen, Y and Li, R and Wang, B},
title = {Toralactone alleviates cisplatin-induced acute kidney injury by modulating the gut microbiota-renal axis.},
journal = {International immunopharmacology},
volume = {142},
number = {Pt A},
pages = {113115},
doi = {10.1016/j.intimp.2024.113115},
pmid = {39276451},
issn = {1878-1705},
abstract = {BACKGROUND: Gut microbiota has been reported to be perturbed by cisplatin and to modulate the nephrotoxicity of chemotherapeutic agents. However, the critical role of toralactone, a bioactive components of Cassia obtusifolia L. seeds, in modulating the gut microbiota in the pathogenesis of cisplatin-induced nephrotoxicity remains to be elucidated.

METHODS: In this study, we verified the reno-protective effects of toralactone and compared the composition and function of the gut microbiota in the normal, cisplatin-treated and low or high dose of toralactone-treated mice using 16S rDNA gene sequencing. We also investigated the gut microbiota related LPS/TLR4/NF-κB/TNF-α pathway in renal tissue. To elucidate the causal relationship between gut dysbiosis and cisplatin nephrotoxicity, an antibiotic cocktail was administered to deplete the gut microbiota and fecal microbiota transplantation (FMT) was performed prior to cisplatin treatment.

RESULTS: The renal histopathology showed that toralactone significantly alleviated cisplatin-induced renal injury. 16S rDNA gene sequencing analysis demonstrated that toralactone treatment effectively reversed cisplatin-induced gut microbiota dysbiosis in mice. FMT from toralactone-treated mice to cisplatin-induced kidney injury mice was observed to have the reno-protective effects, and deletion of gut microbiota by antibiotics was found to negate the reno-protective effect of toralactone. Interestingly, the renal tissue of cisplatin-associated kidney injury mice showed activation of the LPS/TLR4/NF-κB pathway and increase in TNF-α within the renal tissue, whereas toralactone treatment was observed to inhibit the LPS/TLR4/NF-κB/TNF-α pathway.

CONCLUSION: This study elucidated the reno-protective effects for the first time, demonstrating that it exerts its beneficial effects through the gut microbiota, which mediate the LPS/TLR4/NF-κB/TNF-α inflammatory pathway. It may help to develop therapeutic approaches using toralactone and targeted restoration of the gut microbiota.},
}

@article {pmid39273662,
year = {2024},
author = {Acevedo-Román, A and Pagán-Zayas, N and Velázquez-Rivera, LI and Torres-Ventura, AC and Godoy-Vitorino, F},
title = {Insights into Gut Dysbiosis: Inflammatory Diseases, Obesity, and Restoration Approaches.},
journal = {International journal of molecular sciences},
volume = {25},
number = {17},
pages = {},
pmid = {39273662},
issn = {1422-0067},
support = {P20 GM103475/GM/NIGMS NIH HHS/United States ; U54 GM133807/GM/NIGMS NIH HHS/United States ; U54 MD007600//MD/NIMHD NIH HHS/United States ; S21 MD001830/MD/NIMHD NIH HHS/United States ; T32 GM148406/GM/NIGMS NIH HHS/United States ; U54 MD007600/MD/NIMHD NIH HHS/United States ; },
mesh = {Humans ; *Dysbiosis/microbiology/therapy ; *Gastrointestinal Microbiome ; *Obesity/microbiology ; *Fecal Microbiota Transplantation ; *Probiotics/therapeutic use ; Animals ; Inflammation/microbiology ; Prebiotics/administration & dosage ; },
abstract = {The gut microbiota is one of the most critical factors in human health. It involves numerous physiological processes impacting host health, mainly via immune system modulation. A balanced microbiome contributes to the gut's barrier function, preventing the invasion of pathogens and maintaining the integrity of the gut lining. Dysbiosis, or an imbalance in the gut microbiome's composition and function, disrupts essential processes and contributes to various diseases. This narrative review summarizes key findings related to the gut microbiota in modern multifactorial inflammatory conditions such as ulcerative colitis or Crohn's disease. It addresses the challenges posed by antibiotic-driven dysbiosis, particularly in the context of C. difficile infections, and the development of novel therapies like fecal microbiota transplantation and biotherapeutic drugs to combat these infections. An emphasis is given to restoration of the healthy gut microbiome through dietary interventions, probiotics, prebiotics, and novel approaches for managing gut-related diseases.},
}

Humans
*Dysbiosis/microbiology/therapy
*Gastrointestinal Microbiome
*Obesity/microbiology
*Fecal Microbiota Transplantation
*Probiotics/therapeutic use
Animals
Inflammation/microbiology
Prebiotics/administration & dosage

@article {pmid39272235,
year = {2024},
author = {Li, H and Han, L and Zhou, F and Wu, Z and Zhang, L and Xie, R and Jiang, F and Tian, Q and Huang, X},
title = {Ningxiang Pig-Derived Microbiota Affects the Growth Performance, Gut Microbiota, and Serum Metabolome of Nursery Pigs.},
journal = {Animals : an open access journal from MDPI},
volume = {14},
number = {17},
pages = {},
pmid = {39272235},
issn = {2076-2615},
support = {U20A2055//National Natural Science Foundation of China/ ; },
abstract = {The gut microbiota is crucial for maintaining the host's intestinal homeostasis and metabolism. This study investigated the effects of fecal microbiota transplantation (FMT) from Ningxiang pigs on the growth performance, fecal microbiota, and serum metabolites of the same-old DLY pigs. The results indicated that the average daily gain of FMT pigs was significantly greater than that of the control (CON) group. Compared to the CON group, the FMT group significantly improved the apparent digestibility of crude fiber, crude ash, gross energy, and calcium of the pigs. The analysis of serum antioxidant status revealed that the activities of total superoxide dismutase and catalase in the serum of pigs in the FMT group were significantly elevated, whereas the level of malondialdehyde was significantly reduced. Furthermore, 16S rRNA sequencing analysis revealed that the Ningxiang pig-derived microbiota altered the fecal microbiota structure and modulated the diversity of the gut microbiota in the DLY pigs. Untargeted LC-MS metabolomics demonstrated that pigs in the FMT group exhibited distinct metabolomic profiles compared to those in the CON group. Significant changes were observed in key metabolites involved in amino acid, lipid, and carbohydrate metabolism. Additionally, a correlation analysis between serum differential metabolites and the gut microbiota revealed that the relative abundance of Lachnospiraceae_NK4A136_group and Corynebacterium was highly correlated with lipid compounds. In conclusion, Ningxiang pig-derived microbiota can alleviate oxidative stress and enhance growth performance in DLY pigs by modulating their gut microbiota and metabolic features.},
}

@article {pmid39271443,
year = {2024},
author = {López Zúñiga, MÁ and Sánchez Cabello, A and López Ruz, MÁ},
title = {Diagnostic and therapeutic management of Clostridioides difficile infection.},
journal = {Medicina clinica},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.medcli.2024.06.004},
pmid = {39271443},
issn = {1578-8989},
abstract = {A review of the diagnostic and therapeutic management algorithm of the pathogen Clostridioides difficile for daily practice is presented. Its diagnosis, in any unformed stool sample sent to the laboratory, is based on a two-step algorithm, with demonstration of the pathogen by means of its enzyme glutamate dehydrogenase by immunoassay and subsequent PCR (polymerase chain reaction) of its toxin. The mainstay of step therapy, reserved for symptomatic patients, is fidaxomicin, over vancomycin. Metronidazole is not an adequate treatment. Emerging therapies, such as faecal microbiota transplantation or the antibody bezlotoxumab, are gaining importance in patients with risk factors or relapses. Surgery is indicated in patients with worse prognosis and complications. Prevention is essential, based on vigilance and contact precautions, in addition to the elimination of spores from the environment.},
}

@article {pmid39271107,
year = {2024},
author = {Drekonja, DM and Shaukat, A and Huang, Y and Zhang, JH and Reinink, AR and Nugent, S and Dominitz, JA and Davis-Karim, A and Gerding, DN and Kyriakides, TC},
title = {A randomized controlled trial of efficacy and safety of Fecal Microbiota Transplant for preventing recurrent Clostridioides difficile infection.},
journal = {Clinical infectious diseases : an official publication of the Infectious Diseases Society of America},
volume = {},
number = {},
pages = {},
doi = {10.1093/cid/ciae467},
pmid = {39271107},
issn = {1537-6591},
abstract = {BACKGROUND: Clostridioides difficile infection (CDI) is the most common cause of healthcare-associated infections in US hospitals with 15%-30% of patients experiencing recurrence. The aim of our randomized, double-blind clinical trial was to assess the efficacy of capsule-delivered fecal microbiota transplantation (FMT) versus placebo in reducing recurrent diarrhea and CDI recurrence. The secondary aim was FMT safety assessment.

METHODS: Between 2018 and 2022, Veterans across the Veterans Health Administration system with recurrent CDI who responded to antibiotic treatment were randomized in a 1:1 ratio to oral FMT or placebo capsules. Randomization was stratified by number of prior CDI recurrences (1 or ≥2). The primary endpoint was clinical recurrence by day 56, defined as >3 unformed stools daily for ≥2 days with or without laboratory confirmation of C. difficile, or death within 56 days.

RESULTS: The study was stopped due to futility after meeting pre-specified criteria. Of 153 participants (76 FMT, 77 placebo) with an average age of 66.5 years, 25 participants (32.9%) in the FMT arm and 23 (29.9%) in the placebo arm experienced the primary endpoint of diarrhea and possible or definite CDI recurrence or death within 56 days of capsule administration (absolute difference 3.0%; 95% CI [-11.7%, 17.7%]). Stratification by number of recurrences revealed no statistically significant differences. There were no clinically important differences in adverse events.

CONCLUSIONS: FMT therapy vs. placebo did not reduce CDI recurrence or death at 56 days. There were no meaningful differences in adverse events between treatment groups.},
}

@article {pmid39270883,
year = {2024},
author = {Li, F and Han, Q and Cai, Y and Li, Y and Yang, Y and Li, J and Wu, R and Chen, R and Liu, R},
title = {Si-Ni-San ameliorates cholestatic liver injury by favoring P. goldsteinii colonization.},
journal = {Journal of ethnopharmacology},
volume = {337},
number = {Pt 1},
pages = {118804},
doi = {10.1016/j.jep.2024.118804},
pmid = {39270883},
issn = {1872-7573},
abstract = {Current treatment options for cholestatic liver diseases are limited, and addressing impaired intestinal barrier has emerged as a promising therapeutic approach. Si-Ni-San (SNS) is a Traditional Chinese Medicine (TCM) formula commonly utilized in the management of chronic liver diseases. Our previous studies have indicated that SNS effectively enhanced intestinal barrier function through the modulation of gut microbiota.

AIM OF THE STUDY: This study aims to verify the therapeutic effects of SNS on cholestatic liver injury, focusing on elucidating the underlying mechanism involving the gut-liver axis.

MATERIALS AND METHODS: The 16s RNA gene sequencing, non-targeted metabolomics were used to investigate the effects of SNS on the gut microbiota dysbiosis. Fecal microbiota transplantation (FMT) was conducted to identify potential beneficial probiotics underlying the therapeutic effects of SNS.

RESULTS: Our results demonstrated that SNS significantly ameliorated cholestatic liver injury induced by partial bile duct ligation (pBDL). Additionally, SNS effectively suppressed cholestasis-induced inflammation and barrier dysfunction in both the small intestine and colon. While SNS did not impact the intestinal FXR-FGF15-hepatic CYP7A1 axis, it notably improved gut microbiota dysbiosis and modulated the profile of microbial metabolites, including beneficial secondary bile acids and tryptophan derivatives. Furthermore, gut microbiota depletion experiments and FMT confirmed that the therapeutic benefits of SNS in cholestatic liver disease are dependent on gut microbiota modulation, particularly through the promotion of the growth of potential probiotic P. goldsteinii. Moreover, a synergistic improvement in cholestatic liver injury was observed with the co-administration of P. goldsteinii and SNS.

CONCLUSION: Our study underscores that SNS effectively alleviates cholestatic liver injury by addressing gut microbiota dysbiosis and enhancing intestinal barrier function, supporting its rational clinical utilization. Furthermore, we highlight P. goldsteinii as a promising probiotic candidate for the management of cholestatic liver diseases.},
}

@article {pmid39270730,
year = {2024},
author = {Poutanen, SM and Hota, SS},
title = {Déjà vu: Unanswered Questions about Fecal Microbiota Transplantation for Recurrent Clostridioides difficile Infection.},
journal = {Clinical infectious diseases : an official publication of the Infectious Diseases Society of America},
volume = {},
number = {},
pages = {},
doi = {10.1093/cid/ciae468},
pmid = {39270730},
issn = {1537-6591},
}

@article {pmid39269473,
year = {2024},
author = {Singh, V and Choi, SD and Mahra, K and Son, H and Lee, H and Lee, YJ and Kim, ES and Shin, JH},
title = {Cultured fecal microbial community and its impact as fecal microbiota transplantation treatment in mice gut inflammation.},
journal = {Applied microbiology and biotechnology},
volume = {108},
number = {1},
pages = {463},
pmid = {39269473},
issn = {1432-0614},
support = {2021R1A6C101A416//Korea Basic Science Institute/ ; },
mesh = {*Fecal Microbiota Transplantation/methods ; Animals ; *Feces/microbiology ; Mice ; *Gastrointestinal Microbiome ; Humans ; *Inflammatory Bowel Diseases/therapy/microbiology ; *Disease Models, Animal ; *Cytokines/metabolism ; *RNA, Ribosomal, 16S/genetics ; Mice, Inbred C57BL ; Dextran Sulfate ; Male ; Culture Media/chemistry ; Bacteria/classification/genetics/isolation & purification ; },
abstract = {The fecal microbiome is identical to the gut microbial communities and provides an easy access to the gut microbiome. Therefore, fecal microbial transplantation (FMT) strategies have been used to alter dysbiotic gut microbiomes with healthy fecal microbiota, successfully alleviating various metabolic disorders, such as obesity, type 2 diabetes, and inflammatory bowel disease (IBD). However, the success of FMT treatment is donor-dependent and variations in gut microbes cannot be avoided. This problem may be overcome by using a cultured fecal microbiome. In this study, a human fecal microbiome was cultured using five different media; growth in brain heart infusion (BHI) media resulted in the highest microbial community cell count. The microbiome (16S rRNA) data demonstrated that the cultured microbial communities were similar to that of the original fecal sample. Therefore, the BHI-cultured fecal microbiome was selected for cultured FMT (cFMT). Furthermore, a dextran sodium sulfate (DSS)-induced mice-IBD model was used to confirm the impact of cFMT. Results showed that cFMT effectively alleviated IBD-associated symptoms, including improved gut permeability, restoration of the inflamed gut epithelium, decreased expression of pro-inflammatory cytokines (IFN-γ, TNF-α, IL-1, IL-6, IL-12, and IL-17), and increased expression of anti-inflammatory cytokines (IL-4 and IL-10). Thus, study's findings suggest that cFMT can be a potential alternative to nFMT. KEY POINTS: • In vitro fecal microbial communities were grown in a batch culture using five different media. • Fecal microbial transplantation was performed on DSS-treated mice using cultured and normal fecal microbes. • Cultured fecal microbes effectively alleviated IBD-associated symptoms.},
}

*Fecal Microbiota Transplantation/methods
Animals
*Feces/microbiology
Mice
*Gastrointestinal Microbiome
Humans
*Inflammatory Bowel Diseases/therapy/microbiology
*Disease Models, Animal
*Cytokines/metabolism
*RNA, Ribosomal, 16S/genetics
Mice, Inbred C57BL
Dextran Sulfate
Male
Culture Media/chemistry
Bacteria/classification/genetics/isolation & purification

@article {pmid39267518,
year = {2024},
author = {Gan, Y and Wu, ZH and Li, QL and Lu, ZX and Chen, LL},
title = {[Advances in the treatment of Clostridium difficile infection in children].},
journal = {Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics},
volume = {26},
number = {9},
pages = {995-1001},
pmid = {39267518},
issn = {1008-8830},
mesh = {Humans ; *Clostridium Infections/therapy ; *Fecal Microbiota Transplantation ; Child ; Clostridioides difficile ; Risk Factors ; Anti-Bacterial Agents/therapeutic use ; },
abstract = {Clostridium difficile infection (CDI) is a major cause of hospital-acquired gastrointestinal infections in children. Current treatment for pediatric CDI primarily involves antibiotics; however, some children experience recurrence after antibiotic treatment, and those with initial recurrence remain at risk for further recurrences following subsequent antibiotic therapy. In such cases, careful consideration of treatment options is necessary. Fecal microbiota transplantation has been shown to be effective for recurrent CDI and has a high safety profile. This article reviews the latest research on the pathogenesis, risk factors, diagnosis, and treatment of pediatric CDI domestically and internationally, with a particular focus on fecal microbiota transplantation therapy.},
}

Humans
*Clostridium Infections/therapy
*Fecal Microbiota Transplantation
Child
Clostridioides difficile
Risk Factors
Anti-Bacterial Agents/therapeutic use

@article {pmid39267235,
year = {2024},
author = {},
title = {Correction to "Long-Term Effects of Fecal Microbiota Transplantation on Gut Microbiota After Helicobacter pylori Eradication With Bismuth Quadruple Therapy: A Randomized Controlled Trial".},
journal = {Helicobacter},
volume = {29},
number = {5},
pages = {e13127},
doi = {10.1111/hel.13127},
pmid = {39267235},
issn = {1523-5378},
}

@article {pmid39267080,
year = {2024},
author = {Wei, X and Xing, F and Xu, Y and Zhang, F and Cheng, D and Zhou, Y and Zheng, F and Zhang, W},
title = {Preoperative gut microbiota of POCD patients induces pre- and postoperative cognitive impairment and systemic inflammation in rats.},
journal = {Journal of neuroinflammation},
volume = {21},
number = {1},
pages = {221},
pmid = {39267080},
issn = {1742-2094},
support = {82002086//National Natural Science Foundation of China/ ; 82001187//National Natural Science Foundation of China/ ; 82071240//National Natural Science Foundation of China/ ; },
mesh = {*Gastrointestinal Microbiome/physiology ; Animals ; Rats ; *Postoperative Cognitive Complications/etiology ; Male ; Humans ; Female ; Aged ; *Inflammation ; Rats, Sprague-Dawley ; Middle Aged ; Retrospective Studies ; Cognitive Dysfunction/etiology/microbiology ; },
abstract = {BACKGROUND: Postoperative cognitive dysfunction (POCD) is common following surgery in elderly patients. The role of the preoperative gut microbiota in POCD has attracted increasing attention, but the potential underlying mechanisms remain unclear. This research aimed to investigate the impact of the preoperative gut microbiota on POCD.

METHODS: Herein, we analyzed the preoperative gut microbiota of POCD patients through a prospective specimen collection and retrospective blinded evaluation study. Then, we transferred the preoperative gut microbiota of POCD patients to antibiotic-treated rats and established POCD model by abdominal surgery to explore the impact of the preoperative gut microbiota on pre- and postoperative cognitive function and systemic inflammation. The gut microbiota was analyzed using 16S rRNA sequencing analysis. The Morris water maze test was performed to evaluate learning and memory abilities. The inflammatory cytokines TNF-α, IL-1β and IL-6 in the serum and hippocampus were measured by ELISA. Microglia were examined by immunofluorescence staining for Iba-1.

RESULTS: Based on the decrease in the postoperative MMSE score, 24 patients were identified as having POCD and were matched with 24 control patients. Compared with control patients, POCD patients exhibited higher BMI and lower preoperative MMSE score. The preoperative gut microbiota of POCD patients had lower bacterial richness but a larger distribution, decreased abundance of Firmicutes and increased abundance of Proteobacteria than did that of control patients. Compared with rats that received preoperative fecal samples of control patients, rats that received preoperative fecal samples of POCD patients presented an increased abundance of Desulfobacterota, decreased cognitive function, increased levels of TNF-α and IL-1β in the serum, increased levels of TNF-α and greater microglial activation in the hippocampus. Additionally, correlation analysis revealed a positive association between the abundance of Desulfobacterota and the level of serum TNF-α in rats. Then, we performed abdominal surgery to investigate the impact of the preoperative gut microbiota on postoperative conditions, and the surgery did indeed cause POCD and inflammatory response. Notably, compared with rats that received preoperative fecal samples of control patients, rats that received preoperative fecal samples of POCD patients displayed exacerbated cognitive impairment; increased levels of TNF-α, IL-1β and IL-6 in the serum and hippocampus; and increased activation of microglia in the hippocampus.

CONCLUSIONS: Our findings suggest that the preoperative gut microbiota of POCD patients can induce preoperative and aggravate postoperative cognitive impairment and systemic inflammation in rats. Modulating inflammation by targeting the gut microbiota might be a promising approach for preventing POCD.},
}

*Gastrointestinal Microbiome/physiology
Animals
Rats
*Postoperative Cognitive Complications/etiology
Male
Humans
Female
Aged
*Inflammation
Rats, Sprague-Dawley
Middle Aged
Retrospective Studies
Cognitive Dysfunction/etiology/microbiology

@article {pmid39266472,
year = {2024},
author = {Bell, J and Radial, SL and Cuming, RS and Trope, G and Hughes, KJ},
title = {Effects of fecal microbiota transplantation on clinical outcomes and fecal microbiota of foals with diarrhea.},
journal = {Journal of veterinary internal medicine},
volume = {},
number = {},
pages = {},
doi = {10.1111/jvim.17185},
pmid = {39266472},
issn = {1939-1676},
support = {//Agrifutures Australia/ ; },
abstract = {BACKGROUND: Diarrhea in foals can be associated with disruption of the intestinal microbiota (dysbiosis). Effective management of intestinal dysbiosis in foals has not been demonstrated.

HYPOTHESIS/OBJECTIVES: Fecal microbiota transplantation (FMT) in foals with diarrhea influences the intestinal microbiota and improves clinical and clinicopathological outcomes.

ANIMALS: Twenty-five foals <6 months of age with diarrhea and systemic inflammatory response syndrome at 3 veterinary hospitals.

METHODS: A prospective randomized placebo-controlled cohort study. Foals in the FMT group (n = 19) or control group (n = 9) received FMT or electrolyte solution once daily for 3 days. Fecal samples were obtained on Day 0 (D0), D1, D2, D3, and D7. Within group and between group data analyses were performed for clinical, clinicopathological, and microbiota variables.

RESULTS: Treatment had no effect on survival (FMT 79%; control 100%, P = .3) or resolution of diarrhea (FMT 68%; control 55%, P = .4). On D3, the white blood cell count of the FMT group was lower than the control group (D3 FMT group median 6.4 g/L [5-8.3 g/L]; D3 control group median 14.3 g/L [6.7-18.9 g/L] P = .04). Heart rate reduced over time in the FMT group (D0 median 80 bpm [60-150 bpm]; D2 median 70 bpm [52-110 bpm] [P = .005]; and D3 median 64, [54-102 bpm] [P < .001]). Phylum Verrucomicrobiota, genus Akkermansia, and family Prevotellaceae were enriched in the FMT group on D1 (linear discriminate analysis > 4).

In foals with diarrhea, FMT appears safe and can be associated with some clinical and microbiota changes suggestive of beneficial effect.},
}

@article {pmid39263354,
year = {2024},
author = {Zhang, C and Wang, G and Yin, X and Gou, L and Guo, M and Suo, F and Zhuang, T and Yuan, Z and Liu, Y and Gu, M and Yao, R},
title = {Hepatic protein phosphatase 1 regulatory subunit 3G alleviates obesity and liver steatosis by regulating the gut microbiota and bile acid metabolism.},
journal = {Journal of pharmaceutical analysis},
volume = {14},
number = {8},
pages = {100976},
pmid = {39263354},
issn = {2214-0883},
abstract = {Intestinal dysbiosis and disrupted bile acid (BA) homeostasis are associated with obesity, but the precise mechanisms remain insufficiently explored. Hepatic protein phosphatase 1 regulatory subunit 3G (PPP1R3G) plays a pivotal role in regulating glycolipid metabolism; nevertheless, its obesity-combatting potency remains unclear. In this study, a substantial reduction was observed in serum PPP1R3G levels in high-body mass index (BMI) and high-fat diet (HFD)-exposed mice, establishing a positive correlation between PPP1R3G and non-12α-hydroxylated (non-12-OH) BA content. Additionally, hepatocyte-specific overexpression of Ppp1r3g (PPP1R3G HOE) mitigated HFD-induced obesity as evidenced by reduced weight, fat mass, and an improved serum lipid profile; hepatic steatosis alleviation was confirmed by normalized liver enzymes and histology. PPP1R3G HOE considerably impacted systemic BA homeostasis, which notably increased the non-12-OH BAs ratio, particularly lithocholic acid (LCA). 16S ribosomal DNA (16S rDNA) sequencing assay indicated that PPP1R3G HOE reversed HFD-induced gut dysbiosis by reducing the Firmicutes/Bacteroidetes ratio and Lactobacillus population, and elevating the relative abundance of Blautia, which exhibited a positive correlation with serum LCA levels. A fecal microbiome transplantation test confirmed that the anti-obesity effect of hepatic PPP1R3G was gut microbiota-dependent. Mechanistically, PPP1R3G HOE markedly suppressed hepatic cholesterol 7α-hydroxylase (CYP7A1) and sterol-12α-hydroxylase (CYP8B1), and concurrently upregulated oxysterol 7-α hydroxylase and G protein-coupled BA receptor 5 (TGR5) expression under HFD conditions. Furthermore, LCA administration significantly mitigated the HFD-induced obesity phenotype and elevated non-12-OH BA levels. These findings emphasize the significance of hepatic PPP1R3G in ameliorating diet-induced adiposity and hepatic steatosis through the gut microbiota-BA axis, which may serve as potential therapeutic targets for obesity-related disorders.},
}

@article {pmid39262376,
year = {2024},
author = {Wang, T and Hao, L and Yang, K and Feng, W and Guo, Z and Liu, M and Xiao, R},
title = {Fecal microbiota transplantation derived from mild cognitive impairment individuals impairs cerebral glucose uptake and cognitive function in wild-type mice: Bacteroidetes and TXNIP-GLUT signaling pathway.},
journal = {Gut microbes},
volume = {16},
number = {1},
pages = {2395907},
doi = {10.1080/19490976.2024.2395907},
pmid = {39262376},
issn = {1949-0984},
mesh = {Animals ; *Fecal Microbiota Transplantation ; *Cognitive Dysfunction/metabolism/microbiology ; Mice ; *Gastrointestinal Microbiome ; *Glucose/metabolism ; *Brain/metabolism ; *Bacteroidetes/metabolism ; *Signal Transduction ; *Dysbiosis/microbiology/metabolism ; Male ; Humans ; *Cognition ; Mice, Inbred C57BL ; Carrier Proteins/metabolism/genetics ; Glucose Transport Proteins, Facilitative/metabolism/genetics ; Thioredoxins ; },
abstract = {Gut microbiome dysbiosis has been widely implicated in cognitive impairment, but the identity of the specific bacterial taxa and mechanisms are not fully elucidated. Brain glucose hypometabolism coincides with the cognitive decline. This study explored the link among cognition, gut microbiota and glucose uptake based on the fecal microbiota transplantation from mild cognitive impairment individuals (MCI-FMT) and investigated whether similar mechanisms were involved in 27-hydroxycholesterol (27-OHC)-induced cognitive decline. Our results showed that the MCI-FMT mice exhibited learning and memory decline and morphological lesions in the brain and colon tissues. There were reduced [18]F-fluorodeoxyglucose uptake, downregulated expression of glucose transporters (GLUT1,3,4) and upregulated negative regulator of glucose uptake (TXNIP) in the brain. MCI-FMT altered the bacterial composition and diversity of the recipient mice, and the microbial signatures highlighted by the increased abundance of Bacteroides recapitulated the negative effects of MCI bacterial colonization. However, inhibiting Bacteroidetes or TXNIP increased the expression of GLUT1 and GLUT4, significantly improving brain glucose uptake and cognitive performance in 27-OHC-treated mice. Our study verified that cognitive decline and abnormal cerebral glucose uptake were associated with gut microbiota dysbiosis; we also revealed the involvement of Bacteroidetes and molecular mechanisms of TXNIP-related glucose uptake in cognitive deficits caused by 27-OHC.},
}

Animals
*Fecal Microbiota Transplantation
*Cognitive Dysfunction/metabolism/microbiology
Mice
*Gastrointestinal Microbiome
*Glucose/metabolism
*Brain/metabolism
*Bacteroidetes/metabolism
*Signal Transduction
*Dysbiosis/microbiology/metabolism
Male
Humans
*Cognition
Mice, Inbred C57BL
Carrier Proteins/metabolism/genetics
Glucose Transport Proteins, Facilitative/metabolism/genetics
Thioredoxins

@article {pmid39262248,
year = {2024},
author = {Mu, X and Zhang, J and Li, H and Li, H and Mu, Z and Ye, F and Li, J and Ye, F},
title = {Effects of intestinal flora on cerebral hemorrhage area and brain tissue inflammation in acute hemorrhagic stroke.},
journal = {Cellular and molecular biology (Noisy-le-Grand, France)},
volume = {70},
number = {8},
pages = {153-157},
doi = {10.14715/cmb/2024.70.8.21},
pmid = {39262248},
issn = {1165-158X},
mesh = {Animals ; Male ; *Cerebral Hemorrhage/complications/pathology/microbiology/metabolism ; *Mice, Inbred C57BL ; *Gastrointestinal Microbiome ; *Hemorrhagic Stroke/pathology/metabolism ; *Brain/pathology/metabolism ; Inflammation/pathology/metabolism ; Disease Models, Animal ; Mice ; Brain Edema/pathology/metabolism ; Hematoma/pathology/metabolism/complications ; },
abstract = {To explore the impacts of intestinal flora on cerebral hemorrhage area and brain tissue inflammation in acute hemorrhagic stroke, seventy-two male C57BL/6 mice were randomly separated into 6 groups (n=12), the experimental group (EG, day 1, day 3 and day 7) and the control group (CG, day 1, day 3 and day 7). The mouse cerebral hemorrhage model was established by collagenase injection, and the EG received 0.4 mL fecal filtrate of healthy mice once a day, and the CG received the same amount of normal saline transplantation. The mNSS score, hematoma volume and cerebral edema content were used to evaluate nerve function injury and brain injury degree at each time point after operation. The expressions of inflammatory factors were detected by western blot. We found that at each time point after operation, compared with the CG, nerve function deficit scores of mice in the EG declined (P<0.05), the water content of mice brain tissue in the EG declined (P<0.05), and the protein expressions of inflammatory factors in the EG were decreased (P<0.05). Relative to the CG, the volume of hematoma in the EG declined on day 3 along with day 7 after operation (P<0.05). In conclusion, intestinal flora can reduce cerebral hemorrhage area and brain tissue inflammation, and then improve the performance of nerve function deficit in acute hemorrhagic stroke.},
}

Animals
Male
*Cerebral Hemorrhage/complications/pathology/microbiology/metabolism
*Mice, Inbred C57BL
*Gastrointestinal Microbiome
*Hemorrhagic Stroke/pathology/metabolism
*Brain/pathology/metabolism
Inflammation/pathology/metabolism
Disease Models, Animal
Mice
Brain Edema/pathology/metabolism
Hematoma/pathology/metabolism/complications

@article {pmid39261424,
year = {2024},
author = {Evrensel, A},
title = {Probiotics and Fecal Microbiota Transplantation in Major Depression: Doxa or Episteme?.},
journal = {Advances in experimental medicine and biology},
volume = {1456},
number = {},
pages = {67-83},
pmid = {39261424},
issn = {0065-2598},
mesh = {*Fecal Microbiota Transplantation/methods ; Humans ; *Probiotics/therapeutic use ; *Gastrointestinal Microbiome ; *Depressive Disorder, Major/therapy/microbiology ; Antidepressive Agents/therapeutic use ; Animals ; },
abstract = {In the human body, eukaryotic somatic cells and prokaryotic microorganisms live together. In this state, the body can be viewed as a "superorganism." Symbiotic life with commensal microorganisms can be observed in almost every part of the body. Intestinal microbiota plays an important role in health and disease, and in shaping and regulating neuronal functions from the intrauterine period to the end of life. Microbiota-based treatment opportunities are becoming more evident in both understanding the etiopathogenesis and treatment of neuropsychiatric disorders, especially depression. Antidepressant drugs, which are the first choice in the treatment of depression, also have antimicrobial and immunomodulatory mechanisms of action. From these perspectives, direct probiotics and fecal microbiota transplantation are treatment options to modulate microbiota composition. There are few preclinical and clinical studies on the effectiveness and safety of these applications in depression. The information obtained from these studies may still be at a doxa level. However, the probability that this information will become episteme in the future seems to be increasing.},
}

*Fecal Microbiota Transplantation/methods
Humans
*Probiotics/therapeutic use
*Gastrointestinal Microbiome
*Depressive Disorder, Major/therapy/microbiology
Antidepressive Agents/therapeutic use
Animals

@article {pmid39259805,
year = {2024},
author = {Sawaed, J and Zelik, L and Levin, Y and Feeney, R and Naama, M and Gordon, A and Zigdon, M and Rubin, E and Telpaz, S and Modilevsky, S and Ben-Simon, S and Awad, A and Harshuk-Shabso, S and Nuriel-Ohayon, M and Werbner, M and Schroeder, BO and Erez, A and Bel, S},
title = {Antibiotics damage the colonic mucus barrier in a microbiota-independent manner.},
journal = {Science advances},
volume = {10},
number = {37},
pages = {eadp4119},
pmid = {39259805},
issn = {2375-2548},
mesh = {Animals ; *Anti-Bacterial Agents/pharmacology/adverse effects ; Mice ; *Intestinal Mucosa/metabolism/microbiology/drug effects/pathology ; *Gastrointestinal Microbiome/drug effects ; *Colon/metabolism/drug effects/pathology/microbiology ; *Mucus/metabolism ; Inflammatory Bowel Diseases/chemically induced/metabolism/pathology/microbiology ; Endoplasmic Reticulum Stress/drug effects ; Disease Models, Animal ; Fecal Microbiota Transplantation ; Mice, Inbred C57BL ; Humans ; },
abstract = {Antibiotic use is a risk factor for development of inflammatory bowel diseases (IBDs). IBDs are characterized by a damaged mucus layer, which does not separate the intestinal epithelium from the microbiota. Here, we hypothesized that antibiotics affect the integrity of the mucus barrier, which allows bacterial penetrance and predisposes to intestinal inflammation. We found that antibiotic treatment led to breakdown of the colonic mucus barrier and penetration of bacteria into the mucus layer. Using fecal microbiota transplant, RNA sequencing followed by machine learning, ex vivo mucus secretion measurements, and antibiotic treatment of germ-free mice, we determined that antibiotics induce endoplasmic reticulum stress in the colon that inhibits colonic mucus secretion in a microbiota-independent manner. This antibiotic-induced mucus secretion flaw led to penetration of bacteria into the colonic mucus layer, translocation of microbial antigens into circulation, and exacerbation of ulcerations in a mouse model of IBD. Thus, antibiotic use might predispose to intestinal inflammation by impeding mucus production.},
}

Animals
*Anti-Bacterial Agents/pharmacology/adverse effects
Mice
*Intestinal Mucosa/metabolism/microbiology/drug effects/pathology
*Gastrointestinal Microbiome/drug effects
*Colon/metabolism/drug effects/pathology/microbiology
*Mucus/metabolism
Inflammatory Bowel Diseases/chemically induced/metabolism/pathology/microbiology
Endoplasmic Reticulum Stress/drug effects
Disease Models, Animal
Fecal Microbiota Transplantation
Mice, Inbred C57BL
Humans

@article {pmid39256134,
year = {2024},
author = {Sono, M and Iimori, K and Nagao, M and Ogawa, S and Maruno, T and Nakanishi, Y and Anazawa, T and Nagai, K and Masui, T and Mori, H and Hosomi, K and Kunisawa, J and Yokota, H and Tanaka, Y and Ohno, H and Hatano, E and Fukuda, A and Seno, H},
title = {Reduction of butyrate-producing bacteria in the gut microbiome of Japanese patients with pancreatic cancer.},
journal = {Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.pan.2024.09.002},
pmid = {39256134},
issn = {1424-3911},
abstract = {BACKGROUND: The incidence of pancreatic cancer is on the rise, and its prognosis remains poor. Recent reports have established a link between the gut and oral microbiome and pancreatic cancer. However, the intricacies of this association within the Japanese population remain unclear. In this study, we investigated the gut and oral microbiomes of Japanese patients with pancreatic cancer, comparing them with those of healthy individuals.

METHODS: We recruited 30 patients with untreated pancreatic cancer and 18 healthy controls at Kyoto University Hospital (2018-2022). We performed a comprehensive 16S rRNA gene sequencing to analyze their gut and oral microbiomes.

RESULTS: Analysis revealed that the diversity of the gut and oral microbiomes of patients with pancreatic cancer was reduced compared to that of the healthy controls. Specifically, we observed an increase in the genus Streptococcus in both the gut and oral microbiomes and a significant decrease in several butyrate-producing bacteria in fecal samples. Moreover, bacteria such as Streptococcus mitis and Holdemanella biformis were present in pancreatic cancer tissues, suggesting that they might influence the carcinogenesis and progression of pancreatic cancer.

CONCLUSIONS: The gut and oral microbiome differed between patients with pancreatic cancer and healthy controls, with a notable decrease in butyrate-producing bacteria in the gut microbiome of the patients. This suggests that there may be a distinct microbial signature associated with pancreatic cancer in the Japanese population. Further studies are required to elucidate the microbiome's causal role in this cancer and help develop prognostic markers or targeted therapies.},
}

@article {pmid39253878,
year = {2024},
author = {Jangi, S and Hecht, G},
title = {Microbiome 2.0: lessons from the 2024 Gut Microbiota for Health World Summit.},
journal = {Gut microbes},
volume = {16},
number = {1},
pages = {2400579},
doi = {10.1080/19490976.2024.2400579},
pmid = {39253878},
issn = {1949-0984},
mesh = {*Gastrointestinal Microbiome ; Humans ; *Fecal Microbiota Transplantation ; *Probiotics/administration & dosage ; Congresses as Topic ; },
abstract = {This Meeting Summary highlights the key insights from the 12th meeting of the Gut Microbiota for Health World Summit, held in Washington, DC, organized by the American Gastroenterological Association (AGA) and the European Society of Neurogastroenterology and Motility (ESNM). Through a 2-day series of plenary sessions, workshops, a poster session, and live discussions involving thought leaders, physicians, researchers, and representatives from the Food and Drug Administration and the pharmaceutical industry, the conference attendees focused on the strategies and challenges in developing microbiome-based therapies to prevent and treat human disease. The conference highlighted progress in the field, including the recently successful introduction of 2 new fecal microbial transplantation-based products into the clinical setting, and the continuing development of next-generation probiotics. However, to continue to advance microbiome-directed treatments, three key themes emerged during the meeting, including (1) better methods to identify actionable targets in the microbiome (2) developing effective strategies to manipulate the microbiome (3) aligning microbiome-based therapies with existing treatment paradigms in the real world.},
}

*Gastrointestinal Microbiome
Humans
*Fecal Microbiota Transplantation
*Probiotics/administration & dosage
Congresses as Topic

@article {pmid39252488,
year = {2024},
author = {Park, J and Hong, SN and Lee, HS and Shin, J and Oh, EH and Nam, K and Seong, G and Kim, HG and Kim, JO and Jeon, SR and , },
title = {Perception of fecal microbiota transplantation in patients with ulcerative colitis in Korea: a KASID multicenter study.},
journal = {The Korean journal of internal medicine},
volume = {39},
number = {5},
pages = {783-792},
pmid = {39252488},
issn = {2005-6648},
support = {//Soonchunhyang University/ ; },
mesh = {Humans ; *Fecal Microbiota Transplantation ; *Colitis, Ulcerative/therapy/microbiology/diagnosis ; Male ; Female ; Adult ; Republic of Korea ; Middle Aged ; Prospective Studies ; *Health Knowledge, Attitudes, Practice ; Patient Education as Topic ; Patient Preference ; Treatment Outcome ; Patient Acceptance of Health Care ; Young Adult ; Aged ; Perception ; },
abstract = {BACKGROUND/AIMS: Fecal microbiota transplantation (FMT) is a promising therapy for inducing and maintaining remission in patients with ulcerative colitis (UC). However, FMT has not been approved for UC treatment in Korea. Our study aimed to investigate patient perceptions of FMT under the national medical policy.

METHODS: This was a prospective, multicenter study. Patients with UC ≥ 19 years of age were included. Patients were surveyed using 22 questions on FMT. Changes in perceptions of FMT before and after education were also compared.

RESULTS: A total of 210 patients with UC were enrolled. We found that 51.4% of the patients were unaware that FMT was an alternative treatment option for UC. After reading the educational materials on FMT, more patients were willing to undergo this procedure (27.1% vs. 46.7%; p < 0.001). The preferred fecal donor was the one recommended by a physician (41.0%), and the preferred transplantation method was the oral capsule (30.4%). A large proportion of patients (50.0%) reported that the national medical policy influenced their choice of FMT treatment. When patients felt severe disease activity, their willingness to undergo FMT increased (92.3% vs. 43.1%; p = 0.001).

CONCLUSION: Education can increase preference for FMT in patients with UC. When patients have severe disease symptoms or their quality of life decreases their willingness to undergo FMT increases. Moreover, national medical policies may influence patient choices regarding FMT.},
}

Humans
*Fecal Microbiota Transplantation
*Colitis, Ulcerative/therapy/microbiology/diagnosis
Male
Female
Adult
Republic of Korea
Middle Aged
Prospective Studies
*Health Knowledge, Attitudes, Practice
Patient Education as Topic
Patient Preference
Treatment Outcome
Patient Acceptance of Health Care
Young Adult
Aged
Perception

@article {pmid39252487,
year = {2024},
author = {Kim, YC and Sohn, KH and Kang, HR},
title = {Gut microbiota dysbiosis and its impact on asthma and other lung diseases: potential therapeutic approaches.},
journal = {The Korean journal of internal medicine},
volume = {39},
number = {5},
pages = {746-758},
pmid = {39252487},
issn = {2005-6648},
support = {RS-2023-00217157//National Research Foundation of Korea/ ; //Ministry of Science and ICT/ ; },
mesh = {Humans ; *Dysbiosis ; *Gastrointestinal Microbiome ; *Probiotics/therapeutic use ; *Asthma/microbiology/immunology/therapy ; *Fecal Microbiota Transplantation ; *Prebiotics ; Animals ; Lung/microbiology/immunology/metabolism ; Lung Diseases/microbiology/therapy/immunology ; },
abstract = {The emerging field of gut-lung axis research has revealed a complex interplay between the gut microbiota and respiratory health, particularly in asthma. This review comprehensively explored the intricate relationship between these two systems, focusing on their influence on immune responses, inflammation, and the pathogenesis of respiratory diseases. Recent studies have demonstrated that gut microbiota dysbiosis can contribute to asthma onset and exacerbation, prompting investigations into therapeutic strategies to correct this imbalance. Probiotics and prebiotics, known for their ability to modulate gut microbial compositions, were discussed as potential interventions to restore immune homeostasis. The impact of antibiotics and metabolites, including short-chain fatty acids produced by the gut microbiota, on immune regulation was examined. Fecal microbiota transplantation has shown promise in various diseases, but its role in respiratory disorders is not established. Innovative approaches, including mucus transplants, inhaled probiotics, and microencapsulation strategies, have been proposed as novel therapeutic avenues. Despite challenges, including the sophisticated adaptability of microbial communities and the need for mechanistic clarity, the potential for microbiota-based interventions is considerable. Collaboration between researchers, clinicians, and other experts is essential to unravel the complexities of the gut-lung axis, paving a way for innovative strategies that could transform the management of respiratory diseases.},
}

Humans
*Dysbiosis
*Gastrointestinal Microbiome
*Probiotics/therapeutic use
*Asthma/microbiology/immunology/therapy
*Fecal Microbiota Transplantation
*Prebiotics
Animals
Lung/microbiology/immunology/metabolism
Lung Diseases/microbiology/therapy/immunology