@article {pmid38690018,
year = {2024},
author = {Dai, C and Huang, YH and Jiang, M},
title = {Fecal microbiota transplantation for irritable bowel syndrome: Current evidence and perspectives.},
journal = {World journal of gastroenterology},
volume = {30},
number = {16},
pages = {2179-2183},
pmid = {38690018},
issn = {2219-2840},
mesh = {*Irritable Bowel Syndrome/therapy/microbiology ; *Fecal Microbiota Transplantation/methods ; Humans ; Treatment Outcome ; *Gastrointestinal Microbiome ; Feces/microbiology ; Randomized Controlled Trials as Topic ; Clostridioides difficile/pathogenicity ; Clostridium Infections/therapy/microbiology ; },
abstract = {In this editorial we comment on the article published in the recent issue of the World journal of Gastroenterology. We focus specifically on the mechanisms un-derlying the effects of fecal microbiota transplantation (FMT) for irritable bowel syndrome (IBS), the factors which affect the outcomes of FMT in IBS patients, and challenges. FMT has emerged as a efficacious intervention for clostridium difficile infection and holds promise as a therapeutic modality for IBS. The utilization of FMT in the treatment of IBS has undergone scrutiny in numerous randomized controlled trials, yielding divergent outcomes. The current frontier in this field seeks to elucidate these variations, underscore the existing knowledge gaps that necessitate exploration, and provide a guideline for successful FMT imple-mentation in IBS patients. At the same time, the application of FMT as a treatment for IBS confronts several challenges.},
}

*Irritable Bowel Syndrome/therapy/microbiology
*Fecal Microbiota Transplantation/methods
Humans
Treatment Outcome
*Gastrointestinal Microbiome
Feces/microbiology
Randomized Controlled Trials as Topic
Clostridioides difficile/pathogenicity
Clostridium Infections/therapy/microbiology

@article {pmid38689371,
year = {2024},
author = {Gooch, HCC and Labedan, M and Hall, LJ and Maxwell, A},
title = {Transplanting human infant gut microbiome species into Galleria mellonella.},
journal = {BMC research notes},
volume = {17},
number = {1},
pages = {123},
pmid = {38689371},
issn = {1756-0500},
support = {NC/R001782/1/NC3RS_/National Centre for the Replacement, Refinement and Reduction of Animals in Research/United Kingdom ; BB/P012523/1/BB_/Biotechnology and Biological Sciences Research Council/United Kingdom ; BB/P012523/1/BB_/Biotechnology and Biological Sciences Research Council/United Kingdom ; BB/P012523/1/BB_/Biotechnology and Biological Sciences Research Council/United Kingdom ; },
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; Humans ; *Moths/microbiology ; *Larva/microbiology ; Infant ; *Feces/microbiology ; Bifidobacterium/isolation & purification ; Enterococcus/isolation & purification ; },
abstract = {OBJECTIVE: Study of the human infant gut microbiome requires the use of surrogate mammalian species such as mice. We sought to investigate the usefulness of the greater wax moth larva, Galleria mellonella, as an alternative.

RESULTS: We have analysed the native gut microbiome of Galleria and developed methods for clearing the native microbiome and introducing species from human infant faecal samples. We find that some species, e.g. enterococci, are more successful at recolonisation, but that others, e.g. Bifidobacterium, are less so. The work paves the way for using Galleria rather than mice in this and similar work.},
}

Animals
*Gastrointestinal Microbiome/physiology
Humans
*Moths/microbiology
*Larva/microbiology
Infant
*Feces/microbiology
Bifidobacterium/isolation & purification
Enterococcus/isolation & purification

@article {pmid38687096,
year = {2024},
author = {Song, XL and Liang, J and Lin, SZ and Xie, YW and Ke, CH and Ao, D and Lu, J and Chen, XM and He, YZ and Liu, XH and Li, W},
title = {Gut-lung axis and asthma: A historical review on mechanism and future perspective.},
journal = {Clinical and translational allergy},
volume = {14},
number = {5},
pages = {e12356},
pmid = {38687096},
issn = {2045-7022},
support = {32100602//National Natural Science Foundation of China/ ; 2023A1515012755//Guangdong Natural Science Foundation of China/ ; GCC2021009//Scientific Research Start-up Fund for High-level Talents of Affiliated Hospital of Guangdong Medical University/ ; },
abstract = {BACKGROUND: Gut microbiota are closely related to the development and regulation of the host immune system by regulating the maturation of immune cells and the resistance to pathogens, which affects the host immunity. Early use of antibiotics disrupts the homeostasis of gut microbiota and increases the risk of asthma. Gut microbiota actively interact with the host immune system via the gut-lung axis, a bidirectional communication pathway between the gut and lung. The manipulation of gut microbiota through probiotics, helminth therapy, and fecal microbiota transplantation (FMT) to combat asthma has become a hot research topic. BODY: This review mainly describes the current immune pathogenesis of asthma, gut microbiota and the role of the gut-lung axis in asthma. Moreover, the potential of manipulating the gut microbiota and its metabolites as a treatment strategy for asthma has been discussed.

CONCLUSION: The gut-lung axis has a bidirectional effect on asthma. Gut microecology imbalance contributes to asthma through bacterial structural components and metabolites. Asthma, in turn, can also cause intestinal damage through inflammation throughout the body. The manipulation of gut microbiota through probiotics, helminth therapy, and FMT can inform the treatment strategies for asthma by regulating the maturation of immune cells and the resistance to pathogens.},
}

@article {pmid38686220,
year = {2024},
author = {Bruggeman, A and Vandendriessche, C and Hamerlinck, H and De Looze, D and Tate, DJ and Vuylsteke, M and De Commer, L and Devolder, L and Raes, J and Verhasselt, B and Laukens, D and Vandenbroucke, RE and Santens, P},
title = {Safety and efficacy of faecal microbiota transplantation in patients with mild to moderate Parkinson's disease (GUT-PARFECT): a double-blind, placebo-controlled, randomised, phase 2 trial.},
journal = {EClinicalMedicine},
volume = {71},
number = {},
pages = {102563},
pmid = {38686220},
issn = {2589-5370},
abstract = {BACKGROUND: Dysregulation of the gut microbiome has been implicated in Parkinson's disease (PD). This study aimed to evaluate the clinical effects and safety of a single faecal microbiota transplantation (FMT) in patients with early-stage PD.

METHODS: The GUT-PARFECT trial, a single-centre randomised, double-blind, placebo-controlled trial was conducted at Ghent University Hospital between December 01, 2020 and December 12, 2022. Participants (aged 50-65 years, Hoehn and Yahr stage 2) were randomly assigned to receive nasojejunal FMT with either healthy donor stool or their own stool. Computer-generated randomisation was done in a 1:1 ratio through permutated-block scheduling. Treatment allocation was concealed for participants and investigators. The primary outcome measure at 12 months was the change in the Movement Disorders Society-Unified Parkinson's Disease Rating Scale (MDS-UPDRS) motor score obtained during off-medication evaluations. Intention-to-treat analysis was performed using a mixed model for repeated measures analysis. This completed trial is registered on ClinicalTrials.gov (NCT03808389).

FINDINGS: Between December 2020 and December 2021, FMT procedures were conducted on 46 patients with PD: 22 in the healthy donor group and 24 in the placebo group. Clinical evaluations were performed at baseline, 3, 6, and 12 months post-FMT. Full data analysis was possible for 21 participants in the healthy donor group and 22 in the placebo group. After 12 months, the MDS-UPDRS motor score significantly improved by a mean of 5.8 points (95% CI -11.4 to -0.2) in the healthy donor group and by 2.7 points (-8.3 to 2.9) in the placebo group (p = 0.0235). Adverse events were limited to temporary abdominal discomfort.

INTERPRETATION: Our findings suggested a single FMT induced mild, but long-lasting beneficial effects on motor symptoms in patients with early-stage PD. These findings highlight the potential of modulating the gut microbiome as a therapeutic approach and warrant a further exploration of FMT in larger cohorts of patients with PD in various disease stages.

FUNDING: Flemish PD patient organizations (VPL and Parkili), Research Foundation Flanders (FWO), Biocodex Microbiota Foundation.},
}

@article {pmid38685762,
year = {2024},
author = {Ishnaiwer, M and Le Bastard, Q and Naour, M and Zeman, M and Dailly, E and Montassier, E and Batard, E and Dion, M},
title = {Efficacy of an inulin-based treatment on intestinal colonization by multidrug-resistant E. coli: insight into the mechanism of action.},
journal = {Gut microbes},
volume = {16},
number = {1},
pages = {2347021},
pmid = {38685762},
issn = {1949-0984},
mesh = {Animals ; *Inulin/pharmacology/metabolism ; Mice ; *Gastrointestinal Microbiome/drug effects ; *Escherichia coli/drug effects/genetics ; *Feces/microbiology ; *Amoxicillin/pharmacology ; *Pantoprazole/pharmacology ; *Drug Resistance, Multiple, Bacterial ; beta-Lactamases/metabolism/genetics ; Dysbiosis/microbiology/drug therapy ; Anti-Bacterial Agents/pharmacology ; Escherichia coli Infections/drug therapy/microbiology ; Female ; Prebiotics/administration & dosage ; },
abstract = {Inulin, an increasingly studied dietary fiber, alters intestinal microbiota. The aim of this study was to assess whether inulin decreases intestinal colonization by multidrug resistant E. coli and to investigate its potential mechanisms of action. Mice with amoxicillin-induced intestinal dysbiosis mice were inoculated with extended spectrum beta-lactamase producing E. coli (ESBL-E. coli). The combination of inulin and pantoprazole (IP) significantly reduced ESBL-E. coli fecal titers, whereas pantoprazole alone did not and inulin had a delayed and limited effect. Fecal microbiome was assessed using shotgun metagenomic sequencing and qPCR. The efficacy of IP was predicted by increased abundance of 74 taxa, including two species of Adlercreutzia. Preventive treatments with A. caecimuris or A. muris also reduced ESBL-E. coli fecal titers. Fecal microbiota of mice effectively treated by IP was enriched in genes involved in inulin catabolism, production of propionate and expression of beta-lactamases. They also had increased beta-lactamase activity and decreased amoxicillin concentration. These results suggest that IP act through production of propionate and degradation of amoxicillin by the microbiota. The combination of pantoprazole and inulin is a potential treatment of intestinal colonization by multidrug-resistant E. coli. The ability of prebiotics to promote propionate and/or beta-lactamase producing bacteria may be used as a screening tool to identify potential treatments of intestinal colonization by multidrug resistant Enterobacterales.},
}

Animals
*Inulin/pharmacology/metabolism
Mice
*Gastrointestinal Microbiome/drug effects
*Escherichia coli/drug effects/genetics
*Feces/microbiology
*Amoxicillin/pharmacology
*Pantoprazole/pharmacology
*Drug Resistance, Multiple, Bacterial
beta-Lactamases/metabolism/genetics
Dysbiosis/microbiology/drug therapy
Anti-Bacterial Agents/pharmacology
Escherichia coli Infections/drug therapy/microbiology
Female
Prebiotics/administration & dosage

@article {pmid38685731,
year = {2024},
author = {Zhang, Z and Mocanu, V and Deehan, EC and Hotte, N and Zhu, Y and Wei, S and Kao, DH and Karmali, S and Birch, DW and Walter, J and Madsen, KL},
title = {Recipient microbiome-related features predicting metabolic improvement following fecal microbiota transplantation in adults with severe obesity and metabolic syndrome: a secondary analysis of a phase 2 clinical trial.},
journal = {Gut microbes},
volume = {16},
number = {1},
pages = {2345134},
pmid = {38685731},
issn = {1949-0984},
mesh = {Humans ; *Fecal Microbiota Transplantation ; *Metabolic Syndrome/therapy/microbiology ; Male ; Female ; *Gastrointestinal Microbiome ; Adult ; Middle Aged ; *Feces/microbiology ; *Bile Acids and Salts/metabolism/blood ; *Bacteria/classification/isolation & purification/genetics/metabolism ; Obesity/therapy/microbiology ; Dietary Fiber/administration & dosage/metabolism ; Insulin Resistance ; Treatment Outcome ; },
abstract = {Microbial-based therapeutics in clinical practice are of considerable interest, and a recent study demonstrated fecal microbial transplantation (FMT) followed by dietary fiber supplements improved glucose homeostasis. Previous evidence suggests that donor and recipient compatibility and FMT protocol are key determinants, but little is known about the involvement of specific recipient factors. Using data from our recent randomized placebo-control phase 2 clinical trial in adults with obesity and metabolic syndrome, we grouped participants that received FMT from one of 4 donors with either fiber supplement into HOMA-IR responders (n = 21) and HOMA-IR non-responders (n = 8). We further assessed plasma bile acids using targeted metabolomics and performed subgroup analyzes to evaluate the effects of recipient parameters and gastrointestinal factors on microbiota engraftment and homeostatic model assessment of insulin resistance (HOMA2-IR) response. The baseline fecal microbiota composition at genus level of recipients could predict the improvements in HOMA2-IR at week 6 (ROC-AUC = 0.70). Prevotella was identified as an important predictor, with responders having significantly lower relative abundance than non-responders (p = .02). In addition, recipients displayed a highly individualized degree of microbial engraftment from donors. Compared to the non-responders, the responders had significantly increased bacterial richness (Chao1) after FMT and a more consistent engraftment of donor-specific bacteria ASVs (amplicon sequence variants) such as Faecalibacillus intestinalis (ASV44), Roseburia spp. (ASV103), and Christensenellaceae spp. (ASV140) (p < .05). Microbiota engraftment was strongly associated with recipients' factors at baseline including initial gut microbial diversity, fiber and nutrient intakes, inflammatory markers, and bile acid derivative levels. This study identified that responders to FMT therapy had a higher engraftment rate in the transplantation of specific donor-specific microbes, which were strongly correlated with insulin sensitivity improvements. Further, the recipient baseline gut microbiota and related factors were identified as the determinants for responsiveness to FMT and fiber supplementation. The findings provide a basis for the development of precision microbial therapeutics for the treatment of metabolic syndrome.},
}

Humans
*Fecal Microbiota Transplantation
*Metabolic Syndrome/therapy/microbiology
Male
Female
*Gastrointestinal Microbiome
Adult
Middle Aged
*Feces/microbiology
*Bile Acids and Salts/metabolism/blood
*Bacteria/classification/isolation & purification/genetics/metabolism
Obesity/therapy/microbiology
Dietary Fiber/administration & dosage/metabolism
Insulin Resistance
Treatment Outcome

@article {pmid38684800,
year = {2024},
author = {Liu, MT and Zhang, Y and Xiang, CG and Yang, T and Wang, XH and Lu, QK and Lu, HM and Fan, C and Feng, CL and Yang, XQ and Zou, DW and Li, H and Tang, W},
title = {Methionine-choline deficient diet deteriorates DSS-induced murine colitis through disturbance of gut microbes and infiltration of macrophages.},
journal = {Acta pharmacologica Sinica},
volume = {},
number = {},
pages = {},
pmid = {38684800},
issn = {1745-7254},
abstract = {Ulcerative colitis (UC) is associated with changed dietary habits and mainly linked with the gut microbiota dysbiosis, necroptosis of epithelial cells, and mucosal ulcerations. Liver dysfunction and abnormal level of liver metabolism indices were identified in UC patients, suggesting a close interaction between gut and liver disorders. Methionine-choline deficient diet (MCD) has been shown to induce persistent alterations of gut microbiota and metabolome during hepatitis. In this study we further explored the disease phenotypes in UC patients and investigated whether MCD functioned as a trigger for UC susceptibility. After assessing 88 serum specimens from UC patients, we found significant liver dysfunction and dyslipidemia including abnormal ALT, AST, TG, TC, LDL-c and HDL-c. Liver dysfunction and dyslipidemia were confirmed in DSS-induced colitis mice. We fed mice with MCD for 14 days to cause mild liver damage, and then treated with DSS for 7 days. We found that MCD intake significantly exacerbated the pathogenesis of mucosal inflammation in DSS-induced acute, progressive, and chronic colitis, referring to promotion of mucosal ulcers, colon shortening, diarrhea, inflammatory immune cell infiltration, cytokines release, and abnormal activation of inflammatory macrophages in colon and liver specimens. Intraperitoneal injection of clodronate liposomes to globally delete macrophages dramatically compromised the pathogenesis of MCD-triggering colitis. In addition, MCD intake markedly changed the production pattern of short-chain fatty acids (SCFAs) in murine stools, colons, and livers. We demonstrated that MCD-induced colitis pathogenesis largely depended on the gut microbes and the disease phenotypes could be transmissible through fecal microbiota transplantation (FMT). In conclusion, this study supports the concept that intake of MCD predisposes to experimental colitis and enhances its pathogenesis via modulating gut microbes and macrophages in mice.},
}

@article {pmid38682201,
year = {2024},
author = {Ayabe, RI and White, MG},
title = {Metastasis and the Microbiome: The Impact of Bacteria in Disseminated Colorectal Cancer.},
journal = {Frontiers in bioscience (Landmark edition)},
volume = {29},
number = {4},
pages = {152},
doi = {10.31083/j.fbl2904152},
pmid = {38682201},
issn = {2768-6698},
mesh = {Humans ; *Colorectal Neoplasms/microbiology/pathology/therapy ; *Gastrointestinal Microbiome/physiology ; *Neoplasm Metastasis ; Dysbiosis/microbiology ; Bacteria/classification/genetics ; Fecal Microbiota Transplantation ; },
abstract = {Metastasis remains a leading cause of mortality for patients with solid tumors. An expanding body of literature suggests interplay between the host, gut, and tumoral microbiomes may play a role in cancer initiation and distant dissemination. These associations have been particularly well-studied in colorectal cancer, where gut dysbiosis and an endotoxin-induced inflammatory milieu foster premalignant polyp formation, setting the stage for carcinogenesis. Subsequent violation of the gut vascular barrier enables dissemination of bacterial agents to sites such as the liver, where they contribute to establishment of pre-metastatic niches, which promote tumor cell extravasation and metastatic outgrowth. Intriguingly, breakdown of this vascular barrier has been shown to be aided by the presence of tumoral bacteria. The presence of similar species, including Fusobacterium nucleatum and Escherichia Coli, in both primary and metastatic colorectal tumors, supports this hypothesis and their presence is associated with chemotherapy resistance and an overall poor prognosis. Specific gut microbial populations are also associated with differential response to immunotherapy, which has a growing role in microsatellite unstable colorectal cancers. Recent work suggests that modulation of gut microbiome using dietary modification, targeted antibiotics, or fecal microbiota transplantation may improve response to immunotherapy and oncologic outcomes. Elucidation of the precise mechanistic links between the microbiome and cancer dissemination will open the doors to additional therapeutic possibilities.},
}

Humans
*Colorectal Neoplasms/microbiology/pathology/therapy
*Gastrointestinal Microbiome/physiology
*Neoplasm Metastasis
Dysbiosis/microbiology
Bacteria/classification/genetics
Fecal Microbiota Transplantation

@article {pmid38680517,
year = {2024},
author = {Patel, P and Robinson, PD and Fisher, BT and Phillips, R and Morgan, JE and Lehrnbecher, T and Kuczynski, S and Koenig, C and Haeusler, GM and Esbenshade, A and Elgarten, C and Duong, N and Diorio, C and Castagnola, E and Beauchemin, MP and Ammann, RA and Dupuis, LL and Sung, L},
title = {Guideline for the management of Clostridioides difficile infection in pediatric patients with cancer and hematopoietic cell transplantation recipients: 2024 update.},
journal = {EClinicalMedicine},
volume = {72},
number = {},
pages = {102604},
pmid = {38680517},
issn = {2589-5370},
abstract = {Our objective was to update a clinical practice guideline for the prevention and treatment of Clostridioides difficile infection (CDI) in pediatric patients with cancer and hematopoietic cell transplantation recipients. We reconvened an international multi-disciplinary panel. A systematic review of randomized controlled trials (RCTs) for the prevention or treatment of CDI in any population was updated and identified 31 new RCTs. Strong recommendations were made to use either oral metronidazole or oral vancomycin for non-severe CDI treatment, and to use either oral vancomycin or oral fidaxomicin for severe CDI. A strong recommendation that fecal microbiota transplantation should not be routinely used to treat CDI was also made. The panel made two new good practice statements to follow infection control practices including isolation in patients experiencing CDI, and to minimize systemic antibacterial administration where feasible, especially in patients who have experienced CDI.},
}

@article {pmid38679396,
year = {2024},
author = {Benech, N and Cassir, N and Galperine, T and Alric, L and Scanzi, J and Sokol, H and , },
title = {Fecal microbiota transplantation for recurrent C. difficile infection can be the best therapeutic option in severely immunocompromised patients depending on a case-by-case assessment of the benefit/risk ratio.},
journal = {Gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.1053/j.gastro.2024.04.022},
pmid = {38679396},
issn = {1528-0012},
}

@article {pmid38679228,
year = {2024},
author = {Rondinella, D and Quaranta, G and Rozera, T and Dargenio, P and Fancello, G and Venturini, I and Guarnaccia, A and Porcari, S and Bibbò, S and Sanguinetti, M and Gasbarrini, A and Masucci, L and Cammarota, G and Ianiro, G},
title = {Donor screening for fecal microbiota transplantation with a direct stool testing-based strategy: a prospective cohort study.},
journal = {Microbes and infection},
volume = {},
number = {},
pages = {105341},
doi = {10.1016/j.micinf.2024.105341},
pmid = {38679228},
issn = {1769-714X},
abstract = {Fecal microbiota transplantation (FMT) is effective against recurrent Clostridioides difficile infection (rCDI), but its safety is jeopardized by the potential transmission of pathogens, so international guidelines recommend either a quarantine or a direct stool testing. Whereas reports of the quarantine-based approach are emerging, data on the direct testing-based approach are not available. Our aim is to report outcomes of a donor screening framework for FMT including direct stool testing. In this prospective cohort study, all donor candidates recruited at our FMT centre underwent a four-step screening process to be enrolled as actual donors. Each collected stool donation was then evaluated with a direct stool testing including a molecular assay for gut pathogens and a culture assay for multi-drug resistant organisms (MDRO). From January 2019 to June 2023, 72 of 227 candidates (32%) were considered eligible and provided 277 stool donations. Ninety-nine donations (36%) were discarded for positivity to intestinal pathogens, most commonly enteropathogenic Escherichia coli (n= 37) and Blastocystis hominis (n= 20). Overall, 337 stool aliquots were obtained from 165 approved donations. All suspensions were used for patients with rCDI, and no serious adverse events or clinically evident infections were observed at 12 weeks after procedures. In our study, screening of donor faeces including direct stool testing led to the discard of a considerable rate of stool donations but was also extremely safe. This approach may represent a reliable strategy to guarantee the safety of FMT programs, especially in countries with high prevalence of MDRO.},
}

@article {pmid38678155,
year = {2024},
author = {Corriero, A and Giglio, M and Soloperto, R and Inchingolo, F and Varrassi, G and Puntillo, F},
title = {Microbial Symphony: Exploring the Role of the Gut in Osteoarthritis-Related Pain. A Narrative Review.},
journal = {Pain and therapy},
volume = {},
number = {},
pages = {},
pmid = {38678155},
issn = {2193-8237},
abstract = {One of the most common musculoskeletal disorders, osteoarthritis (OA), causes worldwide disability, morbidity, and poor quality of life by degenerating articular cartilage, modifying subchondral bone, and inflaming synovial membranes. OA pathogenesis pathways must be understood to generate new preventative and disease-modifying therapies. In recent years, it has been acknowledged that gut microbiota (GM) can significantly contribute to the development of OA. Dysbiosis of GM can disrupt the "symphony" between the host and the GM, leading to a host immunological response that activates the "gut-joint" axis, ultimately worsening OA. This narrative review summarizes research supporting the "gut-joint axis" hypothesis, focusing on the interactions between GM and the immune system in its two main components, innate and adaptive immunity. Furthermore, the pathophysiological sequence of events that link GM imbalance to OA and OA-related pain is broken down and further investigated. We also suggest that diet and prebiotics, probiotics, nutraceuticals, exercise, and fecal microbiota transplantation could improve OA management and represent a new potential therapeutic tool in the light of the scarce panorama of disease-modifying osteoarthritis drugs (DMOADs). Future research is needed to elucidate these complex interactions, prioritizing how a particular change in GM, i.e., a rise or a drop of a specific bacterial strain, correlates with a certain OA subset to pinpoint the associated signaling pathway that leads to OA.},
}

@article {pmid38674860,
year = {2024},
author = {Wang, X and Jin, Y and Di, C and Zeng, Y and Zhou, Y and Chen, Y and Pan, Z and Li, Z and Ling, W},
title = {Supplementation of Silymarin Alone or in Combination with Salvianolic Acids B and Puerarin Regulates Gut Microbiota and Its Metabolism to Improve High-Fat Diet-Induced NAFLD in Mice.},
journal = {Nutrients},
volume = {16},
number = {8},
pages = {},
pmid = {38674860},
issn = {2072-6643},
support = {81973022//National Natural Science Foundation of China/ ; TY202101003//BYHEALTH Nutrition and Health Research Foundation/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Non-alcoholic Fatty Liver Disease/etiology/drug therapy ; *Diet, High-Fat/adverse effects ; *Mice, Inbred C57BL ; *Isoflavones/pharmacology ; Male ; Mice ; *Silymarin/pharmacology ; *Dietary Supplements ; Benzofurans/pharmacology ; Liver/metabolism/drug effects ; Disease Models, Animal ; Bile Acids and Salts/metabolism ; Plant Extracts/pharmacology ; *Depsides ; },
abstract = {Silymarin, salvianolic acids B, and puerarin were considered healthy food agents with tremendous potential to ameliorate non-alcoholic fatty liver disease (NAFLD). However, the mechanisms by which they interact with gut microbiota to exert benefits are largely unknown. After 8 weeks of NAFLD modeling, C57BL/6J mice were randomly divided into five groups and fed a normal diet, high-fat diet (HFD), or HFD supplemented with a medium or high dose of Silybum marianum extract contained silymarin or polyherbal extract contained silymarin, salvianolic acids B, and puerarin for 16 weeks, respectively. The untargeted metabolomics and 16S rRNA sequencing were used for molecular mechanisms exploration. The intervention of silymarin and polyherbal extract significantly improved liver steatosis and recovered liver function in the mice, accompanied by an increase in probiotics like Akkermansia and Blautia, and suppressed Clostridium, which related to changes in the bile acids profile in feces and serum. Fecal microbiome transplantation confirmed that this alteration of microbiota and its metabolites were responsible for the improvement in NAFLD. The present study substantiated that alterations of the gut microbiota upon silymarin and polyherbal extract intervention have beneficial effects on HFD-induced hepatic steatosis and suggested the pivotal role of gut microbiota and its metabolites in the amelioration of NAFLD.},
}

Animals
*Gastrointestinal Microbiome/drug effects
*Non-alcoholic Fatty Liver Disease/etiology/drug therapy
*Diet, High-Fat/adverse effects
*Mice, Inbred C57BL
*Isoflavones/pharmacology
Male
Mice
*Silymarin/pharmacology
*Dietary Supplements
Benzofurans/pharmacology
Liver/metabolism/drug effects
Disease Models, Animal
Bile Acids and Salts/metabolism
Plant Extracts/pharmacology
*Depsides

@article {pmid38674803,
year = {2024},
author = {Arteaga-Muller, GY and Flores-Treviño, S and Bocanegra-Ibarias, P and Robles-Espino, D and Garza-González, E and Fabela-Valdez, GC and Camacho-Ortiz, A},
title = {Changes in the Progression of Chronic Kidney Disease in Patients Undergoing Fecal Microbiota Transplantation.},
journal = {Nutrients},
volume = {16},
number = {8},
pages = {},
pmid = {38674803},
issn = {2072-6643},
mesh = {Humans ; *Renal Insufficiency, Chronic/therapy/microbiology ; *Fecal Microbiota Transplantation ; Male ; Female ; *Disease Progression ; Middle Aged ; Double-Blind Method ; *Gastrointestinal Microbiome ; Aged ; *Feces/microbiology ; Dysbiosis/therapy ; Treatment Outcome ; Adult ; Creatinine/blood ; },
abstract = {Chronic kidney disease (CKD) is a progressive loss of renal function in which gut dysbiosis is involved. Fecal microbiota transplantation (FMT) may be a promising alternative for restoring gut microbiota and treating CKD. This study evaluated the changes in CKD progression in patients treated with FMT. Patients with diabetes and/or hypertension with CKD clinical stages 2, 3, and 4 in this single-center, double-blind, randomized, placebo-controlled clinical trial (NCT04361097) were randomly assigned to receive either FMT or placebo capsules for 6 months. Laboratory and stool metagenomic analyses were performed. A total of 28 patients were included (15 FMT and 13 placebo). Regardless of CKD stages, patients responded similarly to FMT treatment. More patients (53.8%) from the placebo group progressed to CKD than the FMT group (13.3%). The FMT group maintained stable renal function parameters (serum creatinine and urea nitrogen) compared to the placebo group. Adverse events after FMT treatment were mild or moderate gastrointestinal symptoms. The abundance of Firmicutes and Actinobacteria decreased whereas Bacteroidetes, Proteobacteria and Roseburia spp. increased in the FMT group. CKD patients showed less disease progression after FMT administration. The administration of oral FMT in patients with CKD is a safe strategy, does not represent a risk, and has potential benefits.},
}

Humans
*Renal Insufficiency, Chronic/therapy/microbiology
*Fecal Microbiota Transplantation
Male
Female
*Disease Progression
Middle Aged
Double-Blind Method
*Gastrointestinal Microbiome
Aged
*Feces/microbiology
Dysbiosis/therapy
Treatment Outcome
Adult
Creatinine/blood

@article {pmid38674209,
year = {2024},
author = {Abenavoli, L and Gambardella, ML and Scarlata, GGM and Lenci, I and Baiocchi, L and Luzza, F},
title = {The Many Faces of Metabolic Dysfunction-Associated Fatty Liver Disease Treatment: From the Mediterranean Diet to Fecal Microbiota Transplantation.},
journal = {Medicina (Kaunas, Lithuania)},
volume = {60},
number = {4},
pages = {},
pmid = {38674209},
issn = {1648-9144},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; *Diet, Mediterranean ; *Non-alcoholic Fatty Liver Disease/therapy/microbiology ; Probiotics/therapeutic use/administration & dosage ; Gastrointestinal Microbiome/physiology ; },
abstract = {The gastrointestinal tract is inhabited by the gut microbiota. The main phyla are Firmicutes and Bacteroidetes. In non-alcoholic fatty liver disease, now renamed metabolic dysfunction-associated fatty liver disease (MAFLD), an alteration in Firmicutes and Bacteroidetes abundance promotes its pathogenesis and evolution into non-alcoholic steatohepatitis, liver cirrhosis, and hepatocellular carcinoma. For this reason, early treatment is necessary to counteract its progression. The aim of the present narrative review is to evaluate the different therapeutic approaches to MAFLD. The most important treatment for MAFLD is lifestyle changes. In this regard, the Mediterranean diet could be considered the gold standard in the prevention and treatment of MAFLD. In contrast, a Western diet should be discouraged. Probiotics and fecal microbiota transplantation seem to be valid, safe, and effective alternatives for MAFLD treatment. However, more studies with a longer follow-up and with a larger cohort of patients are needed to underline the more effective approaches to contrasting MAFLD.},
}

Humans
*Fecal Microbiota Transplantation/methods
*Diet, Mediterranean
*Non-alcoholic Fatty Liver Disease/therapy/microbiology
Probiotics/therapeutic use/administration & dosage
Gastrointestinal Microbiome/physiology

@article {pmid38673510,
year = {2024},
author = {Bragazzi, MC and Pianigiani, F and Venere, R and Ridola, L},
title = {Dysbiosis in Inflammatory Bowel Disease and Spondyloarthritis: Still a Long Way to Go?.},
journal = {Journal of clinical medicine},
volume = {13},
number = {8},
pages = {},
pmid = {38673510},
issn = {2077-0383},
abstract = {The association between Inflammatory Bowel Disease (IBD) and Spondyloarthritis (SpA) has been known for years, as has the concept that IBD is associated with an altered intestinal bacterial composition, a condition known as "dysbiosis". Recently, a state of intestinal dysbiosis has also been found in SpA. Dysbiosis in the field of IBD has been well characterized so far, as well as in SpA. The aim of this review is to summarize what is known to date and to emphasize the similarities between the microbiota conditions in these two diseases: particularly, an altered distribution in the gut of Enterobacteriaceae, Streptococcus, Haemophilus, Clostridium, Akkermansia, Ruminococcus, Faecalibacterium Prausnitzii, Bacteroides Vulgatus, Dialister Invisus, and Bifidubacterium Adolescentis is common to both IBD and SpA. At the same time, little is known about intestinal dysbiosis in IBD-related SpA. Only a single recent study has found an increase in Escherichia and Shigella abundances and a decrease in Firmicutes, Ruminococcaceae, and Faecalibacterium abundances in an IBD-related SpA group. Based on what has been discovered so far about the altered distribution of bacteria that unite both pathologies, it is appropriate to carry out further studies aiming to improve the understanding of IBD-related SpA for the purpose of developing new therapeutic strategies.},
}

@article {pmid38672797,
year = {2024},
author = {Nayak, G and Dimitriadis, K and Pyrpyris, N and Manti, M and Kamperidis, N and Kamperidis, V and Ziakas, A and Tsioufis, K},
title = {Gut Microbiome and Its Role in Valvular Heart Disease: Not a "Gutted" Relationship.},
journal = {Life (Basel, Switzerland)},
volume = {14},
number = {4},
pages = {},
pmid = {38672797},
issn = {2075-1729},
abstract = {The role of the gut microbiome (GM) and oral microbiome (OM) in cardiovascular disease (CVD) has been increasingly being understood in recent years. It is well known that GM is a risk factor for various CVD phenotypes, including hypertension, dyslipidemia, heart failure and atrial fibrillation. However, its role in valvular heart disease (VHD) is less well understood. Research shows that, direct, microbe-mediated and indirect, metabolite-mediated damage as a result of gut dysbiosis and environmental factors results in a subclinical, chronic, systemic inflammatory state, which promotes inflammatory cell infiltration in heart valves and subsequently, via pro-inflammatory molecules, initiates a cascade of reaction, resulting in valve calcification, fibrosis and dysfunction. This relationship between GM and VHD adds a pathophysiological link to the pathogenesis of VHD, which can be aimed therapeutically, in order to prevent or regress any risk for valvular pathologies. Therapeutic interventions include dietary modifications and lifestyle interventions, in order to influence environmental factors that can promote gut dysbiosis. Furthermore, the combination of probiotics and prebiotics, as well as fecal m transplantation and targeted treatment with inducers or inhibitors of microbial enzymes have showed promising results in animal and/or clinical studies, with the potential to reduce the inflammatory state and restore the normal gut flora in patients. This review, thus, is going to discuss the pathophysiological links behind the relationship of GM, CVD and VHD, as well as explore the recent data regarding the effect of GM-altering treatment in CVD, cardiac function and systemic inflammation.},
}

@article {pmid38672155,
year = {2024},
author = {Shin, J and Baek, GH and Cha, B and Park, SH and Lee, JH and Kim, JS and Kwon, KS},
title = {Complementary Therapeutic Effect of Fecal Microbiota Transplantation in Ulcerative Colitis after the Response to Anti-Tumor Necrosis Factor Alpha Agent Was Lost: A Case Report.},
journal = {Biomedicines},
volume = {12},
number = {4},
pages = {},
pmid = {38672155},
issn = {2227-9059},
support = {2021R1G1A1095241//National Research Foundation of Korea/ ; },
abstract = {In patients with ulcerative colitis (UC), the development of an antidrug antibody (ADA) to anti-tumor necrosis factor (TNF)α agent is a crucial problem which aggravates the clinical course of the disease, being cited as one of the most common causes for discontinuing anti-TNFα treatment. This is due to ADA eventually causing secondary LOR, leading to discontinuation of anti-TNFα treatment. Recently, research on the microbiome and relationship between worsening UC and dysbiosis has been conducted. Further, investigations on the association between the microbiome and secondary LOR are increasing. Here, we present the therapeutic effect of fecal microbiota transplantation (FMT) on a 42-year-old man with secondary LOR and high ADA levels. FMT has recently been used for the treatment of, and for overcoming, drug resistance through microbiome modification. Stool samples were collected from the patient before and 4 weeks after FMT. Symptoms, including hematochezia and Mayo endoscopy sub-scores, improved after FMT, while ADA levels decreased by one-third to less than half the value (29 ng/mL) compared to before FMT (79 ng/mL). Additionally, the trough level of infliximab became measurable, which reflects the improvement in the area under the concentration (AUC). Butyricicoccus, Faecalibacterium, Bifidobacterium, Ligilactobacillus, Alistipes, and Odoribacter, which regulate immune responses and alleviate inflammation, also increased after FMT. We report a case in which microbiome modification by FMT increased the AUC of anti-TNFα in a patient who developed secondary LOR during anti-TNFα treatment, thereby improving symptoms and mucosal inflammation.},
}

@article {pmid38667013,
year = {2024},
author = {Losurdo, G and Mezzapesa, M and Ditonno, I and Piazzolla, M and Pricci, M and Girardi, B and Celiberto, F and Galeano, G and Riezzo, G and Russo, F and Iannone, A and Ierardi, E and Di Leo, A},
title = {Helicobacter pylori Secondary Antibiotic Resistance after One or More Eradication Failure: A Genotypic Stool Analysis Study.},
journal = {Antibiotics (Basel, Switzerland)},
volume = {13},
number = {4},
pages = {},
pmid = {38667013},
issn = {2079-6382},
abstract = {Helicobacter pylori (H. pylori) antibiotic resistance is the leading cause for unsuccessful eradication therapy. After one or more failures, the chance of encountering secondary antibiotic resistance increases. The aim of this study was to characterize genotypic secondary resistance in a cohort of southern Italian H. pylori patients with at least one previous failure. Such patients collected stool samples using a dedicated kit (THD fecal test[TM]), and bacterial DNA was extracted and amplified using RT-PCR. Resistance to clarithromycin, amoxicillin, metronidazole, levofloxacin, and tetracycline was assessed using a high-resolution melting curve. We enrolled 50 patients. A total of 72% of patients failed one previous antibiotic course, 16% failed two, 10% failed three, and 2% failed four. The rate of secondary antibiotic resistance was 16% for clarithromycin, 18% for metronidazole, 14% for amoxicillin, 14% for levofloxacin, and 2% for tetracycline. Among the eight clarithromycin-resistant patients, five (62.5%) previously received a clarithromycin-based regimen. The same rate was 33.3% (3/9) for metronidazole. The only tetracycline-resistant patient had received Pylera. In conclusion, our data seem to show that, even though secondary resistance is not very high, resistance to clarithromycin could be very likely related to previous exposure to this antibiotic.},
}

@article {pmid38666855,
year = {2024},
author = {Long, C and Zhou, X and Xia, F and Zhou, B},
title = {Intestinal Barrier Dysfunction and Gut Microbiota in Non-Alcoholic Fatty Liver Disease: Assessment, Mechanisms, and Therapeutic Considerations.},
journal = {Biology},
volume = {13},
number = {4},
pages = {},
pmid = {38666855},
issn = {2079-7737},
support = {2022A1515010833//Natural Science Foundation of Guangdong Province/ ; 82074078//National Natural Science Foundation of China/ ; 81803816//National Natural Science Foundation of China/ ; ZDSYS20220606100801003//Shenzhen Key Laboratory of Chinese Medicine Active Substance Screening and Translational Re-search/ ; },
abstract = {Non-alcoholic fatty liver disease (NAFLD) is a type of metabolic stress liver injury closely related to insulin resistance (IR) and genetic susceptibility without alcohol consumption, which encompasses a spectrum of liver disorders ranging from simple hepatic lipid accumulation, known as steatosis, to the more severe form of steatohepatitis (NASH). NASH can progress to cirrhosis and hepatocellular carcinoma (HCC), posing significant health risks. As a multisystem disease, NAFLD is closely associated with systemic insulin resistance, central obesity, and metabolic disorders, which contribute to its pathogenesis and the development of extrahepatic complications, such as cardiovascular disease (CVD), type 2 diabetes mellitus, chronic kidney disease, and certain extrahepatic cancers. Recent evidence highlights the indispensable roles of intestinal barrier dysfunction and gut microbiota in the onset and progression of NAFLD/NASH. This review provides a comprehensive insight into the role of intestinal barrier dysfunction and gut microbiota in NAFLD, including intestinal barrier function and assessment, inflammatory factors, TLR4 signaling, and the gut-liver axis. Finally, we conclude with a discussion on the potential therapeutic strategies targeting gut permeability and gut microbiota in individuals with NAFLD/NASH, such as interventions with medications/probiotics, fecal transplantation (FMT), and modifications in lifestyle, including exercise and diet.},
}

@article {pmid38664425,
year = {2024},
author = {Chui, ZSW and Chan, LML and Zhang, EWH and Liang, S and Choi, EPH and Lok, KYW and Tun, HM and Kwok, JYY},
title = {Effects of microbiome-based interventions on neurodegenerative diseases: a systematic review and meta-analysis.},
journal = {Scientific reports},
volume = {14},
number = {1},
pages = {9558},
pmid = {38664425},
issn = {2045-2322},
mesh = {Humans ; *Neurodegenerative Diseases/microbiology/therapy ; *Gastrointestinal Microbiome ; *Fecal Microbiota Transplantation/methods ; Probiotics/therapeutic use ; Microbiota ; },
abstract = {Neurodegenerative diseases (NDDs) are characterized by neuronal damage and progressive loss of neuron function. Microbiome-based interventions, such as dietary interventions, biotics, and fecal microbiome transplant, have been proposed as a novel approach to managing symptoms and modulating disease progression. Emerging clinical trials have investigated the efficacy of interventions modulating the GM in alleviating or reversing disease progression, yet no comprehensive synthesis have been done. A systematic review of the literature was therefore conducted to investigate the efficacy of microbiome-modulating methods. The search yielded 4051 articles, with 15 clinical trials included. The overall risk of bias was moderate in most studies. Most microbiome-modulating interventions changed the GM composition. Despite inconsistent changes in GM composition, the meta-analysis showed that microbiome-modulating interventions improved disease burden (SMD, - 0.57; 95% CI - 0.93 to - 0.21; I[2] = 42%; P = 0.002) with a qualitative trend of improvement in constipation. However, current studies have high methodological heterogeneity and small sample sizes, requiring more well-designed and controlled studies to elucidate the complex linkage between microbiome, microbiome-modulating interventions, and NDDs.},
}

Humans
*Neurodegenerative Diseases/microbiology/therapy
*Gastrointestinal Microbiome
*Fecal Microbiota Transplantation/methods
Probiotics/therapeutic use
Microbiota

@article {pmid38664378,
year = {2024},
author = {Holmberg, SM and Feeney, RH and Prasoodanan P K, V and Puértolas-Balint, F and Singh, DK and Wongkuna, S and Zandbergen, L and Hauner, H and Brandl, B and Nieminen, AI and Skurk, T and Schroeder, BO},
title = {The gut commensal Blautia maintains colonic mucus function under low-fiber consumption through secretion of short-chain fatty acids.},
journal = {Nature communications},
volume = {15},
number = {1},
pages = {3502},
pmid = {38664378},
issn = {2041-1723},
support = {2018-02095//Vetenskapsrådet (Swedish Research Council)/ ; SMK-1959//Kempestiftelserna (Kempe Foundations)/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome ; *Dietary Fiber/metabolism ; *Fatty Acids, Volatile/metabolism ; Mice ; *Colon/metabolism/microbiology ; Humans ; *Intestinal Mucosa/metabolism/microbiology ; Male ; Receptors, G-Protein-Coupled/metabolism/genetics ; Female ; Mice, Inbred C57BL ; Mucus/metabolism ; Fecal Microbiota Transplantation ; Symbiosis ; Propionates/metabolism ; Clostridiales/metabolism ; Acetates/metabolism ; Adult ; *Receptors, Cell Surface ; },
abstract = {Beneficial gut bacteria are indispensable for developing colonic mucus and fully establishing its protective function against intestinal microorganisms. Low-fiber diet consumption alters the gut bacterial configuration and disturbs this microbe-mucus interaction, but the specific bacteria and microbial metabolites responsible for maintaining mucus function remain poorly understood. By using human-to-mouse microbiota transplantation and ex vivo analysis of colonic mucus function, we here show as a proof-of-concept that individuals who increase their daily dietary fiber intake can improve the capacity of their gut microbiota to prevent diet-mediated mucus defects. Mucus growth, a critical feature of intact colonic mucus, correlated with the abundance of the gut commensal Blautia, and supplementation of Blautia coccoides to mice confirmed its mucus-stimulating capacity. Mechanistically, B. coccoides stimulated mucus growth through the production of the short-chain fatty acids propionate and acetate via activation of the short-chain fatty acid receptor Ffar2, which could serve as a new target to restore mucus growth during mucus-associated lifestyle diseases.},
}

Animals
*Gastrointestinal Microbiome
*Dietary Fiber/metabolism
*Fatty Acids, Volatile/metabolism
Mice
*Colon/metabolism/microbiology
Humans
*Intestinal Mucosa/metabolism/microbiology
Male
Receptors, G-Protein-Coupled/metabolism/genetics
Female
Mice, Inbred C57BL
Mucus/metabolism
Fecal Microbiota Transplantation
Symbiosis
Propionates/metabolism
Clostridiales/metabolism
Acetates/metabolism
Adult
*Receptors, Cell Surface

@article {pmid38663650,
year = {2024},
author = {Fang, H and Hou, Q and Zhang, W and Su, Z and Zhang, J and Li, J and Lin, J and Wang, Z and Yu, X and Yang, Y and Wang, Q and Li, X and Li, Y and Hu, L and Li, S and Wang, X and Liao, L},
title = {Fecal Microbiota Transplantation Improves Clinical Symptoms of Fibromyalgia: An open-label, Randomized, Nonplacebo-Controlled Study.},
journal = {The journal of pain},
volume = {},
number = {},
pages = {104535},
doi = {10.1016/j.jpain.2024.104535},
pmid = {38663650},
issn = {1528-8447},
abstract = {Fibromyalgia (FM) is a complex and poorly understood disorder characterized by chronic and widespread musculoskeletal pain, of which the etiology remains unknown. Now, the disorder of the gut microbiome is considered as one of the main causes of FM. This study was aimed to investigate the potential benefits of fecal microbiota transplantation (FMT) in patients with FM. A total of 45 patients completed this open-label randomized, nonplacebo-controlled clinical study. The Numerical Rating Scale (NRS) scores in the FMT group were slightly lower than the control group at 1 month (P> 0.05), and they decreased significantly at 2, 3, 6, and 12 months after treatment (P < 0.001). Besides, compared with the control group, the Widespread Pain Index (WPI), Symptom Severity (SS), Hospital Anxiety and Depression Scale (HADS) and Pittsburgh Sleep Quality Index (PSQI) scores were significantly lower in the FMT group at different time points (P < 0.001). After 6 months of treatment, there was a significant increase in serotonin (5-HT) and gamma-aminobutyric acid (GABA) levels (P < 0.001), while glutamate levels significantly decreased in the FMT group (P < 0.001). The total effective rate was higher in the FMT group (90.9%) compared to the control group (56.5%) after 6 months of treatment (P < 0.05). FMT can effectively improve the clinical symptoms of FM. With the close relations between the changes of neurotransmitters and FM, certain neurotransmitters may serve as a diagnostic marker or potential target for FM patients. PERSPECTIVE: Fecal microbiota transplantation (FMT) is a novel therapy that aims to restore the gut microbial balance and modulate the gut-brain axis. It is valuable to further explore the therapeutic effect of FMT on FM. Furthermore, certain neurotransmitters may become a diagnostic marker or a new therapeutic target for FM patients.},
}

@article {pmid38663540,
year = {2024},
author = {Liang, L and Zhang, J and Chen, J and Tian, Y and Li, W and Shi, M and Cheng, S and Zheng, Y and Wang, C and Liu, H and Yang, X and Ye, W},
title = {Bazedoxifene attenuates dextran sodium sulfate-induced colitis in mice through gut microbiota modulation and inhibition of STAT3 and NF-κB pathways.},
journal = {European journal of pharmacology},
volume = {},
number = {},
pages = {176611},
doi = {10.1016/j.ejphar.2024.176611},
pmid = {38663540},
issn = {1879-0712},
abstract = {Inflammatory bowel disease (IBD) is a chronic and relapsing inflammatory disorder of the gastrointestinal tract for which treatment options remain limited. In this study, we used a dual-luciferase-based screening of an FDA-approved drug library, identifying Bazedoxifene (BZA) as an inhibitor of the NF-κB pathway. We further investigated its therapeutic effects in a dextran sodium sulfate (DSS)-induced colitis model and explored its impact on gut microbiota regulation and the underlying molecular mechanisms. Our results showed that BZA significantly reduced DSS-induced colitis symptoms in mice, evidenced by decreased colon length shortening, lower histological scores, and increased expression of intestinal mucosal barrier-associated proteins, such as Claudin 1, Occludin, Zo-1, Mucin 2 (Muc2), and E-cadherin. Used independently, BZA showed therapeutic effects comparable to those of infliximab (IFX). In addition, BZA modulated the abundance of gut microbiota especially Bifidobacterium pseudolongum, and influenced microbial metabolite production. Crucially, BZA's alleviation of DSS-induced colitis in mice was linked to change in gut microbiota composition, as evidenced by in vivo gut microbiota depletion and fecal microbiota transplantation (FMT) mice model. Molecularly, BZA inhibited STAT3 and NF-κB activation in DSS-induced colitis in mice. In general, BZA significantly reduced DSS-induced colitis in mice through modulating the gut microbiota and inhibiting STAT3 and NF-κB activation, and its independent use demonstrated a therapeutic potential comparable to IFX. This study highlights gut microbiota's role in IBD drug development, offering insights for BZA's future development and its clinical applications.},
}

@article {pmid38663526,
year = {2024},
author = {Zhang, S and Tang, S and Liu, Z and Lv, H and Cai, X and Zhong, R and Chen, L and Zhang, H},
title = {Baicalin restore intestinal damage after early-life antibiotic therapy: the role of the MAPK signaling pathway.},
journal = {Pharmacological research},
volume = {},
number = {},
pages = {107194},
doi = {10.1016/j.phrs.2024.107194},
pmid = {38663526},
issn = {1096-1186},
abstract = {Antibiotic related intestinal injury in early life affects subsequent health and susceptibility. Here, we employed weaned piglets as a model to investigate the protective effects of baicalin against early-life antibiotic exposure-induced microbial dysbiosis. Piglets exposed to lincomycin showed a marked reduction in body weight (p < 0.05) and deterioration of jejunum intestinal morphology, alongside an increase in antibiotic-resistant bacteria such as Staphylococcus, Dolosicoccus, Escherichia-Shigella, and Raoultella. In contrast, baicalin treatment resulted in body weights, intestinal morphology, and microbial profiles that closely resembled those of the control group (p > 0.05), with a significant increase in norank_f_Muribaculaceae and Prevotellaceae_NK3B31_group colonization compared with lincomycin group (p < 0.05). Further analysis through fecal microbial transplantation into mice revealed that lincomycin exposure led to significant alterations in intestinal morphology and microbial composition, notably increasing harmful microbes and decreasing beneficial ones such as norank_Muribaculaceae and Akkermansia (p < 0.05). This shift was associated with an increase in harmful metabolites and disruption of the calcium signaling pathway gene expression. Conversely, baicalin supplementation not only counteracted these effects but also enhanced beneficial metabolites and regulated genes within the MAPK signaling pathway (MAP3K11, MAP4K2, MAPK7, MAPK13) and calcium channel proteins (ORA13, CACNA1S, CACNA1F and CACNG8), suggesting a mechanism through which baicalin mitigates antibiotic-induced intestinal and microbial disturbances. These findings highlight baicalin's potential as a plant extract-based intervention for preventing antibiotic-related intestinal injury and offer new targets for therapeutic strategies.},
}

@article {pmid38663295,
year = {2024},
author = {Liu, A and Li, Y and Li, L and Chen, K and Tan, M and Zou, F and Zhang, X and Meng, X},
title = {Bile acid metabolism is altered in learning and memory impairment induced by chronic lead exposure.},
journal = {Journal of hazardous materials},
volume = {471},
number = {},
pages = {134360},
doi = {10.1016/j.jhazmat.2024.134360},
pmid = {38663295},
issn = {1873-3336},
abstract = {Lead is a neurotoxic contaminant that exists widely in the environment. Although lead neurotoxicity has been found to be tightly linked to gut microbiota disturbance, the effect of host metabolic disorders caused by gut microbiota disturbance on lead neurotoxicity has not been investigated. In this work, the results of new object recognition tests and Morris water maze tests showed that chronic low-dose lead exposure caused learning and memory dysfunction in mice. The results of 16 S rRNA sequencing of cecal contents and fecal microbiota transplantation showed that the neurotoxicity of lead could be transmitted through gut microbiota. The results of untargeted metabolomics and bile acid targeted metabolism analysis showed that the serum bile acid metabolism profile of lead-exposed mice was significantly changed. In addition, supplementation with TUDCA or INT-777 significantly alleviated chronic lead exposure-induced learning and memory impairment, primarily through inhibition of the NLRP3 inflammasome in the hippocampus to relieve neuroinflammation. In conclusion, our findings suggested that dysregulation of host bile acid metabolism may be one of the mechanisms of lead-induced neurotoxicity, and supplementation of specific bile acids may be a possible therapeutic strategy for lead-induced neurotoxicity.},
}

@article {pmid38660489,
year = {2024},
author = {Zhang, J and Wang, H and Liu, Y and Shi, M and Zhang, M and Zhang, H and Chen, J},
title = {Advances in fecal microbiota transplantation for the treatment of diabetes mellitus.},
journal = {Frontiers in cellular and infection microbiology},
volume = {14},
number = {},
pages = {1370999},
pmid = {38660489},
issn = {2235-2988},
mesh = {*Fecal Microbiota Transplantation/methods ; Humans ; *Gastrointestinal Microbiome ; *Diabetes Mellitus/therapy/microbiology ; Dysbiosis/therapy ; Animals ; Feces/microbiology ; },
abstract = {Diabetes mellitus (DM) refers to a group of chronic diseases with global prevalence, characterized by persistent hyperglycemia resulting from various etiologies. DM can harm various organ systems and lead to acute or chronic complications, which severely endanger human well-being. Traditional treatment mainly involves controlling blood sugar levels through replacement therapy with drugs and insulin; however, some patients still find a satisfactory curative effect difficult to achieve. Extensive research has demonstrated a close correlation between enteric dysbacteriosis and the pathogenesis of various types of DM, paving the way for novel therapeutic approaches targeting the gut microbiota to manage DM. Fecal microbiota transplantation (FMT), a method for re-establishing the intestinal microbiome balance, offers new possibilities for treating diabetes. This article provides a comprehensive review of the correlation between DM and the gut microbiota, as well as the current advancements in FMT treatment for DM, using FMT as an illustrative example. This study aims to offer novel perspectives and establish a theoretical foundation for the clinical diagnosis and management of DM.},
}

*Fecal Microbiota Transplantation/methods
Humans
*Gastrointestinal Microbiome
*Diabetes Mellitus/therapy/microbiology
Dysbiosis/therapy
Animals
Feces/microbiology

@article {pmid38659636,
year = {2024},
author = {Herman, C and Barker, BM and Bartelli, TF and Chandra, V and Krajmalnik-Brown, R and Jewell, M and Li, L and Liao, C and McAllister, F and Nirmalkar, K and Xavier, JB and Caporaso, JG},
title = {Assessing Engraftment Following Fecal Microbiota Transplant.},
journal = {ArXiv},
volume = {},
number = {},
pages = {},
pmid = {38659636},
issn = {2331-8422},
abstract = {Fecal Microbiota Transplant (FMT) is an FDA approved treatment for recurrent Clostridium difficile infections, and is being explored for other clinical applications, from alleviating digestive and neurological disorders, to priming the microbiome for cancer treatment, and restoring microbiomes impacted by cancer treatment. Quantifying the extent of engraftment following an FMT is important in determining if a recipient didn't respond because the engrafted microbiome didn't produce the desired outcomes (a successful FMT, but negative treatment outcome), or the microbiome didn't engraft (an unsuccessful FMT and negative treatment outcome). The lack of a consistent methodology for quantifying FMT engraftment extent hinders the assessment of FMT success and its relation to clinical outcomes, and presents challenges for comparing FMT results and protocols across studies. Here we review 46 studies of FMT in humans and model organisms and group their approaches for assessing the extent to which an FMT engrafts into three criteria: 1) Chimeric Asymmetric Community Coalescence investigates microbiome shifts following FMT engraftment. 2) Donated Microbiome Indicator Features tracks donated microbiome features as a signal of engraftment with methods such as differential abundance testing based on the current sample collection, or tracking changes in feature abundances that have been previously identified. 3) Temporal Stability examines how resistant post-FMT recipient's microbiomes are to reverting back to their baseline microbiome. Investigated together, these criteria provide a clear assessment of microbiome engraftment. We discuss the pros and cons of each of these criteria, providing illustrative examples of their application. We also introduce key terminology and recommendations on how FMT studies can be analyzed for rigorous engraftment extent assessment.},
}

@article {pmid38659317,
year = {2024},
author = {Xiao, N and He, W and Chen, S and Yao, Y and Wu, N and Xu, M and Du, H and Zhao, Y and Tu, Y},
title = {Protective Effect of Egg Yolk Lipids against Dextran Sulfate Sodium-Induced Colitis: The Key Role of Gut Microbiota and Short-Chain Fatty Acids.},
journal = {Molecular nutrition & food research},
volume = {},
number = {},
pages = {e2400048},
doi = {10.1002/mnfr.202400048},
pmid = {38659317},
issn = {1613-4133},
support = {82260642//National Natural Science Foundation of China/ ; 20224ACB205015//Key Program of Natural Science Foundation of Jiangxi Province, China/ ; 29202300002//Training Project of High-level and High-skilled Leading Talents of Jiangxi Province/ ; },
abstract = {Egg yolk lipids significantly alleviate dextran sulfate sodium (DSS)-induced colitis by inhibiting NLRP3 inflammasome, reversing gut microbiota dysbiosis, and increasing short chain fatty acids (SCFAs) concentrations. However, the role of gut microbiota and the relationship between SCFAs and NLRP3 inflammasome are still unknown. Here, this study confirms that antibiotic treatment abolishes the protective effect of egg yolk lipids on DSS-induced colonic inflammation, intestinal barrier damage, and lipopolysaccharide translocation. Fecal microbiota transplantation also supports that egg yolk lipids alleviate colitis in a gut microbiota-dependent manner. Then, the study investigates the relationship between SCFAs and NLRP3 inflammasome, and finds that SCFAs significantly suppress colitis via inhibiting colonic NLRP3 inflammasome activation and proinflammatory cytokines secretions (interleukin, IL)-1β and IL-18, and combined treatment of SCFAs and MCC950 (NLRP3 inhibitor) shows a better activity against colitis and NLRP3 inflammasome activation. Together, these findings provide positive evidence for gut microbiorta-SCFAs-NLRP3 axis as a novel target involving in the therapy of inflammatory bowel disease.},
}

@article {pmid38655401,
year = {2024},
author = {Shi, W and Li, Z and Wang, W and Liu, X and Wu, H and Chen, X and Zhou, X and Zhang, S},
title = {Dynamic gut microbiome-metabolome in cationic bovine serum albumin induced experimental immune-complex glomerulonephritis and effect of losartan and mycophenolate mofetil on microbiota modulation.},
journal = {Journal of pharmaceutical analysis},
volume = {14},
number = {4},
pages = {100931},
pmid = {38655401},
issn = {2214-0883},
abstract = {Dynamic changes in gut dysbiosis and metabolomic dysregulation are associated with immune-complex glomerulonephritis (ICGN). However, an in-depth study on this topic is currently lacking. Herein, we report an ICGN model to address this gap. ICGN was induced via the intravenous injection of cationized bovine serum albumin (c-BSA) into Sprague-Dawley (SD) rats for two weeks, after which mycophenolate mofetil (MMF) and losartan were administered orally. Two and six weeks after ICGN establishment, fecal samples were collected and 16S ribosomal DNA (rDNA) sequencing and untargeted metabolomic were conducted. Fecal microbiota transplantation (FMT) was conducted to determine whether gut normalization caused by MMF and losartan contributed to their renal protective effects. A gradual decline in microbial diversity and richness was accompanied by a loss of renal function. Approximately 18 genera were found to have significantly different relative abundances between the early and later stages, and Marvinbryantia and Allobaculum were markedly upregulated in both stages. Untargeted metabolomics indicated that the tryptophan metabolism was enhanced in ICGN, characterized by the overproduction of indole and kynurenic acid, while the serotonin pathway was reduced. Administration of losartan and MMF ameliorated microbial dysbiosis and reduced the accumulation of indoxyl conjugates in feces. FMT using feces from animals administered MMF and losartan improved gut dysbiosis by decreasing the Firmicutes/Bacteroidetes (F/B) ratio but did not improve renal function. These findings indicate that ICGN induces serous gut dysbiosis, wherein an altered tryptophan metabolism may contribute to its progression. MMF and losartan significantly reversed the gut microbial and metabolomic dysbiosis, which partially contributed to their renoprotective effects.},
}

@article {pmid38654015,
year = {2024},
author = {Lachance, G and Robitaille, K and Laaraj, J and Gevariya, N and Varin, TV and Feldiorean, A and Gaignier, F and Julien, IB and Xu, HW and Hallal, T and Pelletier, JF and Bouslama, S and Boufaied, N and Derome, N and Bergeron, A and Ellis, L and Piccirillo, CA and Raymond, F and Fradet, Y and Labbé, DP and Marette, A and Fradet, V},
title = {The gut microbiome-prostate cancer crosstalk is modulated by dietary polyunsaturated long-chain fatty acids.},
journal = {Nature communications},
volume = {15},
number = {1},
pages = {3431},
pmid = {38654015},
issn = {2041-1723},
support = {400345//Canadian Cancer Society Research Institute (Société Canadienne du Cancer)/ ; },
mesh = {Male ; *Gastrointestinal Microbiome ; *Prostatic Neoplasms/metabolism/diet therapy/microbiology ; Animals ; Humans ; Mice ; *Fecal Microbiota Transplantation ; *Feces/microbiology ; Fatty Acids, Omega-3/metabolism/administration & dosage ; Mice, Inbred C57BL ; Fatty Acids, Unsaturated/metabolism ; },
abstract = {The gut microbiota modulates response to hormonal treatments in prostate cancer (PCa) patients, but whether it influences PCa progression remains unknown. Here, we show a reduction in fecal microbiota alpha-diversity correlating with increase tumour burden in two distinct groups of hormonotherapy naïve PCa patients and three murine PCa models. Fecal microbiota transplantation (FMT) from patients with high PCa volume is sufficient to stimulate the growth of mouse PCa revealing the existence of a gut microbiome-cancer crosstalk. Analysis of gut microbial-related pathways in mice with aggressive PCa identifies three enzymes responsible for the metabolism of long-chain fatty acids (LCFA). Supplementation with LCFA omega-3 MAG-EPA is sufficient to reduce PCa growth in mice and cancer up-grading in pre-prostatectomy PCa patients correlating with a reduction of gut Ruminococcaceae in both and fecal butyrate levels in PCa patients. This suggests that the beneficial effect of omega-3 rich diet is mediated in part by modulating the crosstalk between gut microbes and their metabolites in men with PCa.},
}

Male
*Gastrointestinal Microbiome
*Prostatic Neoplasms/metabolism/diet therapy/microbiology
Animals
Humans
Mice
*Fecal Microbiota Transplantation
*Feces/microbiology
Fatty Acids, Omega-3/metabolism/administration & dosage
Mice, Inbred C57BL
Fatty Acids, Unsaturated/metabolism

@article {pmid38653643,
year = {2024},
author = {Taghaddos, D and Saqib, Z and Bai, X and Bercik, P and Collins, SM},
title = {Post-infectious ibs following Clostridioides difficile infection; role of microbiota and implications for treatment.},
journal = {Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.dld.2024.03.008},
pmid = {38653643},
issn = {1878-3562},
abstract = {Up to 25% of patients recovering from antibiotic-treated Clostridioides difficile infection (CDI) develop functional symptoms reminiscent of Post-Infectious Irritable Bowel Syndrome (PI-IBS). For patients with persistent symptoms following infection, a clinical dilemma arises as to whether to provide additional antibiotic treatment or to adopt a conservative symptom-based approach. Here, we review the literature on CDI-related PI-IBS and compare the findings with PI-IBS. We review proposed mechanisms, including the role of C. difficile toxins and the microbiota, and discuss implications for therapy. We suggest that gut dysfunction post-CDI may be initiated by toxin-induced damage to enteroglial cells and that a dysbiotic gut microbitota maintains the clinical phenotype over time, prompting consideration of microbiota-directed therapies. While Fecal Microbial Transplant (FMT) is currently reserved for recurrent CDI (rCDI), we propose that microbiota-directed therapies may have a role in primary CDI in order to avoid or mitigate futher antibiotic treatment that further disrupts the microbiota and thus prevent PI-IBS. We discuss novel microbial transfer therapies and as they emerge, we recommend clinical trials to determine whether microbial transfer therapy of the primary infection prevents both rCDI and CDI-related PI- IBS.},
}

@article {pmid38648368,
year = {2024},
author = {Muchhala, KH and Kallurkar, PS and Kang, M and Koseli, E and Poklis, JL and Xu, Q and Dewey, WL and Fettweis, JM and Jimenez, NR and Akbarali, HI},
title = {The role of morphine- and fentanyl-induced impairment of intestinal epithelial antibacterial activity in dysbiosis and its impact on the microbiota-gut-brain axis.},
journal = {FASEB journal : official publication of the Federation of American Societies for Experimental Biology},
volume = {38},
number = {8},
pages = {e23603},
doi = {10.1096/fj.202301590RR},
pmid = {38648368},
issn = {1530-6860},
support = {P30DA033934//HHS | National Institutes of Health (NIH)/ ; R01DA024009//HHS | National Institutes of Health (NIH)/ ; T32DA007027//HHS | National Institutes of Health (NIH)/ ; 2214-A//TUBITAK/ ; },
abstract = {Recent evidence suggests that chronic exposure to opioid analgesics such as morphine disrupts the intestinal epithelial layer and causes intestinal dysbiosis. Depleting gut bacteria can preclude the development of tolerance to opioid-induced antinociception, suggesting an important role of the gut-brain axis in mediating opioid effects. The mechanism underlying opioid-induced dysbiosis, however, remains unclear. Host-produced antimicrobial peptides (AMPs) are critical for the integrity of the intestinal epithelial barrier as they prevent the pathogenesis of the enteric microbiota. Here, we report that chronic morphine or fentanyl exposure reduces the antimicrobial activity in the ileum, resulting in changes in the composition of bacteria. Fecal samples from morphine-treated mice had increased levels of Akkermansia muciniphila with a shift in the abundance ratio of Firmicutes and Bacteroidetes. Fecal microbial transplant (FMT) from morphine-naïve mice or oral supplementation with butyrate restored (a) the antimicrobial activity, (b) the expression of the antimicrobial peptide, Reg3γ, (c) prevented the increase in intestinal permeability and (d) prevented the development of antinociceptive tolerance in morphine-dependent mice. Improved epithelial barrier function with FMT or butyrate prevented the enrichment of the mucin-degrading A. muciniphila in morphine-dependent mice. These data implicate impairment of the antimicrobial activity of the intestinal epithelium as a mechanism by which opioids disrupt the microbiota-gut-brain axis.},
}

@article {pmid38647627,
year = {2023},
author = {Zhuang, X and Zhao, M and Ji, X and Yang, S and Yin, H and Zhao, L},
title = {Chitobiose exhibited a lipid-lowering effect in ob/ob[-/-] mice via butyric acid enrolled liver-gut crosstalk.},
journal = {Bioresources and bioprocessing},
volume = {10},
number = {1},
pages = {79},
pmid = {38647627},
issn = {2197-4365},
support = {23ZR1417300//Shanghai Natural Science Foundation General program/ ; 2022153//Shanghai post-doctoral Excellence Program/ ; 2019YFD090180302//National key R&D Program of China/ ; B18022//111 Project/ ; },
abstract = {Chitobiose (COS2) efficiently lowers lipids in vivo and facilitates butyric acid enrichment during human fecal fermentation. However, whether COS2 can interact with butyric acid to generate a hypolipidemic effect remains unclear. This study examined the hypolipidemic mechanism of COS2 involving butyric acid, which could alleviate non-alcoholic fatty liver disease (NAFLD). The results revealed that COS2 administration modulated the β-oxidation pathway in the liver and restructured the short chain fatty acids in the fecal of ob/ob[-/-] mice. Moreover, the hypolipidemic effect of COS2 and its specific accumulated metabolite butyric acid was verified in sodium oleate-induced HepG2 cells. Butyric acid was more effective to reverse lipid accumulation and up-regulate β-oxidation pathway at lower concentrations. Furthermore, structural analysis suggested that butyric acid formed hydrogen bonds with key residues in hydrophilic ligand binding domains (LBDs) of PPARα and activated the transcriptional activity of the receptor. Therefore, the potential mechanism behind the lipid-lowering effect of COS2 in vivo involved restoring hepatic lipid disorders via butyric acid accumulation and liver-gut axis signaling.},
}

@article {pmid38647957,
year = {2024},
author = {Singh, V and Mahra, K and Jung, D and Shin, JH},
title = {Gut Microbes in Polycystic Ovary Syndrome and Associated Comorbidities; Type 2 Diabetes, Non-Alcoholic Fatty Liver Disease (NAFLD), Cardiovascular Disease (CVD), and the Potential of Microbial Therapeutics.},
journal = {Probiotics and antimicrobial proteins},
volume = {},
number = {},
pages = {},
pmid = {38647957},
issn = {1867-1314},
support = {2021R1A6C101A416//Korea Basic Science Institute/ ; },
abstract = {Polycystic ovary syndrome (PCOS) is one of the most common endocrine anomalies among females of reproductive age, highlighted by hyperandrogenism. PCOS is multifactorial as it can be associated with obesity, insulin resistance, low-grade chronic inflammation, and dyslipidemia. PCOS also leads to dysbiosis by lowering microbial diversity and beneficial microbes, such as Faecalibacterium, Roseburia, Akkermenisa, and Bifidobacterium, and by causing a higher load of opportunistic pathogens, such as Escherichia/Shigella, Fusobacterium, Bilophila, and Sutterella. Wherein, butyrate producers and Akkermansia participate in the glucose uptake by inducing glucagon-like peptide-1 (GLP-1) and glucose metabolism, respectively. The abovementioned gut microbes also maintain the gut barrier function and glucose homeostasis by releasing metabolites such as short-chain fatty acids (SCFAs) and Amuc_1100 protein. In addition, PCOS-associated gut is found to be higher in gut-microbial enzyme β-glucuronidase, causing the de-glucuronidation of conjugated androgen, making it susceptible to reabsorption by entero-hepatic circulation, leading to a higher level of androgen in the circulatory system. Overall, in PCOS, such dysbiosis increases the gut permeability and LPS in the systemic circulation, trimethylamine N-oxide (TMAO) in the circulatory system, chronic inflammation in the adipose tissue and liver, and oxidative stress and lipid accumulation in the liver. Thus, in women with PCOS, dysbiosis can promote the progression and severity of type 2 diabetes, non-alcoholic fatty liver disease (NAFLD), and cardiovascular diseases (CVD). To alleviate such PCOS-associated complications, microbial therapeutics (probiotics and fecal microbiome transplantation) can be used without any side effects, unlike in the case of hormonal therapy. Therefore, this study sought to understand the mechanistic significance of gut microbes in PCOS and associated comorbidities, along with the role of microbial therapeutics that can ease the life of PCOS-affected women.},
}

@article {pmid38647087,
year = {2024},
author = {Zhou, F and Zhang, Q and Zheng, X and Shi, F and Ma, K and Ji, F and Meng, N and Li, R and Lv, J and Li, Q},
title = {Antiaging Effects of Human Fecal Transplants with Different Combinations of Bifidobacterium bifidum LTBB21J1 and Lactobacillus casei LTL1361 in d-Galactose-Induced Mice.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.3c09815},
pmid = {38647087},
issn = {1520-5118},
abstract = {The feces of healthy middle-aged and old people were first transplanted into d-galactose-induced aging mice to construct humanized aging mice with gut microbiota (FMTC) to confirm the antiaging effect of probiotics produced from centenarians. The mouse model was then treated with centenarian-derived Bifidobacterium bifidum (FMTL), Lactobacillus casei (FMTB), and their mixtures (FMTM), and young mice were used as the control. Compared with the FMTC group, the results demonstrated that the probiotics and their combinations alleviated neuronal damage, increased antioxidant capacity, decreased inflammation, and enhanced cognitive and memory functions in aging mice. In the gut microbiota, the relative abundance of Lactobacillus, Ligilactobacillus, and Akkermansia increased and that of Desulfovibrio and Colidextribacter decreased in the FMTM group compared with that in the FMTC group. The three probiotic groups displayed significant changes in 15 metabolites compared with the FMTC group, with 4 metabolites showing increased expression and 11 metabolites showing decreased expression. The groups were graded as Control > FMTM > FMTB > FMTL > FMTC using a newly developed comprehensive quantitative scoring system that thoroughly analyzed the various indicators of this study. The beneficial antiaging effects of probiotics derived from centenarians were quantitatively described using a novel perspective in this study; it is confirmed that both probiotics and their combinations exert antiaging effects, with the probiotic complex group exhibiting a larger effect.},
}

@article {pmid38646653,
year = {2024},
author = {Liu, Q and Yang, Y and Pan, M and Yang, F and Yu, Y and Qian, Z},
title = {Role of the gut microbiota in tumorigenesis and treatment.},
journal = {Theranostics},
volume = {14},
number = {6},
pages = {2304-2328},
pmid = {38646653},
issn = {1838-7640},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Carcinogenesis ; *Neoplasms/microbiology/therapy ; *Dysbiosis/microbiology ; Animals ; },
abstract = {The gut microbiota is a crucial component of the intricate microecosystem within the human body that engages in interactions with the host and influences various physiological processes and pathological conditions. In recent years, the association between dysbiosis of the gut microbiota and tumorigenesis has garnered increasing attention, as it is recognized as a hallmark of cancer within the scientific community. However, only a few microorganisms have been identified as potential drivers of tumorigenesis, and enhancing the molecular understanding of this process has substantial scientific importance and clinical relevance for cancer treatment. In this review, we delineate the impact of the gut microbiota on tumorigenesis and treatment in multiple types of cancer while also analyzing the associated molecular mechanisms. Moreover, we discuss the utility of gut microbiota data in cancer diagnosis and patient stratification. We further outline current research on harnessing microorganisms for cancer treatment while also analyzing the prospects and challenges associated with this approach.},
}

Humans
*Gastrointestinal Microbiome
*Carcinogenesis
*Neoplasms/microbiology/therapy
*Dysbiosis/microbiology
Animals

@article {pmid38644237,
year = {2024},
author = {, and , and , },
title = {[Chinese expert consensus on the clinical diagnosis and treatment of gut microecology in chronic constipation (2024 edition)].},
journal = {Zhonghua wei chang wai ke za zhi = Chinese journal of gastrointestinal surgery},
volume = {27},
number = {4},
pages = {326-337},
doi = {10.3760/cma.j.cn441530-20240313-00096},
pmid = {38644237},
issn = {1671-0274},
support = {2022YFC2010101//"Thirteenth Five-Year Plan" National Key Research and Development Program "Proactive Health and Aging Science and Technology Response" Key Project/ ; 82100698//National Natural Science Foundation of China/ ; 21Y11908300, 22DZ2203700//Shanghai Municipal Science and Technology Innovation Action Plan/ ; },
mesh = {Humans ; *Constipation/therapy/diagnosis ; *Gastrointestinal Microbiome ; Chronic Disease ; *Fecal Microbiota Transplantation ; China ; *Consensus ; Dysbiosis/therapy/diagnosis ; Quality of Life ; },
abstract = {Chronic constipation is one of the common gastrointestinal disorders, with an incidence rate that is gradually increasing yearly and becoming an important chronic disease that affects people's health and quality of life. In recent years, significant progress has been made in the basic and clinical research of chronic constipation, especially the gut microbiota therapy methods have received increasing attention. Therefore, under the initiative of the Parenteral and Enteral Nutrition Branch of the Chinese Medical Association, Chinese Society for the Promotion of Human Health Science and Technology, and Committee on Gut Microecology and Fecal Microbiota Transplantation, experts from relevant fields in China have been organized to establish the "Chinese Expert Consensus on the Clinical Diagnosis and Treatment of Gut Microecology in Chronic Constipation (2024 Edition)" committee. Focusing on the dysbiosis of gut microbiota, the indications for gut microbiota therapy, and the protocols for fecal microbiota transplantation, 16 consensus opinions were proposed based on the review of domestic and international literature and the clinical experience of experts, aiming to standardize the clinical application of gut microbiota in chronic constipation.},
}

Humans
*Constipation/therapy/diagnosis
*Gastrointestinal Microbiome
Chronic Disease
*Fecal Microbiota Transplantation
China
*Consensus
Dysbiosis/therapy/diagnosis
Quality of Life

@article {pmid38642272,
year = {2024},
author = {Chen, LA and Boyle, K},
title = {The Role of the Gut Microbiome in Health and Disease in the Elderly.},
journal = {Current gastroenterology reports},
volume = {},
number = {},
pages = {},
pmid = {38642272},
issn = {1534-312X},
abstract = {PURPOSE OF REVIEW: Growing evidence supports the contribution of age in the composition and function of the gut microbiome, with specific findings associated with health in old age and longevity.

RECENT FINDINGS: Current studies have associated certain microbiota, such as Butyricimonas, Akkermansia, and Odoribacter, with healthy aging and the ability to survive into extreme old age. Furthermore, emerging clinical and pre-clinical research have shown promising mechanisms for restoring a healthy microbiome in elderly populations through various interventions such as fecal microbiota transplant (FMT), dietary interventions, and exercise programs. Despite several conceptually exciting interventional studies, the field of microbiome research in the elderly remains limited. Specifically, large longitudinal studies are needed to better understand causative relationships between the microbiome and healthy aging. Additionally, individualized approaches to microbiome interventions based on patients' co-morbidities and the underlying functional capacity of their microbiomes are needed to achieve optimal results.},
}

@article {pmid38639049,
year = {2024},
author = {Peng, Z and Zhang, J and Zhang, M and Yin, L and Zhou, Z and Lv, C and Wang, Z and Tang, J},
title = {Tryptophan metabolites relieve intestinal Candida albicans infection by altering the gut microbiota to reduce IL-22 release from group 3 innate lymphoid cells of the colon lamina propria.},
journal = {Food & function},
volume = {},
number = {},
pages = {},
doi = {10.1039/d4fo00432a},
pmid = {38639049},
issn = {2042-650X},
abstract = {Invasive candidiasis may be caused by Candida albicans (C. albicans) colonization of the intestinal tract. Preventing intestinal damage caused by Candida albicans infection and protecting intestinal barrier function have become a critical issue. Integrated analyses of the microbiome with metabolome revealed a remarkable shift of the gut microbiota and tryptophan metabolites, kynurenic acid (KynA), and indolacrylic acid (IA) in mice infected with C. albicans. The transcriptome sequencing indicated that differentially expressed genes were significantly associated with innate immune responses and inflammatory responses. The results of this study suggest that KynA and IA (KI) can alleviate intestinal damage caused by Candida albicans infection in mice by reducing intestinal permeability, increasing intestinal firmness, alleviating intestinal inflammation, and reducing the secretion of interleukin-22 (IL-22) in the 3 groups of colon innate lymphoid cells (ILC3). We performed a fecal microbiota transplantation (FMT) experiment and found that the intestinal barrier function, inflammation, and IL-22 secretion of ILC3 in the colon lamina propria of the recipient mice subjected to C. albicans infection and KI treatment were consistent with the trends of the donor mice. Our results suggest that tryptophan metabolites may directly regulate colon lamina ILC3 to promote intestinal resistance to C. albicans invasion, or indirectly regulate the ILC3 secretion of IL-22 to play a protective role in the intestinal barrier by affecting intestinal microorganisms, which may become a potential target for alleviating intestine borne C. albicans infection.},
}

@article {pmid38638595,
year = {2024},
author = {Srikrishnaraj, A and Lanting, BA and Burton, JP and Teeter, MG},
title = {The Microbial Revolution in the World of Joint Replacement Surgery.},
journal = {JB & JS open access},
volume = {9},
number = {2},
pages = {},
pmid = {38638595},
issn = {2472-7245},
abstract = {BACKGROUND: The prevalence of revision surgery due to aseptic loosening and periprosthetic joint infection (PJI) following total hip and knee arthroplasty is growing. Strategies to prevent the need for revision surgery and its associated health-care costs and patient morbidity are needed. Therapies that modulate the gut microbiota to influence bone health and systemic inflammation are a novel area of research.

METHODS: A literature review of preclinical and clinical peer-reviewed articles relating to the role of the gut microbiota in bone health and PJI was performed.

RESULTS: There is evidence that the gut microbiota plays a role in maintaining bone mineral density, which can contribute to osseointegration, osteolysis, aseptic loosening, and periprosthetic fractures. Similarly, the gut microbiota influences gut permeability and the potential for bacterial translocation to the bloodstream, increasing susceptibility to PJI.

CONCLUSIONS: Emerging evidence supports the role of the gut microbiota in the development of complications such as aseptic loosening and PJI after total hip or knee arthroplasty. There is a potential for microbial therapies such as probiotics or fecal microbial transplantation to moderate the risk of developing these complications. However, further investigation is required.

CLINICAL RELEVANCE: Modulation of the gut microbiota may influence patient outcomes following total joint arthroplasty.},
}

@article {pmid38637862,
year = {2024},
author = {Zhao, H and Zhou, Y and Xu, J and Zhang, Y and Wang, H and Zhao, C and Huang, H and Yang, J and Huang, C and Li, Y and Wang, L and Nie, Y},
title = {Short-chain fatty acid-producing bacterial strains attenuate experimental ulcerative colitis by promoting M2 macrophage polarization via JAK/STAT3/FOXO3 axis inactivation.},
journal = {Journal of translational medicine},
volume = {22},
number = {1},
pages = {369},
pmid = {38637862},
issn = {1479-5876},
support = {82270577//National Natural Science Foundation of China/ ; 202201020297//Guangzhou Planned Project of Science and Technology/ ; 202201020248,202002020012//Guangzhou Planned Project of Science and Technology/ ; 202102080044//Guangzhou Planned Project of Science and Technology/ ; KY17010003//Guangzhou Key Laboratory of Digestive Diseases (2022-2023)/ ; 2020A1515011000//Natural Science Foundation of Guangdong Province/ ; 2020ZYGXZR024//Fundamental Research Funds for the Central Universities/ ; },
mesh = {Humans ; Mice ; Animals ; *Colitis, Ulcerative/therapy ; RNA, Ribosomal, 16S/genetics/metabolism ; *Gastrointestinal Microbiome ; *Colitis ; *Inflammatory Bowel Diseases ; Fatty Acids, Volatile/adverse effects/metabolism ; Bacteria/metabolism ; Disease Models, Animal ; Inflammation ; Dextran Sulfate/adverse effects ; Mice, Inbred C57BL ; Colon ; Forkhead Box Protein O3/metabolism ; *STAT3 Transcription Factor ; },
abstract = {BACKGROUND: Patients with inflammatory bowel disease (IBD), dysbiosis, and immunosuppression who receive fecal microbiota transplantation (FMT) from healthy donors are at an increased risk of developing bacteremia. This study investigates the efficacy of a mixture of seven short-chain fatty acid (SCFA)-producing bacterial strains (7-mix), the resulting culture supernatant mixture (mix-sup), and FMT for treating experimental ulcerative colitis (UC) and evaluates underlying mechanisms.

METHODS: Utilizing culturomics, we isolated and cultured SCFA-producing bacteria from the stool of healthy donors. We used a mouse model of acute UC induced by dextran sulfate sodium (DSS) to assess the effects of 7-mix, mix-sup, and FMT on intestinal inflammation and barrier function, microbial abundance and diversity, and gut macrophage polarization by flow cytometry, immunohistochemistry, 16S rRNA gene sequencing, and transwell assays.

RESULTS: The abundance of several SCFA-producing bacterial taxa decreased in patients with UC. Seven-mix and mix-sup suppressed the inflammatory response and enhanced intestinal mucosal barrier function in the mouse model of UC to an extent similar to or superior to that of FMT. Moreover, 7-mix and mix-sup increased the abundance of SCFA-producing bacteria and SCFA concentrations in colitic mice. The effects of these interventions on the inflammatory response and gut barrier function were mediated by JAK/STAT3/FOXO3 axis inactivation in macrophages by inducing M2 macrophage polarization in vivo and in vitro.

CONCLUSIONS: Our approach provides new opportunities to rationally harness live gut probiotic strains and metabolites to reduce intestinal inflammation, restore gut microbial composition, and expedite the development of safe and effective treatments for IBD.},
}

Humans
Mice
Animals
*Colitis, Ulcerative/therapy
RNA, Ribosomal, 16S/genetics/metabolism
*Gastrointestinal Microbiome
*Colitis
*Inflammatory Bowel Diseases
Fatty Acids, Volatile/adverse effects/metabolism
Bacteria/metabolism
Disease Models, Animal
Inflammation
Dextran Sulfate/adverse effects
Mice, Inbred C57BL
Colon
Forkhead Box Protein O3/metabolism
*STAT3 Transcription Factor

@article {pmid38635481,
year = {2024},
author = {Zambrano, LD and Newhams, MM and Simeone, RM and Payne, AB and Wu, M and Orzel-Lockwood, AO and Halasa, NB and Calixte, JM and Pannaraj, PS and Mongkolrattanothai, K and Boom, JA and Sahni, LC and Kamidani, S and Chiotos, K and Cameron, MA and Maddux, AB and Irby, K and Schuster, JE and Mack, EH and Biggs, A and Coates, BM and Michelson, KN and Bline, KE and Nofziger, RA and Crandall, H and Hobbs, CV and Gertz, SJ and Heidemann, SM and Bradford, TT and Walker, TC and Schwartz, SP and Staat, MA and Bhumbra, SS and Hume, JR and Kong, M and Stockwell, MS and Connors, TJ and Cullimore, ML and Flori, HR and Levy, ER and Cvijanovich, NZ and Zinter, MS and Maamari, M and Bowens, C and Zerr, DM and Guzman-Cottrill, JA and Gonzalez, I and Campbell, AP and Randolph, AG and , },
title = {Durability of Original Monovalent mRNA Vaccine Effectiveness Against COVID-19 Omicron-Associated Hospitalization in Children and Adolescents - United States, 2021-2023.},
journal = {MMWR. Morbidity and mortality weekly report},
volume = {73},
number = {15},
pages = {330-338},
doi = {10.15585/mmwr.mm7315a2},
pmid = {38635481},
issn = {1545-861X},
mesh = {Humans ; Adolescent ; Child ; United States/epidemiology ; *COVID-19 Vaccines ; *COVID-19/epidemiology/prevention & control ; mRNA Vaccines ; Vaccine Efficacy ; SARS-CoV-2 ; Hospitalization ; RNA, Messenger ; },
abstract = {Pediatric COVID-19 vaccination is effective in preventing COVID-19-related hospitalization, but duration of protection of the original monovalent vaccine during SARS-CoV-2 Omicron predominance merits evaluation, particularly given low coverage with updated COVID-19 vaccines. During December 19, 2021-October 29, 2023, the Overcoming COVID-19 Network evaluated vaccine effectiveness (VE) of ≥2 original monovalent COVID-19 mRNA vaccine doses against COVID-19-related hospitalization and critical illness among U.S. children and adolescents aged 5-18 years, using a case-control design. Too few children and adolescents received bivalent or updated monovalent vaccines to separately evaluate their effectiveness. Most case-patients (persons with a positive SARS-CoV-2 test result) were unvaccinated, despite the high frequency of reported underlying conditions associated with severe COVID-19. VE of the original monovalent vaccine against COVID-19-related hospitalizations was 52% (95% CI = 33%-66%) when the most recent dose was administered <120 days before hospitalization and 19% (95% CI = 2%-32%) if the interval was 120-364 days. VE of the original monovalent vaccine against COVID-19-related hospitalization was 31% (95% CI = 18%-43%) if the last dose was received any time within the previous year. VE against critical COVID-19-related illness, defined as receipt of noninvasive or invasive mechanical ventilation, vasoactive infusions, extracorporeal membrane oxygenation, and illness resulting in death, was 57% (95% CI = 21%-76%) when the most recent dose was received <120 days before hospitalization, 25% (95% CI = -9% to 49%) if it was received 120-364 days before hospitalization, and 38% (95% CI = 15%-55%) if the last dose was received any time within the previous year. VE was similar after excluding children and adolescents with documented immunocompromising conditions. Because of the low frequency of children who received updated COVID-19 vaccines and waning effectiveness of original monovalent doses, these data support CDC recommendations that all children and adolescents receive updated COVID-19 vaccines to protect against severe COVID-19.},
}

Humans
Adolescent
Child
United States/epidemiology
*COVID-19 Vaccines
*COVID-19/epidemiology/prevention & control
mRNA Vaccines
Vaccine Efficacy
SARS-CoV-2
Hospitalization
RNA, Messenger

@article {pmid38635321,
year = {2024},
author = {Wang, M and Lkhagva, E and Kim, S and Zhai, C and Islam, MM and Kim, HJ and Hong, ST},
title = {The gut microbe pair of Oribacterium sp. GMB0313 and Ruminococcus sp. GMB0270 confers complete protection against SARS-CoV-2 infection by activating CD8+ T cell-mediated immunity.},
journal = {Gut microbes},
volume = {16},
number = {1},
pages = {2342497},
pmid = {38635321},
issn = {1949-0984},
mesh = {Animals ; Cricetinae ; Ruminococcus ; *Gastrointestinal Microbiome ; *COVID-19 ; SARS-CoV-2 ; Clostridiales ; CD8-Positive T-Lymphocytes ; Immunity, Cellular ; },
abstract = {Despite the potential protective role of the gut microbiome against COVID-19, specific microbes conferring resistance to COVID-19 have not yet been identified. In this work, we aimed to identify and validate gut microbes at the species level that provide protection against SARS-CoV-2 infection. To identify gut microbes conferring protection against COVID-19, we conducted a fecal microbiota transplantation (FMT) from an individual with no history of COVID-19 infection or immunization into a lethal COVID-19 hamster model. FMT from this COVID-19-resistant donor resulted in significant phenotypic changes related to COVID-19 sensitivity in the hamsters. Metagenomic analysis revealed distinct differences in the gut microbiome composition among the hamster groups, leading to the identification of two previously unknown bacterial species: Oribacterium sp. GMB0313 and Ruminococcus sp. GMB0270, both associated with COVID-19 resistance. Subsequently, we conducted a proof-of-concept confirmation animal experiment adhering to Koch's postulates. Oral administration of this gut microbe pair, Oribacterium sp. GMB0313 and Ruminococcus sp. GMB0270, to the hamsters provided complete protection against SARS-CoV-2 infection through the activation of CD8+ T cell mediated immunity. The prophylactic efficacy of the gut microbe pair against SARS-CoV-2 infection was comparable to, or even superior to, current mRNA vaccines. This strong prophylactic efficacy suggests that the gut microbe pair could be developed as a host-directed universal vaccine for all betacoronaviruses, including potential future emerging viruses.},
}

Animals
Cricetinae
Ruminococcus
*Gastrointestinal Microbiome
*COVID-19
SARS-CoV-2
Clostridiales
CD8-Positive T-Lymphocytes
Immunity, Cellular

@article {pmid38635003,
year = {2024},
author = {Lee, SH and Lee, JH and Lee, SW},
title = {Application of Microbiome-Based Therapies in Chronic Respiratory Diseases.},
journal = {Journal of microbiology (Seoul, Korea)},
volume = {},
number = {},
pages = {},
pmid = {38635003},
issn = {1976-3794},
support = {2020R1A2C1008431//National Research Foundation of Korea/ ; 2023R1A2C2006688//National Research Foundation of Korea/ ; RS-2023-00222687//National Research Foundation of Korea/ ; 2022M3A9G8017220//National Research Foundation of Korea/ ; },
abstract = {The application of microbiome-based therapies in various areas of human disease has recently increased. In chronic respiratory disease, microbiome-based clinical applications are considered compelling options due to the limitations of current treatments. The lung microbiome is ecologically dynamic and affected by various conditions, and dysbiosis is associated with disease severity, exacerbation, and phenotype as well as with chronic respiratory disease endotype. However, it is not easy to directly modulate the lung microbiome. Additionally, studies have shown that chronic respiratory diseases can be improved by modulating gut microbiome and administrating metabolites. Although the composition, diversity, and abundance of the microbiome between the gut and lung are considerably different, modulation of the gut microbiome could improve lung dysbiosis. The gut microbiome influences that of the lung via bacterial-derived components and metabolic degradation products, including short-chain fatty acids. This phenomenon might be associated with the cross-talk between the gut microbiome and lung, called gut-lung axis. There are multiple alternatives to modulate the gut microbiome, such as prebiotics, probiotics, and postbiotics ingestion and fecal material transplantation. Several studies have shown that high-fiber diets, for example, present beneficial effects through the production of short-chain fatty acids. Additionally, genetically modified probiotics to secrete some beneficial molecules might also be utilized to treat chronic respiratory diseases. Further studies on microbial modulation to regulate immunity and potentiate conventional pharmacotherapy will improve microbiome modulation techniques, which will develop as a new therapeutic area in chronic respiratory diseases.},
}

@article {pmid38631415,
year = {2024},
author = {Lee, CYQ and Margolis, KG},
title = {Unlocking the potential of fecal virome transplants (FVT): modulating the gut-brain axis in stress-related disorders.},
journal = {Gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.1053/j.gastro.2024.04.006},
pmid = {38631415},
issn = {1528-0012},
}

@article {pmid38631285,
year = {2024},
author = {Kang, X and Lau, HC and Yu, J},
title = {Modulating gut microbiome in cancer immunotherapy: Harnessing microbes to enhance treatment efficacy.},
journal = {Cell reports. Medicine},
volume = {5},
number = {4},
pages = {101478},
pmid = {38631285},
issn = {2666-3791},
mesh = {Humans ; *Gastrointestinal Microbiome ; Immunotherapy ; Treatment Outcome ; *Microbiota ; Fecal Microbiota Transplantation ; *Neoplasms ; },
abstract = {Immunotherapy has emerged as a robust approach against cancer, yet its efficacy has varied among individuals, accompanied by the occurrence of immune-related adverse events. As a result, the efficacy of immunotherapy is far from satisfactory, and enormous efforts have been invested to develop strategies to improve patient outcomes. The gut microbiome is now well acknowledged for its critical role in immunotherapy, with better understanding on host-microbes interaction in the context of cancer treatment. Also, an increasing number of trials have been conducted to evaluate the potential and feasibility of microbiome-targeting approaches to enhance efficacy of cancer treatment in patients. Here, the role of the gut microbiome and metabolites (e.g., short-chain fatty acids, tryptophan metabolites) in immunotherapy and the underlying mechanisms are explored. The application of microbiome-targeting approaches that aim to improve immunotherapy efficacy (e.g., fecal microbiota transplantation, probiotics, dietary intervention) is also elaborated, with further discussion on current challenges and suggestions for future research.},
}

Humans
*Gastrointestinal Microbiome
Immunotherapy
Treatment Outcome
*Microbiota
Fecal Microbiota Transplantation
*Neoplasms

@article {pmid38628492,
year = {2024},
author = {Alghamdi, W and Mosli, M and Alqahtani, SA},
title = {Gut microbiota in MAFLD: therapeutic and diagnostic implications.},
journal = {Therapeutic advances in endocrinology and metabolism},
volume = {15},
number = {},
pages = {20420188241242937},
pmid = {38628492},
issn = {2042-0188},
abstract = {Metabolic dysfunction-associated fatty liver disease (MAFLD), formerly known as nonalcoholic fatty liver disease, is becoming a significant contributor to chronic liver disease globally, surpassing other etiologies, such as viral hepatitis. Prevention and early treatment strategies to curb its growing prevalence are urgently required. Recent evidence suggests that targeting the gut microbiota may help treat and alleviate disease progression in patients with MAFLD. This review aims to explore the complex relationship between MAFLD and the gut microbiota in relation to disease pathogenesis. Additionally, it delves into the therapeutic strategies targeting the gut microbiota, such as diet, exercise, antibiotics, probiotics, synbiotics, glucagon-like peptide-1 receptor agonists, and fecal microbiota transplantation, and discusses novel biomarkers, such as microbiota-derived testing and liquid biopsy, for their diagnostic and staging potential. Overall, the review emphasizes the urgent need for preventive and therapeutic strategies to address the devastating consequences of MAFLD at both individual and societal levels and recognizes that further exploration of the gut microbiota may open avenues for managing MAFLD effectively in the future.},
}

@article {pmid38628273,
year = {2024},
author = {Hao, L and Yu, Z and Sun, J and Li, Z and Li, J and Deng, Y and Huang, H and Huo, H and Li, H and Huang, L},
title = {Supplementation of Crataegi fructus alleviates functional dyspepsia and restores gut microbiota in mice.},
journal = {Frontiers in nutrition},
volume = {11},
number = {},
pages = {1385159},
pmid = {38628273},
issn = {2296-861X},
abstract = {INTRODUCTION: Functional dyspepsia (FD), also known as non-ulcerative dyspepsia, is a common digestive system disorder.

METHODS: In this study, an FD model was established using hunger and satiety disorders combined with an intraperitoneal injection of L-arginine. Indices used to evaluate the efficacy of hawthorn in FD mice include small intestinal propulsion rate, gastric residual rate, general condition, food intake, amount of drinking water, gastric histopathological examination, and serum nitric oxide (NO) and gastrin levels. Based on the intestinal flora and their metabolites, short-chain fatty acids (SCFAs), the mechanism of action of Crataegi Fructus (hawthorn) on FD was studied. The fecal microbiota transplantation test was used to verify whether hawthorn altered the structure of the intestinal flora.

RESULTS: The results showed that hawthorn improved FD by significantly reducing the gastric residual rate, increasing the intestinal propulsion rate, the intake of food and drinking water, and the levels of gastrointestinal hormones. Simultaneously, hawthorn elevated substance P and 5-hydroxytryptamine expression in the duodenum, reduced serum NO levels, and increased vasoactive intestinal peptide expression in the duodenum. Notably, hawthorn increased the abundance of beneficial bacteria and SCFA-producing bacteria in the intestines of FD mice, decreased the abundance of conditional pathogenic bacteria, and significantly increased the SCFA content in feces.

DISCUSSION: The mechanism by which hawthorn improves FD may be related to the regulation of intestinal flora structure and the production of SCFAs.},
}

@article {pmid38626129,
year = {2024},
author = {Gong, J and Zhang, Q and Hu, R and Yang, X and Fang, C and Yao, L and Lv, J and Wang, L and Shi, M and Zhang, W and Ma, S and Xiang, H and Zhang, H and Hou, DX and Yin, Y and He, J and Peng, L and Wu, S},
title = {Effects of Prevotella copri on insulin, gut microbiota and bile acids.},
journal = {Gut microbes},
volume = {16},
number = {1},
pages = {2340487},
doi = {10.1080/19490976.2024.2340487},
pmid = {38626129},
issn = {1949-0984},
mesh = {Humans ; Child ; Animals ; Mice ; Insulin ; *Gastrointestinal Microbiome ; *Pediatric Obesity ; Bile Acids and Salts/pharmacology ; Blood Glucose ; *Diabetes Mellitus, Type 2 ; Mice, Obese ; Diet, High-Fat/adverse effects ; Mice, Inbred C57BL ; *Prevotella ; },
abstract = {Obesity is becoming a major global health problem in children that can cause diseases such as type 2 diabetes and metabolic disorders, which are closely related to the gut microbiota. However, the underlying mechanism remains unclear. In this study, a significant positive correlation was observed between Prevotella copri (P. copri) and obesity in children (p = 0.003). Next, the effect of P. copri on obesity was explored by using fecal microbiota transplantation (FMT) experiment. Transplantation of P. copri. increased serum levels of fasting blood glucose (p < 0.01), insulin (p < 0.01) and interleukin-1β (IL-1β) (p < 0.05) in high-fat diet (HFD)-induced obese mice, but not in normal mice. Characterization of the gut microbiota indicated that P. copri reduced the relative abundance of the Akkermansia genus in mice (p < 0.01). Further analysis on bile acids (BAs) revealed that P. copri increased the primary BAs and ursodeoxycholic acid (UDCA) in HFD-induced mice (p < 0.05). This study demonstrated for the first time that P. copri has a significant positive correlation with obesity in children, and can increase fasting blood glucose and insulin levels in HFD-fed obese mice, which are related to the abundance of Akkermansia genus and bile acids.},
}

Humans
Child
Animals
Mice
Insulin
*Gastrointestinal Microbiome
*Pediatric Obesity
Bile Acids and Salts/pharmacology
Blood Glucose
*Diabetes Mellitus, Type 2
Mice, Obese
Diet, High-Fat/adverse effects
Mice, Inbred C57BL
*Prevotella

@article {pmid37368219,
year = {2024},
author = {Tripathi, PR and Srivastava, A},
title = {Approach to a Child with Chronic Diarrhea.},
journal = {Indian journal of pediatrics},
volume = {91},
number = {5},
pages = {472-480},
pmid = {37368219},
issn = {0973-7693},
mesh = {Infant, Newborn ; Child ; Adolescent ; Humans ; *Diarrhea/diagnosis ; *Colonoscopy/adverse effects ; Feces ; Physical Examination/adverse effects ; Chronic Disease ; },
abstract = {Chronic diarrhea in children is challenging both with regards to etiological diagnosis and for management. Etiology and pathophysiological mechanisms vary widely from neonates to adolescents. Congenital or genetic causes are more frequent in neonates, while infections, allergy and immune-mediated mechanisms are more frequent in childhood. A thorough history and proper physical examination are required to decide for further diagnostic evaluation. The approach to a child with chronic diarrhea should be age specific and based predominantly on the pathophysiological mechanism involved. The nature of the stool like watery, bloody or fatty (steatorrhea) can suggest the probable etiology and organ system involved. After routine tests, evaluation with specific serological tests, imaging, endoscopy (gastroscopy/colonoscopy), histopathology of intestinal mucosa, breath tests or radionuclide imaging may be required to make a definitive diagnosis. Genetic evaluation is important in congenital diarrheas, monogenic inflammatory bowel disease (IBD) and immunodeficiency disorders. Management is aimed at stabilization, nutritional support and etiology specific treatment. Specific therapy can be as simple as exclusion of specific nutrient or as complicated as small bowel transplant. Evaluation and management require expertise and thus patients need to be referred in a timely fashion. This will minimise morbidity including nutritional consequences and improve outcome.},
}

Infant, Newborn
Child
Adolescent
Humans
*Diarrhea/diagnosis
*Colonoscopy/adverse effects
Feces
Physical Examination/adverse effects
Chronic Disease

@article {pmid38625103,
year = {2024},
author = {Zhao, Z and Li, C and Huang, J and Yuan, X and Cui, Y and Liu, Y and Zhou, Y and Zhu, Z and Zhang, Z},
title = {Phlorizin Limits Bovine Viral Diarrhea Virus Infection in Mice via Regulating Gut Microbiota Composition.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.4c01228},
pmid = {38625103},
issn = {1520-5118},
abstract = {Phlorizin (PHZ) is one of the main pharmacologically active ingredients in Lithocarpus polystachyus. We have previously shown that PHZ inhibits the replication of bovine viral diarrhea virus (BVDV), but the exact antiviral mechanism, especially in vivo, is still unknown. Here, we further confirm that PHZ has good protective effects in BVDV-infected mice. We analyzed BVDV-induced CD3[+], CD4[+], and CD8[+] T cells among peripheral blood lymphocytes and found that PHZ significantly restored their percentage. Metagenomic analyses revealed that PHZ markedly improved the richness and diversity of intestinal microbiota and increased the abundance of potentially health-related microbes (families Lachnosipiraceae, Ruminococcaceae, and Oscillospiraceae). Specifically, the relative abundance of short chain fatty acid (SCFA)-producing bacteria, including Lachnospiraceae_UCG-006, unclassified_f_Ruminococcaceae, Oscillibacter, Intestinimonas, Blautia, and Lachnoclostridium increased significantly after PHZ treatment. Interestingly, BVDV-infected mice that received fecal microbiota from PHZ-treated mice (PHZ-FMT) had a significantly lower viral load in the duodenum and jejunum than untreated mice. Pathological lesions of duodenum and jejunum were also greatly reduced in the PHZ-FMT group, confirming a significant antiviral effect. These findings show that gut microbiota play an important role in PHZ's antiviral activity and suggest that their targeted intervention might be a promising endogenous strategy to prevent and control BVDV.},
}

@article {pmid38623584,
year = {2024},
author = {Qu, B and Zhang, XE and Feng, H and Yan, B and Bai, Y and Liu, S and He, Y},
title = {Microbial perspective on the skin-gut axis and atopic dermatitis.},
journal = {Open life sciences},
volume = {19},
number = {1},
pages = {20220782},
doi = {10.1515/biol-2022-0782},
pmid = {38623584},
issn = {2391-5412},
abstract = {Atopic dermatitis (AD) is a relapsing inflammatory skin condition that has become a global health issue with complex etiology and mounting prevalence. The association of AD with skin and gut microbiota has been revealed by virtue of the continuous development of sequencing technology and genomics analysis. Also, the gut-brain-skin axis and its mutual crosstalk mechanisms have been gradually verified. Accordingly, the microbiota-skin-gut axis also plays an important role in allergic skin inflammation. Herein, we reviewed the relationship between the microbiota-skin-gut axis and AD, explored the underlying signaling molecules and potential pathways, and focused on the potential mechanisms of probiotics, antimicrobial peptides (AMPs), coagulase-negative staphylococci transplantation, fecal microbiota transplantation, AMPs, and addition of essential fatty acids in alleviating AD, with the aim to provide a new perspective for targeting microbiota in the treatment of allergic skin inflammation.},
}

@article {pmid38622917,
year = {2024},
author = {Lv, C and Cheng, L and Feng, W and Xie, H and Kou, J and Wang, L and Shi, M and Song, X and Wang, X and Chen, S and Xue, L and Zhang, C and Li, X and Zhao, H},
title = {Targeting microbiota-immune-synaptic plasticity to explore the effect of tea polyphenols on improving memory in the aged type 2 diabetic rat model.},
journal = {Nutritional neuroscience},
volume = {},
number = {},
pages = {1-17},
doi = {10.1080/1028415X.2024.2341188},
pmid = {38622917},
issn = {1476-8305},
abstract = {OBJECTIVES: The study aimed to explore whether TP could improve memory in the aged type 2 diabetic rat model by regulating microbiota-immune-synaptic plasticity axis.

METHODS: The experiment was divided into two parts. Firstly, to investigate the effects of TP on the physiopathology of the aged T2DM model rats, rats were randomly divided into the Normal control group, the aged group, the Aged T2DM model group, the TP 75, 150, 300 mg/kg groups, the 150 mg/kg Piracetam group and the 3 mg/kg Rosiglitazone group. Then, to further verify whether TP improved memory in aged T2DM rat model by regulating intestinal flora, the fecal microbiota transplantation (FMT) from the rats in the 300 mg/kg TP group into the rats in the aged T2DM model group was carried out. Effects on gut microbiota, colonic integrity (epithelial tight junction proteins), and endotoxemia (serum LPS) were examined, along with synaptic structure, synaptic plasticity-related structural proteins and inflammation signaling of the hippocampus in our study.

RESULTS: Our results demonstrated that TP alleviated memory impairments in the aged T2DM rat model. The specific outcomes were as follows: TP 300 mg/kg corrected the gut dysbacteriosis, alleviated intestinal permeability reduction and peripheral/central inflammation, inhibited the TLR4/NF-κB signaling pathway. Meanwhile, TP improved the synaptic plasticity in the hippocampus of the aged T2DM model rats, whose expressions of SYN, PSD 95, NMDAR1 and GluR1 in hippocampus were significantly up-regulated. Surprisingly, rats of the FMT group displayed the same changes.

DISCUSSION: TP improves the memory in aged T2DM rat model. The mechanism may be related to the alteration of gut flora, which can inhibit hippocampal TLR4/NF-κB signaling to attenuate neuroinflammation, then improve synaptic plasticity. The study proposes that TP interventions aimed at manipulating the gut microbiota may hold great potential as an effective approach for preventing and treating this disease.},
}

@article {pmid38624958,
year = {2021},
author = {Malhotra, S and Mohandas, S},
title = {Updates and Opinions in Diagnosis and Treatment of Clostridiodes difficile in Pediatrics.},
journal = {Current treatment options in pediatrics},
volume = {7},
number = {4},
pages = {203-216},
pmid = {38624958},
issn = {2198-6088},
abstract = {PURPOSE OF REVIEW: Clostridiodes difficile infection (CDI) has unique challenges for diagnosis and treatment in pediatrics. Though new antibiotics and biologics are being approved or developed for adults, most of the pediatric therapies still rely on multiple or extended antibiotic courses. This review aims to highlight emerging evidence and our clinical experience with CDI in children and can help inform readers' approach to pediatric CDI.

RECENT FINDINGS: Use of fidaxomicin for CDI in pediatrics has been shown to be to be non-inferior to vancomycin and is associated with higher global cure rates and decreased risk of recurrence. Fecal microbiota transplant is a successful emerging therapy with cure rates of up to 90%, though safety alerts should be noted. Diagnostic laboratory testing for C. difficile remains a challenge as it still cannot definitively distinguish between colonization and true infection, and this is particularly relevant to pediatric patients as they have the highest rates of colonization.

SUMMARY: The diagnosis and treatment of C. difficile infection in pediatrics remain challenging and recommendations lag behind advances made in the adult field. Recent data suggests that use of fidaxomicin both as treatment of first episode or recurrences may be beneficial in pediatrics just as in adults. At an experienced center, FMT is associated with high cure rates. Bezlotuxumab a monoclonal antibody to toxin B that is already recommended for use in adults is being studied in children and should be available for clinical use soon. Oral vancomycin prophylaxis is also an emerging strategy for high-risk patients. Finally, a possible vaccine may be on the horizon for pediatrics.},
}

@article {pmid38622523,
year = {2024},
author = {You, X and Qiu, J and Li, Q and Zhang, Q and Sheng, W and Cao, Y and Fu, W},
title = {Astragaloside IV-PESV inhibits prostate cancer tumor growth by restoring gut microbiota and microbial metabolic homeostasis via the AGE-RAGE pathway.},
journal = {BMC cancer},
volume = {24},
number = {1},
pages = {472},
pmid = {38622523},
issn = {1471-2407},
support = {82104853//National Natural Science Foundation of China/ ; BAZYY20220703//Shenzhen Bao'an Chinese Medicine Hospital Research Program/ ; 2023-QNRC2-A10//Young Elite Scientists Sponsorship Program by CACM/ ; 2024A1515012209//Project of Guangdong Provincial Department of Science and Technology/ ; 2021JD082//Bao'an District Science and Technology Innovation Bureau Research Program/ ; },
mesh = {Male ; Humans ; Animals ; Mice ; Mice, Nude ; Receptor for Advanced Glycation End Products ; *Gastrointestinal Microbiome ; *Liver Neoplasms ; *Prostatic Neoplasms/drug therapy ; Homeostasis ; *Saponins ; *Triterpenes ; },
abstract = {BACKGROUND: Prostate cancer (PCa) is becoming the most common malignancy in men worldwide. We investigated the effect of astragaloside IV combined with PESV on the gut microbiota and metabolite of PCa mice and the process of treating PCa.

METHODS: Nude mice were genetically modified to develop tumors characteristic of PCa. The treatment of PCa mice involved the administration of a combination of astragaloside IV and peptides derived from scorpion venom (PESV). Feces were collected for both 16 S rDNA and metabolic analysis. Fecal supernatant was extracted and used for fecal transplantation in PCa mice. Tumor development was observed in both PCa mice and nude mice. Tumor histopathology was examined, and the expression of inflammatory factors and the AGE-RAGE axis in PCa tissues were analyzed.

RESULTS: PCa mice treated with Astragaloside IV in combination with PESV showed a significant reduction in tumor volume and weight, and stabilization of gut microbiota and metabolites. At the Genus level, significant differences were observed in Porphyromonas, Corynebacterium, Arthromitus and Blautia, and the differential metabolites were PA16_016_0, Astragaloside+, Vitamin A acid, Nardosinone, a-Nortestoster, D-Pantethine, Hypoxanthine, Pregnenolone, cinnamic acid, Pyridoxa, Cirtruline and Xanthurenate. There was a correlation between gut microbiota and metabolites. After the fecal transplantation, tumor growth was effectively suppressed in the PCa mice. Notably, both the mRNA and protein levels of the receptor for advanced glycation end products (RAGE) were significantly decreased. Furthermore, the expression of inflammatory factors, namely NF-κB, TNF-α, and IL-6, in the tumor tissues was significantly attenuated. Conversely, upregulation of RAGE led to increased inflammation and reversed tumor growth in the mice.

CONCLUSION: Astragaloside IV combined with PESV could treat PCa by intervening in gut microbiota composition and metabolite by targeting RAGE.},
}

Male
Humans
Animals
Mice
Mice, Nude
Receptor for Advanced Glycation End Products
*Gastrointestinal Microbiome
*Liver Neoplasms
*Prostatic Neoplasms/drug therapy
Homeostasis
*Saponins
*Triterpenes

@article {pmid38621910,
year = {2024},
author = {Yu, HC and Meng, YY and Wang, EK and Yuan, JY and Peng, Y and Li, XB},
title = {[Buzhong Yiqi Decoction ameliorates spleen deficiency syndrome by regulating gut microbiota].},
journal = {Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica},
volume = {49},
number = {4},
pages = {1028-1043},
doi = {10.19540/j.cnki.cjcmm.20231013.701},
pmid = {38621910},
issn = {1001-5302},
mesh = {Humans ; Mice ; Animals ; *Spleen ; Tumor Necrosis Factor-alpha/pharmacology ; *Gastrointestinal Microbiome ; RNA, Ribosomal, 16S/genetics ; Interleukin-2/pharmacology ; Serotonin ; Immunoglobulin A/pharmacology ; },
abstract = {This study aims to decipher the mechanism of Buzhong Yiqi Decoction(BZYQD) in the treatment of spleen deficiency syndrome via gut microbiota. The mouse models of spleen deficiency syndrome were established by fecal microbiota transplantation(FMT, from patients with spleen deficiency syndrome) and administration of Sennae Folium(SF, 10 g·kg~(-1)), respectively, and treated with BZYQD for 5 d. The pseudosterile mice(administrated with large doses of antibiotics) and the mice transplanted with fecal bacteria from healthy human were taken as the controls. The levels of IgA, interleukin(IL)-2, IL-1β, interferon(IFN)-γ, tumor necrosis factor-alpha(TNF-α), and 5-hydroxytryptamine(5-HT) in the intestinal tissue of two models were measured by enzyme-linked immunosorbent assay, and the CD8~+/CD3~+ ratio was determined by flow cytometry. The composition and changes of the gut microbiota were determined by 16S rRNA high-throughput sequencing and qPCR. Furthermore, the correlation analysis was performed to study the mediating role of gut microbiota in the treatment. The results showed that BZYQD elevated the IgA level, lowered the IL-1β, TNF-α, and 5-HT levels, and decreased the CD8~+/CD3~+ ratio in the intestinal tissue of the two models. Moreover, BZYQD had two-way regulatory effects on the levels of IL-2 and IFN-γ. BZYQD inhibited the overgrowth and reduced the richness of gut microbiota in the SF model, and improved the gut microbiota structure in the two models. Algoriphagus, Mycobacterium, and CL500＿29＿marine＿group were the common differential genera in the two models compared with the control. Acinetobacter, Parabacteroides, and Ruminococcus were the differential genera unique to the FMT model, and Sphingorhabdus, Lactobacillus, and Anaeroplasma were the unique differential genera in the SF model. BZYQD was capable of regulating all these genera. The qPCR results showed that BZYQD increased the relative abundance of Akkermansia muciniphila and decreased that of Bacteroides uniformis in the two models. The correlation analysis revealed that the levels of above intestinal cytokines were significantly correlated with characteristic gut microorganisms in different mo-dels. The IL-1β level had a significantly positive correlation with Acinetobacter and CL500＿29＿marine＿group in the two models, while the different levels of IL-2 and IFN-γ in the two models may be related to its different gut microbiota structures. In conclusion, BZYQD could regulate the disordered gut microbiota structure in different animal models of spleen deficiency syndrome to improve the intestinal immune status, which might be one of the mechanisms of BZYQD in treating spleen deficiency syndrome.},
}

Humans
Mice
Animals
*Spleen
Tumor Necrosis Factor-alpha/pharmacology
*Gastrointestinal Microbiome
RNA, Ribosomal, 16S/genetics
Interleukin-2/pharmacology
Serotonin
Immunoglobulin A/pharmacology

@article {pmid38617735,
year = {2024},
author = {Wang, MY and Sang, LX and Sun, SY},
title = {Gut microbiota and female health.},
journal = {World journal of gastroenterology},
volume = {30},
number = {12},
pages = {1655-1662},
pmid = {38617735},
issn = {2219-2840},
mesh = {Female ; Humans ; *Gastrointestinal Microbiome ; Dysbiosis ; *Breast Neoplasms ; *Endometriosis ; Estrogens ; },
abstract = {The gut microbiota is recognized as an endocrine organ with the capacity to influence distant organs and associated biological pathways. Recent advancements underscore the critical role of gut microbial homeostasis in female health; with dysbiosis potentially leading to diseases among women such as polycystic ovarian syndrome, endometriosis, breast cancer, cervical cancer, and ovarian cancer etc. Despite this, there has been limited discussion on the underlying mechanisms. This editorial explores the three potential mechanisms through which gut microbiota dysbiosis may impact the development of diseases among women, namely, the immune system, the gut microbiota-estrogen axis, and the metabolite pathway. We focused on approaches for treating diseases in women by addressing gut microbiota imbalances through probiotics, prebiotics supplementation, and fecal microbiota transplantation (FMT). Future studies should focus on determining the molecular mechanisms underlying associations between dysbiosis of gut microbiota and female diseases to realize precision medicine, with FMT emerging as a promising intervention.},
}

Female
Humans
*Gastrointestinal Microbiome
Dysbiosis
*Breast Neoplasms
*Endometriosis
Estrogens

@article {pmid38617537,
year = {2024},
author = {Yu, X and Li, W and Li, Z and Wu, Q and Sun, S},
title = {Influence of Microbiota on Tumor Immunotherapy.},
journal = {International journal of biological sciences},
volume = {20},
number = {6},
pages = {2264-2294},
pmid = {38617537},
issn = {1449-2288},
mesh = {Humans ; Immunotherapy ; *Microbiota ; *Probiotics/therapeutic use ; *Neoplasms/therapy ; },
abstract = {The role of the microbiome in immunotherapy has recently garnered substantial attention, with molecular studies and clinical trials providing emerging evidence on the pivotal influence of the microbiota in enhancing therapeutic outcomes via immune response modulation. However, the impact of microbial communities can considerably vary across individuals and different immunotherapeutic approaches, posing prominent challenges in harnessing their potential. In this comprehensive review, we outline the current research applications in tumor immunotherapy and delve into the possible mechanisms through which immune function is influenced by microbial communities in various body sites, encompassing those in the gut, extraintestinal barrier, and intratumoral environment. Furthermore, we discuss the effects of diverse microbiome-based strategies, including probiotics, prebiotics, fecal microbiota transplantation, and the targeted modulation of specific microbial taxa, and antibiotic treatments on cancer immunotherapy. All these strategies potentially have a profound impact on immunotherapy and pave the way for personalized therapeutic approaches and predictive biomarkers.},
}

Humans
Immunotherapy
*Microbiota
*Probiotics/therapeutic use
*Neoplasms/therapy

@article {pmid38617453,
year = {2024},
author = {Chen, SJ and Zhang, DY and Wu, X and Zhang, FM and Cui, BT and Huang, YH and Zhang, ZL and Wang, R and Bai, FH},
title = {Washed microbiota transplantation for Crohn's disease: A metagenomic, metatranscriptomic, and metabolomic-based study.},
journal = {World journal of gastroenterology},
volume = {30},
number = {11},
pages = {1572-1587},
pmid = {38617453},
issn = {2219-2840},
mesh = {Humans ; Amino Acids ; *Antifibrinolytic Agents ; *Crohn Disease/diagnosis/therapy ; Escherichia coli ; Metagenome ; *Microbiota ; Prospective Studies ; },
abstract = {BACKGROUND: Fecal microbiota transplantation (FMT) is a promising therapeutic approach for treating Crohn's disease (CD). The new method of FMT, based on the automatic washing process, was named as washed microbiota transplantation (WMT). Most existing studies have focused on observing the clinical phenomena. However, the mechanism of action of FMT for the effective management of CD-particularly in-depth multi-omics analysis involving the metagenome, metatranscriptome, and metabolome-has not yet been reported.

AIM: To assess the efficacy of WMT for CD and explore alterations in the microbiome and metabolome in response to WMT.

METHODS: We conducted a prospective, open-label, single-center clinical study. Eleven CD patients underwent WMT. Their clinical responses (defined as a decrease in their CD Activity Index score of > 100 points) and their microbiome (metagenome, metatranscriptome) and metabolome profiles were evaluated three months after the procedure.

RESULTS: Seven of the 11 patients (63.6%) showed an optimal clinical response three months post-WMT. Gut microbiome diversity significantly increased after WMT, consistent with improved clinical symptoms. Comparison of the metagenome and metatranscriptome analyses revealed consistent alterations in certain strains, such as Faecalibacterium prausnitzii, Roseburia intestinalis, and Escherichia coli. In addition, metabolomics analyses demonstrated that CD patients had elevated levels of various amino acids before treatment compared to the donors. However, levels of vital amino acids that may be associated with disease progression (e.g., L-glutamic acid, gamma-glutamyl-leucine, and prolyl-glutamine) were reduced after WMT.

CONCLUSION: WMT demonstrated therapeutic efficacy in CD treatment, likely due to the effective reconstruction of the patient's microbiome. Multi-omics techniques can effectively help decipher the potential mechanisms of WMT in treating CD.},
}

Humans
Amino Acids
*Antifibrinolytic Agents
*Crohn Disease/diagnosis/therapy
Escherichia coli
Metagenome
*Microbiota
Prospective Studies

@article {pmid38617293,
year = {2024},
author = {Joldrichsen, MR and Kim, E and Steiner, HE and Jeong, YJ and Premanandan, C and Hsueh, W and Ziouzenkova, O and Cormet-Boyaka, E and Boyaka, PN},
title = {Loss of Paneth cells dysregulates gut ILC subsets and enhances weight gain response to high fat diet in a mouse model.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2024.03.29.587349},
pmid = {38617293},
abstract = {Obesity has been associated with dysbiosis, but innate mechanisms linking intestinal epithelial cell subsets and obesity remain poorly understood. Using mice lacking Paneth cells (Sox9 [ΔIEC] mice), small intestinal epithelial cells specialized in the production of antimicrobial products and cytokines, we show that dysbiosis alone does not induce obesity or metabolic disorders. Loss of Paneth cells reduced ILC3 and increased ILC2 numbers in the intestinal lamina propria. High-fat diet (HFD) induced higher weight gain and more severe metabolic disorders in Sox9 [ΔIEC] mice. Further, HFD enhances the number of ILC1 in the intestinal lamina propria of Sox9 [ΔIEC] mice and increases intestinal permeability and the accumulation of immune cells (inflammatory macrophages and T cells, and B cells) in abdominal fat tissues of obese Sox9 [ΔIEC] . Transplantation of fecal materials from Sox9 [ΔIEC] mice in germ-free mice before HFD further confirmed the regulatory role of Paneth cells for gut ILC subsets and the development of obesity.},
}

@article {pmid38616586,
year = {2024},
author = {Joshi, B and Yadav, SK and Shakya Hada, MS and Shrestha, S and Shrestha, KK and Shrestha, PC and Awal, BK},
title = {Post-Transplant Fecal Carriage of Antibiotic Resistant and B-Lactamases-Producing Enterobacteriales among Renal Transplant Recipients.},
journal = {Journal of Nepal Health Research Council},
volume = {21},
number = {4},
pages = {578-586},
doi = {10.33314/jnhrc.v21i4.4801},
pmid = {38616586},
issn = {1999-6217},
mesh = {Humans ; *Anti-Bacterial Agents/pharmacology/therapeutic use ; Ceftazidime ; Transplant Recipients ; *Kidney Transplantation ; Escherichia coli ; Nepal ; beta-Lactamases ; Klebsiella ; },
abstract = {BACKGROUND: The intestinal colonization and transmission of antibiotic-resistant Enterobacteriales to renal transplant recipients may pose a threat to them because they are profoundly immunocompromised and vulnerable to infection. Hence, it is crucial to identify these antibiotic-resistant fecal Enterobacteriales harboring high-risk populations. The objective of this study was to determine antibiotic resistance as well as β-lactamases production in fecal Enterobacteriales among renal transplant recipients.

METHODS: The stool samples, one collected from each transplant recipient, were processed for isolation and identification of Enterobacteriales and were tested for their antibiotic susceptibility, extended-spectrum β-lactamase, and metallo-β-lactamase production by standard methods.

RESULTS: A total of 103 Enterobacteriales comprising of Escherichia coli (86.4%), Klebsiella species (11.7%), and Citrobacter species (1.9%) were isolated and more than 60% of the E. coli were found resistant to ceftazidime and ciprofloxacin and around half of the Klebsiella species were resistant to ceftazidime and fluroquinolones. The extended-spectrum β-lactamase production was seen in 3.4% and 8.3% and metallo-β-lactamase production in 24.7% and 33.3% of E. coli and Klebsiella species, respectively. The high proportion of β-lactamase-producers were resistant to piperacillin-tazobactam, meropenem, gentamicin, and amikacin than β-lactamases non-producers.

CONCLUSION: Since the antibiotic resistance is higher in fecal Enterobacteriales, each renal transplant recipient should be screened for these highly resistant intestinal colonizers after transplantation in order to prevent infections and to reduce the rate of transplant failure due to infections.},
}

Humans
*Anti-Bacterial Agents/pharmacology/therapeutic use
Ceftazidime
Transplant Recipients
*Kidney Transplantation
Escherichia coli
Nepal
beta-Lactamases
Klebsiella

@article {pmid38613431,
year = {2024},
author = {Lee, MA and Questa, M and Wanakumjorn, P and Kol, A and McLaughlin, B and Weimer, BC and Buono, A and Suchodolski, JS and Marsilio, S},
title = {Safety profile and effects on the peripheral immune response of fecal microbiota transplantation in clinically healthy dogs.},
journal = {Journal of veterinary internal medicine},
volume = {},
number = {},
pages = {},
doi = {10.1111/jvim.17061},
pmid = {38613431},
issn = {1939-1676},
support = {//2022 Comparative Gastroenterology Society (CGS)/IDEXX Veterinary Student Summer Scholar Award/ ; NCI P30 CA093373 (Comprehensive Cancer Center), S10 OD018223 (Astrios Cell Sorter), S10 RR 026825 (Fortessa Cytometer)//University of California Davis Flow Cytometry Shared Resource Laboratory/ ; },
abstract = {BACKGROUND: Fecal microbiota transplantation (FMT) is increasingly used for gastrointestinal and extra-gastrointestinal diseases in veterinary medicine. However, its effects on immune responses and possible adverse events have not been systematically investigated.

HYPOTHESIS/OBJECTIVES: Determine the short-term safety profile and changes in the peripheral immune system after a single FMT administration in healthy dogs.

ANIMALS: Ten client-owned, clinically healthy dogs as FMT recipients, and 2 client-owned clinically healthy dogs as FMT donors.

METHODS: Prospective non-randomized clinical trial. A single rectal enema of 5 g/kg was given to clinically healthy canine recipients. During the 28 days after FMT administration, owners self-reported adverse events and fecal scores. On Days 0 (baseline), 1, 4, 10, and 28 after FMT, fecal and blood samples were collected. The canine fecal dysbiosis index (DI) was calculated using qPCR.

RESULTS: No significant changes were found in the following variables: CBC, serum biochemistry, C-reactive protein, serum cytokines (interleukins [IL]-2, -6, -8, tumor necrosis factor [TNF]-α), peripheral leukocytes (B cells, T cells, cluster of differentiation [CD]4+ T cells, CD8+ T cells, T regulatory cells), and the canine DI. Mild vomiting (n = 3), diarrhea (n = 4), decreased activity (n = 2), and inappetence (n = 1) were reported, and resolved without intervention.

Fecal microbiota transplantation did not significantly alter the evaluated variables and recipients experienced minimal adverse events associated with FMT administration. Fecal microbiota transplantation was not associated with serious adverse events, changes in peripheral immunologic variables, or the canine DI in the short-term.},
}

@article {pmid38613119,
year = {2024},
author = {Zhou, Y and Zeng, Y and Wang, R and Pang, J and Wang, X and Pan, Z and Jin, Y and Chen, Y and Yang, Y and Ling, W},
title = {Resveratrol Improves Hyperuricemia and Ameliorates Renal Injury by Modulating the Gut Microbiota.},
journal = {Nutrients},
volume = {16},
number = {7},
pages = {},
pmid = {38613119},
issn = {2072-6643},
support = {81730090//National Natural Science Foundation of China/ ; 81973022//National Natural Science Foundation of China/ ; },
mesh = {Animals ; Mice ; *Hyperuricemia/drug therapy ; *Gastrointestinal Microbiome ; Resveratrol/pharmacology ; Uric Acid ; Kidney Tubules ; Inflammation ; },
abstract = {Resveratrol (RES) has been reported to prevent hyperuricemia (HUA); however, its effect on intestinal uric acid metabolism remains unclear. This study evaluated the impact of RES on intestinal uric acid metabolism in mice with HUA induced by a high-fat diet (HFD). Moreover, we revealed the underlying mechanism through metagenomics, fecal microbiota transplantation (FMT), and 16S ribosomal RNA analysis. We demonstrated that RES reduced the serum uric acid, creatinine, urea nitrogen, and urinary protein levels, and improved the glomerular atrophy, unclear renal tubule structure, fibrosis, and renal inflammation. The results also showed that RES increased intestinal uric acid degradation. RES significantly changed the intestinal flora composition of HFD-fed mice by enriching the beneficial bacteria that degrade uric acid, reducing harmful bacteria that promote inflammation, and improving microbial function via the upregulation of purine metabolism. The FMT results further showed that the intestinal microbiota is essential for the effect of RES on HUA, and that Lactobacillus may play a key role in this process. The present study demonstrated that RES alleviates HFD-induced HUA and renal injury by regulating the gut microbiota composition and the metabolism of uric acid.},
}

Animals
Mice
*Hyperuricemia/drug therapy
*Gastrointestinal Microbiome
Resveratrol/pharmacology
Uric Acid
Kidney Tubules
Inflammation

@article {pmid38613109,
year = {2024},
author = {Byerley, LO and Lorenzen, B and Chang, HM and Hartman, WG and Keenan, MJ and Page, R and Luo, M and Dowd, SE and Taylor, CM},
title = {Gut Microbial Dysbiosis Differs in Two Distinct Cachectic Tumor-Bearing Models Consuming the Same Diet.},
journal = {Nutrients},
volume = {16},
number = {7},
pages = {},
pmid = {38613109},
issn = {2072-6643},
support = {no number//American Institute for Cancer Research/ ; no number//California Walnut Commission/ ; },
mesh = {Male ; Animals ; Rats ; Cachexia/etiology ; Dysbiosis ; *Gastrointestinal Microbiome ; RNA, Ribosomal, 16S/genetics ; Diet ; *Sarcoma ; *Juglans ; },
abstract = {The impact of cancer cachexia on the colonic microbiota is poorly characterized. This study assessed the effect of two cachectic-producing tumor types on the gut microbiota to determine if a similar dysbiosis could be found. In addition, it was determined if a diet containing an immunonutrient-rich food (walnuts) known to promote the growth of probiotic bacteria in the colon could alter the dysbiosis and slow cachexia. Male Fisher 344 rats were randomly assigned to a semi-purified diet with or without walnuts. Then, within each diet group, rats were further assigned randomly to a treatment group: tumor-bearing ad libitum fed (TB), non-tumor-bearing ad libitum fed (NTB-AL), and non-tumor-bearing group pair-fed to the TB (NTB-PF). The TB group was implanted either with the Ward colon carcinoma or MCA-induced sarcoma, both transplantable tumor lines. Fecal samples were collected after the development of cachexia, and bacteria species were identified using 16S rRNA gene analysis. Both TB groups developed cachexia but had a differently altered gut microbiome. Beta diversity was unaffected by treatment (NTB-AL, TB, and NTB-PF) regardless of tumor type but was affected by diet. Also, diet consistently changed the relative abundance of several bacteria taxa, while treatment and tumor type did not. The control diet increased the abundance of A. Anaeroplasma, while the walnut diet increased the genus Ruminococcus. There were no common fecal bacterial changes characteristic of cachexia found. Diet consistently changed the gut microbiota, but these changes were insufficient to slow the progression of cachexia, suggesting cancer cachexia is more complex than a few gut microbiota shifts.},
}

Male
Animals
Rats
Cachexia/etiology
Dysbiosis
*Gastrointestinal Microbiome
RNA, Ribosomal, 16S/genetics
Diet
*Sarcoma
*Juglans

@article {pmid38613058,
year = {2024},
author = {Lombardi, M and Troisi, J and Motta, BM and Torre, P and Masarone, M and Persico, M},
title = {Gut-Liver Axis Dysregulation in Portal Hypertension: Emerging Frontiers.},
journal = {Nutrients},
volume = {16},
number = {7},
pages = {},
pmid = {38613058},
issn = {2072-6643},
mesh = {Humans ; *Esophageal and Gastric Varices ; Gastrointestinal Hemorrhage ; *Hypertension, Portal/etiology ; Ascites ; },
abstract = {Portal hypertension (PH) is a complex clinical challenge with severe complications, including variceal bleeding, ascites, hepatic encephalopathy, and hepatorenal syndrome. The gut microbiota (GM) and its interconnectedness with human health have emerged as a captivating field of research. This review explores the intricate connections between the gut and the liver, aiming to elucidate how alterations in GM, intestinal barrier function, and gut-derived molecules impact the development and progression of PH. A systematic literature search, following PRISMA guidelines, identified 12 original articles that suggest a relationship between GM, the gut-liver axis, and PH. Mechanisms such as dysbiosis, bacterial translocation, altered microbial structure, and inflammation appear to orchestrate this relationship. One notable study highlights the pivotal role of the farnesoid X receptor axis in regulating the interplay between the gut and liver and proposes it as a promising therapeutic target. Fecal transplantation experiments further emphasize the pathogenic significance of the GM in modulating liver maladies, including PH. Recent advancements in metagenomics and metabolomics have expanded our understanding of the GM's role in human ailments. The review suggests that addressing the unmet need of identifying gut-liver axis-related metabolic and molecular pathways holds potential for elucidating pathogenesis and directing novel therapeutic interventions.},
}

Humans
*Esophageal and Gastric Varices
Gastrointestinal Hemorrhage
*Hypertension, Portal/etiology
Ascites

@article {pmid38609760,
year = {2024},
author = {Mullish, BH and Merrick, B and Quraishi, MN and Bak, A and Green, CA and Moore, DJ and Porter, RJ and Elumogo, NT and Segal, JP and Sharma, N and Marsh, B and Kontkowski, G and Manzoor, SE and Hart, AL and Settle, C and Keller, JJ and Hawkey, P and Iqbal, TH and Goldenberg, SD and Williams, HRT},
title = {The use of faecal microbiota transplant as treatment for recurrent or refractory Clostridioides difficile infection and other potential indications: second edition of joint British Society of Gastroenterology (BSG) and Healthcare Infection Society (HIS) guidelines.},
journal = {The Journal of hospital infection},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jhin.2024.03.001},
pmid = {38609760},
issn = {1532-2939},
abstract = {The first British Society of Gastroenterology (BSG) and Healthcare Infection Society (HIS)-endorsed faecal microbiota transplant (FMT) guidelines were published in 2018. Over the past 5 years, there has been considerable growth in the evidence base (including publication of outcomes from large national FMT registries), necessitating an updated critical review of the literature and a second edition of the BSG/HIS FMT guidelines. These have been produced in accordance with National Institute for Health and Care Excellence-accredited methodology, thus have particular relevance for UK-based clinicians, but are intended to be of pertinence internationally. This second edition of the guidelines have been divided into recommendations, good practice points and recommendations against certain practices. With respect to FMT for Clostridioides difficile infection (CDI), key focus areas centred around timing of administration, increasing clinical experience of encapsulated FMT preparations and optimising donor screening. The latter topic is of particular relevance given the COVID-19 pandemic, and cases of patient morbidity and mortality resulting from FMT-related pathogen transmission. The guidelines also considered emergent literature on the use of FMT in non-CDI settings (including both gastrointestinal and non-gastrointestinal indications), reviewing relevant randomised controlled trials. Recommendations are provided regarding special areas (including compassionate FMT use), and considerations regarding the evolving landscape of FMT and microbiome therapeutics.},
}

@article {pmid38609165,
year = {2024},
author = {Mullish, BH and Merrick, B and Quraishi, MN and Bak, A and Green, CA and Moore, DJ and Porter, RJ and Elumogo, NT and Segal, JP and Sharma, N and Marsh, B and Kontkowski, G and Manzoor, SE and Hart, AL and Settle, C and Keller, JJ and Hawkey, P and Iqbal, TH and Goldenberg, SD and Williams, HRT},
title = {The use of faecal microbiota transplant as treatment for recurrent or refractory Clostridioides difficile infection and other potential indications: second edition of joint British Society of Gastroenterology (BSG) and Healthcare Infection Society (HIS) guidelines.},
journal = {Gut},
volume = {},
number = {},
pages = {},
doi = {10.1136/gutjnl-2023-331550},
pmid = {38609165},
issn = {1468-3288},
abstract = {The first British Society of Gastroenterology (BSG) and Healthcare Infection Society (HIS)-endorsed faecal microbiota transplant (FMT) guidelines were published in 2018. Over the past 5 years, there has been considerable growth in the evidence base (including publication of outcomes from large national FMT registries), necessitating an updated critical review of the literature and a second edition of the BSG/HIS FMT guidelines. These have been produced in accordance with National Institute for Health and Care Excellence-accredited methodology, thus have particular relevance for UK-based clinicians, but are intended to be of pertinence internationally. This second edition of the guidelines have been divided into recommendations, good practice points and recommendations against certain practices. With respect to FMT for Clostridioides difficile infection (CDI), key focus areas centred around timing of administration, increasing clinical experience of encapsulated FMT preparations and optimising donor screening. The latter topic is of particular relevance given the COVID-19 pandemic, and cases of patient morbidity and mortality resulting from FMT-related pathogen transmission. The guidelines also considered emergent literature on the use of FMT in non-CDI settings (including both gastrointestinal and non-gastrointestinal indications), reviewing relevant randomised controlled trials. Recommendations are provided regarding special areas (including compassionate FMT use), and considerations regarding the evolving landscape of FMT and microbiome therapeutics.},
}

@article {pmid38608743,
year = {2024},
author = {Yang, X and Zhou, Y and Tan, S and Tian, X and Meng, X and Li, Y and Zhou, B and Zhao, G and Ge, X and He, C and Cheng, W and Zhang, Y and Zheng, K and Yin, K and Yu, Y and Pan, W},
title = {Alterations in gut microbiota contribute to cognitive deficits induced by chronic infection of Toxoplasma gondii.},
journal = {Brain, behavior, and immunity},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.bbi.2024.04.008},
pmid = {38608743},
issn = {1090-2139},
abstract = {Chronic infection with Toxoplasma gondii (T. gondii) emerges as a risk factor for neurodegenerative diseases in animals and humans. However, the underlying mechanisms are largely unknown. We aimed to investigate whether gut microbiota and its metabolites play a role in T. gondii-induced cognitive deficits. We found that T. gondii infection induced cognitive deficits in mice, which was characterized by synaptic ultrastructure impairment and neuroinflammation in the hippocampus. Moreover, the infection led to gut microbiota dysbiosis, barrier integrity impairment, and inflammation in the colon. Interestingly, broad-spectrum antibiotic ablation of gut microbiota attenuated the adverse effects of the parasitic infection on the cognitive function in mice; cognitive deficits and hippocampal pathological changes were transferred from the infected mice to control mice by fecal microbiota transplantation. In addition, the abundance of butyrate-producing bacteria and the production of serum butyrate were decreased in infected mice. Interestingly, dietary supplementation of butyrate ameliorated T. gondii-induced cognitive impairment in mice. Notably, compared to the healthy controls, the decreased butyrate production was negatively correlated with the levels of anti-T. gondii IgG antibody in the serum of human subjects. Overall, this study demonstrates that gut microbiota is a key regulator of T. gondii-induced cognitive impairment.},
}

@article {pmid38608488,
year = {2024},
author = {Bai, X and Deng, J and Duan, Z and Fu, R and Zhu, C and Fan, D},
title = {Ginsenoside Rh4 alleviates gastrointestinal mucositis and enhances chemotherapy efficacy through modulating gut microbiota.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {128},
number = {},
pages = {155577},
doi = {10.1016/j.phymed.2024.155577},
pmid = {38608488},
issn = {1618-095X},
abstract = {BACKGROUND: Gastrointestinal mucositis stands as one of the most severe side effects of irinotecan (CPT-11). however, only palliative treatment is available at present. Therefore, there is an urgent need for adjunctive medications to alleviate the side effects of CPT-11.

PURPOSE: In this study, our objective was to explore whether ginsenoside Rh4 could serve as a modulator of the gut microbiota and an adjunctive agent for chemotherapy, thereby alleviating the side effects of CPT-11 and augmenting its anti-tumor efficacy.

STUDY DESIGN: A CPT-11-induced gastrointestinal mucositis model was used to investigate whether ginsenoside Rh4 alleviated CPT-11-induced gastrointestinal mucositis and enhanced the anti-tumor activity of CPT-11.

METHODS: In this study, we utilized CT26 cells to establish a xenograft tumor model, employing transcriptomics, genomics, and metabolomics techniques to investigate the impact of ginsenoside Rh4 on CPT-11-induced gastrointestinal mucositis and the effect on the anti-tumor activity of CPT-11. Furthermore, we explored the pivotal role of gut microbiota and their metabolites through fecal microbiota transplantation (FMT) experiments and supplementation of the key differential metabolite, hyodeoxycholic acid (HDCA).

RESULTS: The results showed that ginsenoside Rh4 repaired the impairment of intestinal barrier function and restored intestinal mucosal homeostasis in a gut microbiota-dependent manner. Ginsenoside Rh4 treatment modulated gut microbiota diversity and upregulated the abundance of beneficial bacteria, especially Lactobacillus_reuteri and Akkermansia_muciniphila, which further regulated bile acid biosynthesis, significantly promoted the production of the beneficial secondary bile acid hyodeoxycholic acid (HDCA), thereby alleviating CPT-11-induced gut microbiota dysbiosis. Subsequently, ginsenoside Rh4 further alleviated gastrointestinal mucositis through the TGR5-TLR4-NF-κB signaling pathway. On the other hand, ginsenoside Rh4 combination therapy could further reduce the weight and volume of colon tumors, promote tumor cell apoptosis, and enhance the anti-tumor activity of CPT-11 by inhibiting the PI3K-Akt signaling pathway, thus exerting a synergistic anti-tumor effect.

CONCLUSION: In summary, our findings confirm that ginsenoside Rh4 can alleviate CPT-11-induced gastrointestinal mucositis and enhance the anti-tumor activity of CPT-11 by modulating gut microbiota and its related metabolites. Our study validates the potential of ginsenoside Rh4 as a modulator of the gut microbiota and an adjunctive agent for chemotherapy, offering new therapeutic strategies for addressing chemotherapy side effects and improving chemotherapy efficacy.},
}

@article {pmid38608440,
year = {2024},
author = {Zhang, W and Ling, J and Xu, B and Wang, J and Chen, Z and Li, G},
title = {Gut microbiome-mediated monocytes promote liver metastasis.},
journal = {International immunopharmacology},
volume = {133},
number = {},
pages = {111877},
doi = {10.1016/j.intimp.2024.111877},
pmid = {38608440},
issn = {1878-1705},
abstract = {The gut microbiome plays an important role in tumor growth by regulating immune cell function. However, the role of the gut microbiome-mediated monocytes in liver metastasis remains unclear. In this study, we found that fecal microbiome transplantation (FMT) from the stool of patients with liver metastasis (LM) significantly promoted liver metastasis compared with healthy donors (HD). Monocytes were upregulated in liver tissues by the CCL2/CCR2 axis in LM patients' stool transplanted mouse model. CCL2/CCR2 inhibition and monocyte depletion significantly suppress liver metastasis. FMT using LM patients' stool enhanced the plasma lipopolysaccharides (LPS) concentration. The LPS/TLR4 signaling pathway is crucial for gut microbiome-mediated liver metastasis. These results indicated that monocytes contribute to liver metastasis via the CCL2/CCR2 axis.},
}

@article {pmid38604201,
year = {2024},
author = {Bethlehem, L and Estevinho, MM and Grinspan, A and Magro, F and Faith, JJ and Colombel, JF},
title = {Microbiota therapeutics for inflammatory bowel disease: the way forward.},
journal = {The lancet. Gastroenterology & hepatology},
volume = {9},
number = {5},
pages = {476-486},
doi = {10.1016/S2468-1253(23)00441-7},
pmid = {38604201},
issn = {2468-1253},
abstract = {Microbiota therapeutics that transplant faecal material from healthy donors to people with mild-to-moderate ulcerative colitis have shown the potential to induce remission in about 30% of participants in small, phase 2 clinical trials. Despite this substantial achievement, the field needs to leverage the insights gained from these trials and progress towards phase 3 clinical trials and drug approval, while identifying the distinct clinical niche for this new therapeutic modality within inflammatory bowel disease (IBD) therapeutics. We describe the lessons that can be learned from past studies of microbiota therapeutics, from full spectrum donor stool to defined products manufactured in vitro. We explore the actionable insights these lessons provide on the design of near-term studies and future trajectories for the integration of microbiota therapeutics in the treatment of IBD. If successful, microbiota therapeutics will provide a powerful orthogonal approach (complementing or in combination with existing immunomodulatory drugs) to raise the therapeutic ceiling for the many non-responders and partial responders within the IBD patient population.},
}

@article {pmid38604200,
year = {2024},
author = {Porcari, S and Fusco, W and Spivak, I and Fiorani, M and Gasbarrini, A and Elinav, E and Cammarota, G and Ianiro, G},
title = {Fine-tuning the gut ecosystem: the current landscape and outlook of artificial microbiome therapeutics.},
journal = {The lancet. Gastroenterology & hepatology},
volume = {9},
number = {5},
pages = {460-475},
doi = {10.1016/S2468-1253(23)00357-6},
pmid = {38604200},
issn = {2468-1253},
abstract = {The gut microbiome is acknowledged as a key determinant of human health, and technological progress in the past two decades has enabled the deciphering of its composition and functions and its role in human disorders. Therefore, manipulation of the gut microbiome has emerged as a promising therapeutic option for communicable and non-communicable disorders. Full exploitation of current therapeutic microbiome modulators (including probiotics, prebiotics, and faecal microbiota transplantation) is hindered by several factors, including poor precision, regulatory and safety issues, and the impossibility of providing reproducible and targeted treatments. Artificial microbiota therapeutics (which include a wide range of products, such as microbiota consortia, bacteriophages, bacterial metabolites, and engineered probiotics) have appeared as an evolution of current microbiota modulators, as they promise safe and reproducible effects, with variable levels of precision via different pathways. We describe the landscape of artificial microbiome therapeutics, from those already on the market to those still in the pipeline, and outline the major challenges for positioning these therapeutics in clinical practice.},
}

@article {pmid38599497,
year = {2024},
author = {Xu, Q and Sun, L and Chen, Q and Jiao, C and Wang, Y and Li, H and Xie, J and Zhu, F and Wang, J and Zhang, W and Xie, L and Wu, H and Zuo, Z and Chen, X},
title = {Gut microbiota dysbiosis contributes to depression-like behaviors via hippocampal NLRP3-mediated neuroinflammation in a postpartum depression mouse model.},
journal = {Brain, behavior, and immunity},
volume = {119},
number = {},
pages = {220-235},
doi = {10.1016/j.bbi.2024.04.002},
pmid = {38599497},
issn = {1090-2139},
abstract = {Postpartum depression (PPD) is a severe mental disorder that affects approximately 10---20% of women after childbirth. The precise mechanism underlying PPD pathogenesis remains elusive, thus limiting the development of therapeutics. Gut microbiota dysbiosis is considered to contribute to major depressive disorder. However, the associations between gut microbiota and PPD remain unanswered. Here, we established a mouse PPD model by sudden ovarian steroid withdrawal after hormone-simulated pseudopregnancy-human (HSP-H) in ovariectomy (OVX) mouse. Ovarian hormone withdrawal induced depression-like and anxiety-like behaviors and an altered gut microbiota composition. Fecal microbiota transplantation (FMT) from PPD mice to antibiotic cocktail-treated mice induced depression-like and anxiety-like behaviors and neuropathological changes in the hippocampus of the recipient mice. FMT from healthy mice to PPD mice attenuated the depression-like and anxiety-like behaviors as well as the inflammation mediated by the NOD-like receptor protein (NLRP)-3/caspase-1 signaling pathway both in the gut and the hippocampus, increased fecal short-chain fatty acids (SCFAs) levels and alleviated gut dysbiosis with increased SCFA-producing bacteria and reduced Akkermansia in the PPD mice. Also, downregulation of NLRP3 in the hippocampus mitigated depression-like behaviors in PPD mice and overexpression of NLRP3 in the hippocampal dentate gyrus induced depression-like behaviors in naïve female mice. Intriguingly, FMT from healthy mice failed to alleviate depression-like behaviors in PPD mice with NLRP3 overexpression in the hippocampus. Our results highlighted the NLRP3 inflammasome as a key component within the microbiota-gut-brain axis, suggesting that targeting the gut microbiota may be a therapeutic strategy for PPD.},
}

@article {pmid38599474,
year = {2024},
author = {Wang, H and Zhou, L and Zheng, Q and Song, Y and Huang, W and Yang, L and Xiong, Y and Cai, Z and Chen, Y and Yuan, J},
title = {Kai-Xin-San improves cognitive impairment in D-gal and Aβ25-35 induced AD rats by regulating gut microbiota and reducing neuronal damage.},
journal = {Journal of ethnopharmacology},
volume = {},
number = {},
pages = {118161},
doi = {10.1016/j.jep.2024.118161},
pmid = {38599474},
issn = {1872-7573},
abstract = {Kai-Xin-San (KXS) is a classic herbal formula for the treatment and prevention of AD (Alzheimer's disease) with definite curative effect, but its mechanism, which involves multiple components, pathways, and targets, is not yet fully understood.

AIM OF THE STUDY: To verify the effect of KXS on gut microbiota and explore its anti-AD mechanism related with gut microbiota.

MATERIALS AND METHODS: AD rat model was established and evaluated by intraperitoneal injection of D-gal and bilateral hippocampal CA1 injections of Aβ25-35. The pharmacodynamics of KXS in vivo includes general behavior, Morris water maze test, ELISA, Nissl & HE staining and immunofluorescence. Systematic analysis of gut microbiota was conducted using 16S rRNA gene sequencing technology. The potential role of gut microbiota in the anti-AD effect of KXS was validated with fecal microbiota transplantation (FMT) experiments.

RESULTS: KXS could significantly improve cognitive impairment, reduce neuronal damage and attenuate neuroinflammation and colonic inflammation in vivo in AD model rats. Nine differential intestinal bacteria associated with AD were screened, in which four bacteria (Lactobacillus murinus, Ligilactobacillus, Alloprevotella, Prevotellaceae_NK3B31_group) were very significant.

CONCLUSION: KXS can maintain the ecological balance of intestinal microbiota and exert its anti-AD effect by regulating the composition and proportion of gut microbiota in AD rats through the microbiota-gut-brain axis.},
}

@article {pmid38599367,
year = {2024},
author = {Svačina, MKR and Gao, T and Sprenger-Svačina, A and Lin, J and Ganesh, BP and Lee, J and McCullough, LD and Sheikh, KA and Zhang, G},
title = {Rejuvenating fecal microbiota transplant enhances peripheral nerve repair in aged mice by modulating endoneurial inflammation.},
journal = {Experimental neurology},
volume = {376},
number = {},
pages = {114774},
doi = {10.1016/j.expneurol.2024.114774},
pmid = {38599367},
issn = {1090-2430},
abstract = {Peripheral nerve injury (PNI) resulting from trauma or neuropathies can cause significant disability, and its prognosis deteriorates with age. Emerging evidence suggests that gut dysbiosis and reduced fecal short-chain fatty acids (SCFAs) contribute to an age-related systemic hyperinflammation (inflammaging), which hinders nerve recovery after injury. This study thus aimed to evaluate the pro-regenerative effects of a rejuvenating fecal microbiota transplant (FMT) in a preclinical PNI model using aged mice. Aged C57BL/6 mice underwent bilateral crush injuries to their sciatic nerves. Subsequently, they either received FMT from young donors at three and four days after the injury or retained their aged gut microbiota. We analyzed gut microbiome composition and SCFA concentrations in fecal samples. The integrity of the ileac mucosal barrier was assessed by immunofluorescence staining of Claudin-1. Flow cytometry was utilized to examine immune cells and cytokine production in the ileum, spleen, and sciatic nerve. Various assessments, including behavioural tests, electrophysiological studies, and morphometrical analyses, were conducted to evaluate peripheral nerve function and repair following injury. Rejuvenating FMT reversed age-related gut dysbiosis by increasing Actinobacteria, especially Bifidobacteriales genera. This intervention also led to an elevation of gut SCFA levels and mitigated age-related ileac mucosal leakiness in aged recipients. Additionally, it augmented the number of T-helper 2 (Th2) and regulatory T (Treg) cells in the ileum and spleen, with the majority being positive for anti-inflammatory interleukin-10 (IL-10). In sciatic nerves, rejuvenating FMT resulted in increased M2 macrophage counts and a higher IL-10 production by IL-10[+]TNF-α[-] M2 macrophage subsets. Ultimately, restoring a youthful gut microbiome in aged mice led to improved nerve repair and enhanced functional recovery after PNI. Considering that FMT is already a clinically available technique, exploring novel translational strategies targeting the gut microbiome to enhance nerve repair in the elderly seems promising and warrants further evaluation.},
}

@article {pmid38598636,
year = {2024},
author = {Sizemore, N and Oliphant, K and Zheng, R and Martin, CR and Claud, EC and Chattopadhyay, I},
title = {A digital twin of the infant microbiome to predict neurodevelopmental deficits.},
journal = {Science advances},
volume = {10},
number = {15},
pages = {eadj0400},
pmid = {38598636},
issn = {2375-2548},
mesh = {Infant ; Humans ; Infant, Newborn ; Infant, Premature ; Artificial Intelligence ; *Gastrointestinal Microbiome/genetics ; *Microbiota ; Feces ; },
abstract = {Despite the recognized gut-brain axis link, natural variations in microbial profiles between patients hinder definition of normal abundance ranges, confounding the impact of dysbiosis on infant neurodevelopment. We infer a digital twin of the infant microbiome, forecasting ecosystem trajectories from a few initial observations. Using 16S ribosomal RNA profiles from 88 preterm infants (398 fecal samples and 32,942 abundance estimates for 91 microbial classes), the model (Q-net) predicts abundance dynamics with R[2] = 0.69. Contrasting the fit to Q-nets of typical versus suboptimal development, we can reliably estimate individual deficit risk (Mδ) and identify infants achieving poor future head circumference growth with ≈76% area under the receiver operator characteristic curve, 95% ± 1.8% positive predictive value at 98% specificity at 30 weeks postmenstrual age. We find that early transplantation might mitigate risk for ≈45.2% of the cohort, with potentially negative effects from incorrect supplementation. Q-nets are generative artificial intelligence models for ecosystem dynamics, with broad potential applications.},
}

Infant
Humans
Infant, Newborn
Infant, Premature
Artificial Intelligence
*Gastrointestinal Microbiome/genetics
*Microbiota
Feces

@article {pmid38593970,
year = {2024},
author = {Seida, I and Al Shawaf, M and Mahroum, N},
title = {Fecal microbiota transplantation in autoimmune diseases - An extensive paper on a pathogenetic therapy.},
journal = {Autoimmunity reviews},
volume = {},
number = {},
pages = {103541},
doi = {10.1016/j.autrev.2024.103541},
pmid = {38593970},
issn = {1873-0183},
abstract = {The role of infections in the pathogenesis of autoimmune diseases has long been recognized and reported. In addition to infectious agents, the internal composition of the "friendly" living bacteria, (microbiome) and its correlation to immune balance and dysregulation have drawn the attention of researchers for decades. Nevertheless, only recently, scientific papers regarding the potential role of transferring microbiome from healthy donor subjects to patients with autoimmune diseases has been proposed. Fecal microbiota transplantation or FMT, carries the logic of transferring microorganisms responsible for immune balance from healthy donors to individuals with immune dysregulation or more accurately for our paper, autoimmune diseases. Viewing the microbiome as a pathogenetic player allows us to consider FMT as a pathogenetic-based treatment. Promising results alongside improved outcomes have been demonstrated in patients with different autoimmune diseases following FMT. Therefore, in our current extensive review, we aimed to highlight the implication of FMT in various autoimmune diseases, such as inflammatory bowel disease, autoimmune thyroid and liver diseases, systemic lupus erythematosus, and type 1 diabetes mellitus, among others. Presenting all the aspects of FMT in more than 12 autoimmune diseases in one paper, to the best of our knowledge, is the first time presented in medical literature. Viewing FMT as such could contribute to better understanding and newer application of the model in the therapy of autoimmune diseases, indeed.},
}

@article {pmid38591915,
year = {2024},
author = {Bratkovič, T and Zahirović, A and Bizjak, M and Rupnik, M and Štrukelj, B and Berlec, A},
title = {New treatment approaches for Clostridioides difficile infections: alternatives to antibiotics and fecal microbiota transplantation.},
journal = {Gut microbes},
volume = {16},
number = {1},
pages = {2337312},
pmid = {38591915},
issn = {1949-0984},
mesh = {Humans ; Anti-Bacterial Agents/therapeutic use/pharmacology ; *Clostridioides difficile ; Fecal Microbiota Transplantation ; *Gastrointestinal Microbiome ; Vancomycin/pharmacology ; *Clostridium Infections/drug therapy/prevention & control ; },
abstract = {Clostridioides difficile causes a range of debilitating intestinal symptoms that may be fatal. It is particularly problematic as a hospital-acquired infection, causing significant costs to the health care system. Antibiotics, such as vancomycin and fidaxomicin, are still the drugs of choice for C. difficile infections, but their effectiveness is limited, and microbial interventions are emerging as a new treatment option. This paper focuses on alternative treatment approaches, which are currently in various stages of development and can be divided into four therapeutic strategies. Direct killing of C. difficile (i) includes beside established antibiotics, less studied bacteriophages, and their derivatives, such as endolysins and tailocins. Restoration of microbiota composition and function (ii) is achieved with fecal microbiota transplantation, which has recently been approved, with standardized defined microbial mixtures, and with probiotics, which have been administered with moderate success. Prevention of deleterious effects of antibiotics on microbiota is achieved with agents for the neutralization of antibiotics that act in the gut and are nearing regulatory approval. Neutralization of C. difficile toxins (iii) which are crucial virulence factors is achieved with antibodies/antibody fragments or alternative binding proteins. Of these, the monoclonal antibody bezlotoxumab is already in clinical use. Immunomodulation (iv) can help eliminate or prevent C. difficile infection by interfering with cytokine signaling. Small-molecule agents without bacteriolytic activity are usually selected by drug repurposing and can act via a variety of mechanisms. The multiple treatment options described in this article provide optimism for the future treatment of C. difficile infection.},
}

Humans
Anti-Bacterial Agents/therapeutic use/pharmacology
*Clostridioides difficile
Fecal Microbiota Transplantation
*Gastrointestinal Microbiome
Vancomycin/pharmacology
*Clostridium Infections/drug therapy/prevention & control

@article {pmid37823484,
year = {2024},
author = {Straub, TJ and Lombardo, MJ and Bryant, JA and Diao, L and Lodise, TP and Freedberg, DE and Wortman, JR and Litcofsky, KD and Hasson, BR and McGovern, BH and Ford, CB and Henn, MR},
title = {Impact of a Purified Microbiome Therapeutic on Abundance of Antimicrobial Resistance Genes in Patients With Recurrent Clostridioides difficile Infection.},
journal = {Clinical infectious diseases : an official publication of the Infectious Diseases Society of America},
volume = {78},
number = {4},
pages = {833-841},
pmid = {37823484},
issn = {1537-6591},
support = {//Seres Therapeutics/ ; },
mesh = {Adult ; Humans ; Female ; Aged ; Male ; Anti-Bacterial Agents/pharmacology/therapeutic use ; Fecal Microbiota Transplantation ; *Clostridioides difficile/genetics ; Drug Resistance, Bacterial ; *Microbiota ; *Clostridium Infections/microbiology ; Bacteria ; Firmicutes ; },
abstract = {BACKGROUND: The gastrointestinal microbiota is an important line of defense against colonization with antimicrobial resistant (AR) bacteria. In this post hoc analysis of the phase 3 ECOSPOR III trial, we assessed impact of a microbiota-based oral therapeutic (fecal microbiota spores, live; VOWST Oral Spores [VOS], formerly SER-109]; Seres Therapeutics) compared with placebo, on AR gene (ARG) abundance in patients with recurrent Clostridioides difficile infection (rCDI).

METHODS: Adults with rCDI were randomized to receive VOS or placebo orally for 3 days following standard-of-care antibiotics. ARG and taxonomic profiles were generated using whole metagenomic sequencing of stool at baseline and weeks 1, 2, 8, and 24 posttreatment.

RESULTS: Baseline (n = 151) and serial posttreatment stool samples collected through 24 weeks (total N = 472) from 182 patients (59.9% female; mean age: 65.5 years) in ECOSPOR III as well as 68 stool samples obtained at a single time point from a healthy cohort were analyzed. Baseline ARG abundance was similar between arms and significantly elevated versus the healthy cohort. By week 1, there was a greater decline in ARG abundance in VOS versus placebo (P = .003) in association with marked decline of Proteobacteria and repletion of spore-forming Firmicutes, as compared with baseline. We observed abundance of Proteobacteria and non-spore-forming Firmicutes were associated with ARG abundance, while spore-forming Firmicutes abundance was negatively associated.

CONCLUSIONS: This proof-of-concept analysis suggests that microbiome remodeling with Firmicutes spores may be a potential novel approach to reduce ARG colonization in the gastrointestinal tract.},
}

Adult
Humans
Female
Aged
Male
Anti-Bacterial Agents/pharmacology/therapeutic use
Fecal Microbiota Transplantation
*Clostridioides difficile/genetics
Drug Resistance, Bacterial
*Microbiota
*Clostridium Infections/microbiology
Bacteria
Firmicutes

@article {pmid38591029,
year = {2024},
author = {Maurer, JJ and Cheng, Y and Pedroso, A and Thompson, KK and Akter, S and Kwan, T and Morota, G and Kinstler, S and Porwollik, S and McClelland, M and Escalante-Semerena, JC and Lee, MD},
title = {Peeling back the many layers of competitive exclusion.},
journal = {Frontiers in microbiology},
volume = {15},
number = {},
pages = {1342887},
pmid = {38591029},
issn = {1664-302X},
abstract = {Baby chicks administered a fecal transplant from adult chickens are resistant to Salmonella colonization by competitive exclusion. A two-pronged approach was used to investigate the mechanism of this process. First, Salmonella response to an exclusive (Salmonella competitive exclusion product, Aviguard[®]) or permissive microbial community (chicken cecal contents from colonized birds containing 7.85 Log10Salmonella genomes/gram) was assessed ex vivo using a S. typhimurium reporter strain with fluorescent YFP and CFP gene fusions to rrn and hilA operon, respectively. Second, cecal transcriptome analysis was used to assess the cecal communities' response to Salmonella in chickens with low (≤5.85 Log10 genomes/g) or high (≥6.00 Log10 genomes/g) Salmonella colonization. The ex vivo experiment revealed a reduction in Salmonella growth and hilA expression following co-culture with the exclusive community. The exclusive community also repressed Salmonella's SPI-1 virulence genes and LPS modification, while the anti-virulence/inflammatory gene avrA was upregulated. Salmonella transcriptome analysis revealed significant metabolic disparities in Salmonella grown with the two different communities. Propanediol utilization and vitamin B12 synthesis were central to Salmonella metabolism co-cultured with either community, and mutations in propanediol and vitamin B12 metabolism altered Salmonella growth in the exclusive community. There were significant differences in the cecal community's stress response to Salmonella colonization. Cecal community transcripts indicated that antimicrobials were central to the type of stress response detected in the low Salmonella abundance community, suggesting antagonism involved in Salmonella exclusion. This study indicates complex community interactions that modulate Salmonella metabolism and pathogenic behavior and reduce growth through antagonism may be key to exclusion.},
}

@article {pmid38589422,
year = {2024},
author = {Wei, N and Ju, M and Su, X and Zhang, Y and Huang, Y and Rao, X and Cui, L and Lin, Z and Dong, Y},
title = {Transplantation of gut microbiota derived from patients with schizophrenia induces schizophrenia-like behaviors and dysregulated brain transcript response in mice.},
journal = {Schizophrenia (Heidelberg, Germany)},
volume = {10},
number = {1},
pages = {44},
pmid = {38589422},
issn = {2754-6993},
support = {2022M711171//China Postdoctoral Science Foundation/ ; },
abstract = {Schizophrenia (SCZ), as a neurodevelopmental disorder and devastating disease, affects approximately 1% of the world population. Although numerous studies have attempted to elucidate the causes of SCZ occurrence, it is not clearly understood. Recently, the emerging roles of the gut microbiota in a range of brain disorders, including SCZ, have attracted much attention. While the molecular mechanism of gut microbiota in regulating the pathogenesis of SCZ is still lacking. Here, we first confirmed the difference of gut microbiome between SCZ patients and healthy controls, and then, we performed fecal microbiota transplantation (FMT) to clarify the roles of SCZ patients-derived microbiota in a specific pathogen free (SPF) mice model. 16 S rDNA sequencing confirmed that a significant difference of gut microbiome was present between two groups of FMT mice, which has a similar trend with the above human gut microbiome. Furthermore, we found that transplantation of fecal microbiota from SCZ patients into SPF mice was sufficient to induce schizophrenia-like (SCZ-like) symptoms, such as deficits in sociability and hyperactivity. Furthermore, the brains of mice colonized with SCZ microbiota displayed dysregulated transcript response and alternative splicing of SCZ-relevant genes. Moreover, 10 key genes were identified to be correlated with SCZ by an integrative transcriptome data analysis. Finally, 4 key genes were identified to be correlated with the 12 differential genera between two groups of FMT mice. Our results thus demonstrated that the gut microbiome might modify the transcriptomic profile in the brain, thereby modulating social behavior, and our present study can help better understand the link between gut microbiota and SCZ pathogenesis through the gut-brain axis.},
}

@article {pmid38589392,
year = {2024},
author = {Dokoshi, T and Chen, Y and Cavagnero, KJ and Rahman, G and Hakim, D and Brinton, S and Schwarz, H and Brown, EA and O'Neill, A and Nakamura, Y and Li, F and Salzman, NH and Knight, R and Gallo, RL},
title = {Dermal injury drives a skin to gut axis that disrupts the intestinal microbiome and intestinal immune homeostasis in mice.},
journal = {Nature communications},
volume = {15},
number = {1},
pages = {3009},
pmid = {38589392},
issn = {2041-1723},
support = {R37AI052453//U.S. Department of Health & Human Services | National Institutes of Health (NIH)/ ; R01DK121760//U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (National Institute of Diabetes & Digestive & Kidney Diseases)/ ; },
mesh = {Mice ; Animals ; *Gastrointestinal Microbiome ; Hyaluronic Acid/metabolism ; *Colitis ; Intestinal Mucosa/metabolism ; Fecal Microbiota Transplantation ; Dextran Sulfate/toxicity ; Mice, Inbred C57BL ; Disease Models, Animal ; Colon/metabolism ; },
abstract = {The composition of the microbial community in the intestine may influence the functions of distant organs such as the brain, lung, and skin. These microbes can promote disease or have beneficial functions, leading to the hypothesis that microbes in the gut explain the co-occurrence of intestinal and skin diseases. Here, we show that the reverse can occur, and that skin directly alters the gut microbiome. Disruption of the dermis by skin wounding or the digestion of dermal hyaluronan results in increased expression in the colon of the host defense genes Reg3 and Muc2, and skin wounding changes the composition and behavior of intestinal bacteria. Enhanced expression Reg3 and Muc2 is induced in vitro by exposure to hyaluronan released by these skin interventions. The change in the colon microbiome after skin wounding is functionally important as these bacteria penetrate the intestinal epithelium and enhance colitis from dextran sodium sulfate (DSS) as seen by the ability to rescue skin associated DSS colitis with oral antibiotics, in germ-free mice, and fecal microbiome transplantation to unwounded mice from mice with skin wounds. These observations provide direct evidence of a skin-gut axis by demonstrating that damage to the skin disrupts homeostasis in intestinal host defense and alters the gut microbiome.},
}

Mice
Animals
*Gastrointestinal Microbiome
Hyaluronic Acid/metabolism
*Colitis
Intestinal Mucosa/metabolism
Fecal Microbiota Transplantation
Dextran Sulfate/toxicity
Mice, Inbred C57BL
Disease Models, Animal
Colon/metabolism

@article {pmid38589368,
year = {2024},
author = {Liu, P and Liu, Z and Wang, J and Wang, J and Gao, M and Zhang, Y and Yang, C and Zhang, A and Li, G and Li, X and Liu, S and Liu, L and Sun, N and Zhang, K},
title = {Immunoregulatory role of the gut microbiota in inflammatory depression.},
journal = {Nature communications},
volume = {15},
number = {1},
pages = {3003},
pmid = {38589368},
issn = {2041-1723},
mesh = {Humans ; Mice ; Animals ; *Gastrointestinal Microbiome ; Depression/therapy ; Fecal Microbiota Transplantation ; Feces ; Fatty Acids, Volatile/metabolism ; },
abstract = {Inflammatory depression is a treatment-resistant subtype of depression. A causal role of the gut microbiota as a source of low-grade inflammation remains unclear. Here, as part of an observational trial, we first analyze the gut microbiota composition in the stool, inflammatory factors and short-chain fatty acids (SCFAs) in plasma, and inflammatory and permeability markers in the intestinal mucosa of patients with inflammatory depression (ChiCTR1900025175). Gut microbiota of patients with inflammatory depression exhibits higher Bacteroides and lower Clostridium, with an increase in SCFA-producing species with abnormal butanoate metabolism. We then perform fecal microbiota transplantation (FMT) and probiotic supplementation in animal experiments to determine the causal role of the gut microbiota in inflammatory depression. After FMT, the gut microbiota of the inflammatory depression group shows increased peripheral and central inflammatory factors and intestinal mucosal permeability in recipient mice with depressive and anxiety-like behaviors. Clostridium butyricum administration normalizes the gut microbiota, decreases inflammatory factors, and displays antidepressant-like effects in a mouse model of inflammatory depression. These findings suggest that inflammatory processes derived from the gut microbiota can be involved in neuroinflammation of inflammatory depression.},
}

Humans
Mice
Animals
*Gastrointestinal Microbiome
Depression/therapy
Fecal Microbiota Transplantation
Feces
Fatty Acids, Volatile/metabolism

@article {pmid38585738,
year = {2024},
author = {Hunter, C and Dia, K and Boykins, J and Perry, K and Banerjee, N and Cuffee, J and Armstrong, E and Morgan, G and Banerjee, HN and Banerjee, A and Bhattacharya, S},
title = {An investigation for phylogenetic characterization of human Pancreatic cancer microbiome by 16SrDNA Sequencing and Bioinformatics techniques.},
journal = {Research square},
volume = {},
number = {},
pages = {},
doi = {10.21203/rs.3.rs-4140368/v1},
pmid = {38585738},
abstract = {Pancreatic cancer is a significant public health concern, with increasing incidence rates and limited treatment options. Recent studies have highlighted the role of the human microbiome, particularly the gut microbiota, in the development and progression of this disease. Microbial dysbiosis, characterized by alterations in the composition and function of the gut microbiota, has been implicated in pancreatic carcinogenesis through mechanisms involving chronic inflammation, immune dysregulation, and metabolic disturbances. Researchers have identified specific microbial signatures associated with pancreatic cancer, offering potential biomarkers for early detection and prognostication. By leveraging advanced sequencing and bioinformatics tools, scientists have delineated differences in the gut microbiota between pancreatic cancer patients and healthy individuals, providing insights into disease pathogenesis and potential diagnostic strategies. Moreover, the microbiome holds promise as a therapeutic target in pancreatic cancer treatment. Interventions aimed at modulating the microbiome, such as probiotics, prebiotics, and fecal microbiota transplantation, have demonstrated potential in enhancing the efficacy of existing cancer therapies, including chemotherapy and immunotherapy. These approaches can influence immune responses, alter tumor microenvironments, and sensitize tumors to treatment, offering new avenues for improving patient outcomes and overcoming therapeutic resistance. Overall, understanding the complex interplay between the microbiome and pancreatic cancer is crucial for advancing our knowledge of disease mechanisms and identifying innovative therapeutic strategies. Here we report phylogenetic analysis of the 16S microbial sequences of the pancreatic cancer mice microbiome and corresponding age matched healthy mice microbiome. We successfully identified differentially abundance of microbiota in the pancreatic cancer.},
}

@article {pmid38585101,
year = {2024},
author = {Verma, A and Bhagchandani, T and Rai, A and Nikita, and Sardarni, UK and Bhavesh, NS and Gulati, S and Malik, R and Tandon, R},
title = {Short-Chain Fatty Acid (SCFA) as a Connecting Link between Microbiota and Gut-Lung Axis-A Potential Therapeutic Intervention to Improve Lung Health.},
journal = {ACS omega},
volume = {9},
number = {13},
pages = {14648-14671},
pmid = {38585101},
issn = {2470-1343},
support = {D43 TW009345/TW/FIC NIH HHS/United States ; },
abstract = {The microbiome is an integral part of the human gut, and it plays a crucial role in the development of the immune system and homeostasis. Apart from the gut microbiome, the airway microbial community also forms a distinct and crucial part of the human microbiota. Furthermore, several studies indicate the existence of communication between the gut microbiome and their metabolites with the lung airways, called "gut-lung axis". Perturbations in gut microbiota composition, termed dysbiosis, can have acute and chronic effects on the pathophysiology of lung diseases. Microbes and their metabolites in lung stimulate various innate immune pathways, which modulate the expression of the inflammatory genes in pulmonary leukocytes. For instance, gut microbiota-derived metabolites such as short-chain fatty acids can suppress lung inflammation through the activation of G protein-coupled receptors (free fatty acid receptors) and can also inhibit histone deacetylase, which in turn influences the severity of acute and chronic respiratory diseases. Thus, modulation of the gut microbiome composition through probiotic/prebiotic usage and fecal microbiota transplantation can lead to alterations in lung homeostasis and immunity. The resulting manipulation of immune cells function through microbiota and their key metabolites paves the way for the development of novel therapeutic strategies in improving the lung health of individuals affected with various lung diseases including SARS-CoV-2. This review will shed light upon the mechanistic aspect of immune system programming through gut and lung microbiota and exploration of the relationship between gut-lung microbiome and also highlight the therapeutic potential of gut microbiota-derived metabolites in the management of respiratory diseases.},
}

@article {pmid38584861,
year = {2024},
author = {Biedermann, L and Kreienbühl, A and Rogler, G},
title = {Microbiota Therapy in Inflammatory Bowel Disease.},
journal = {Visceral medicine},
volume = {40},
number = {2},
pages = {92-101},
pmid = {38584861},
issn = {2297-4725},
abstract = {BACKGROUND: In both Crohn's disease (CD) and ulcerative colitis (UC), the two major forms of inflammatory bowel disease (IBD) the immune reaction is - at least partially - directed against components of the luminal microbiota of the gut. These immune responses as well as other factors contribute to a phenomenon frequently described as "dysbiosis" meaning an alteration of the composition of the colonic microbiota. To improve the dysbiosis and to restore the normal composition of the colonic microbiota, fecal microbiota transplantation (FMT) has been tested as a therapeutic option to induce and maintain remission in IBD patients.

SUMMARY: This review will first discuss changes in the composition of the intestinal microbiota found in IBD patients and second the therapeutic potential of microbiological interventions for the treatment of these patients. FMT has been studied in several clinical trials in both, CD and UC. Reported results and subsequent meta-analyses indicate that FMT may be effective to induce remission in UC. However, the optimal route of FMT, the necessary number of administrations and the question whether life bacteria of freshly prepared stool is more effective than frozen are still unclear. Concepts associated with an optimization of FMT such as the "super donor concept" or the "consortia-approach" will be discussed to illustrate open questions and difficulties associated with microbiota therapy in IBD.

KEY MESSAGES: The microbiota composition in IBD patients shows significant alterations compared to healthy individuals termed as "dysbiosis". FMT and other therapeutic approaches to modify the microbiota composition have been studied in clinical trials in recent years. Efficacy has been shown in UC; however, many questions with respect to the optimization of microbiota therapy remain to be answered.},
}

@article {pmid38584858,
year = {2024},
author = {Stallhofer, J and Steube, A and Katzer, K and Stallmach, A},
title = {Microbiota-Based Therapeutics as New Standard-of-Care Treatment for Recurrent Clostridioides difficile Infection.},
journal = {Visceral medicine},
volume = {40},
number = {2},
pages = {82-91},
pmid = {38584858},
issn = {2297-4725},
abstract = {BACKGROUND: Clostridioides difficile (C. difficile) is a spore-forming bacterial species that ubiquitously exists in the environment. Colonization by C. difficile is highly prevalent in infants, while fewer than 5% of adults are asymptomatic carriers. Disruption of the microbiome, such as through antibiotic treatment, triggers the germination of bacterial spores into numerous vegetative cells. These cells then produce enterotoxins that result in watery diarrhea and colonic inflammation. If left untreated, C. difficile infection (CDI) can lead to pseudomembranous colitis with the potentially life-threatening complication of toxic megacolon.

SUMMARY: Over the past few decades, the incidence, morbidity, and mortality associated with CDIs have increased. They have emerged as the primary cause of nosocomial gastrointestinal infections in industrialized countries, posing a significant burden on healthcare systems. Despite antibiotics often being the cause of CDIs, they remain the standard treatment. However, a considerable number of patients treated with antibiotics will experience recurrent CDI (rCDI). Microbiota-based therapies targeting the core issue of CDI - antibiotic-induced dysbiosis - hold promise for rCDI treatment. While data for probiotics are insufficient, numerous studies have highlighted the effectiveness of fecal microbiota transplantation (FMT) as a safe and viable therapeutic option for rCDI. This approach is now endorsed by multiple guidelines. Nonetheless, regulatory prerequisites, such as comprehensive stool donor screening, restrict the widespread adoption of FMT beyond specialized centers. Recently, the US Food and Drug Administration has approved two commercial microbiota-based therapeutics to prevent CDI recurrence. These therapeutics are available by prescription in the USA. RBX2660 (REBYOTA™) comprises a diverse consortium of live microbes derived from human stool and is administered via enema. On the other hand, SER-109 (VOWST™) is an orally administered spore-based medication. In this review, we discuss the potential of microbiota-based treatments for rCDI against the background of medico-legal challenges associated with classical FMT.

KEY MESSAGES: FMT has emerged as a highly effective cure for rCDI. Nonetheless, regulatory prerequisites and laborious preparation procedures impede its widespread use. The establishment of ready-to-use microbiota-based therapeutics in clinical practice is necessary. In the USA, the recent approval of the first two commercial medications, including a spore-based oral preparation, marks a significant step forward.},
}

@article {pmid38584284,
year = {2024},
author = {Chen, C and Xu, JL and Gu, ZC and Zhou, SS and Wei, GL and Gu, JL and Ma, HL and Feng, YQ and Song, ZW and Yan, ZP and Deng, S and Ding, R and Li, SL and Huo, JG},
title = {Danggui Sini decoction alleviates oxaliplatin-induced peripheral neuropathy by regulating gut microbiota and potentially relieving neuroinflammation related metabolic disorder.},
journal = {Chinese medicine},
volume = {19},
number = {1},
pages = {58},
pmid = {38584284},
issn = {1749-8546},
support = {82004339//Natural Science Foundation of China/ ; Z2022005//Medical Scientific Research Project of Jiangsu Provincial Health Commission/ ; No.2021.6//Jiangsu Clinical Innovation Center of Digestive Cancer of Traditional Chinese Medicine/ ; JD2019SZXYB16//Project of National Clinical Research Base of Traditional Chinese Medicine in Jiangsu Province/ ; BE2019767//Jiangsu science and technology department social development-clinical frontier technology/ ; BRA2019100//Jiangsu science and technology department social development-clinical frontier technology/ ; BK20210984//Natural Science Foundation of Jiangsu Province/ ; },
abstract = {BACKGROUND: Danggui Sini decoction (DSD), a traditional Chinese medicine formula, has the function of nourishing blood, warming meridians, and unblocking collaterals. Our clinical and animal studies had shown that DSD can effectively protect against oxaliplatin (OXA)-induced peripheral neuropathy (OIPN), but the detailed mechanisms remain uncertain. Multiple studies have confirmed that gut microbiota plays a crucial role in the development of OIPN. In this study, the potential mechanism of protective effect of DSD against OIPN by regulating gut microbiota was investigated.

METHODS: The neuroprotective effects of DSD against OIPN were examined on a rat model of OIPN by determining mechanical allodynia, biological features of dorsal root ganglia (DRG) as well as proinflammatory indicators. Gut microbiota dysbiosis was characterized using 16S rDNA gene sequencing and metabolism disorders were evaluated using untargeted and targeted metabolomics. Moreover the gut microbiota mediated mechanisms were validated by antibiotic intervention and fecal microbiota transplantation.

RESULTS: DSD treatment significantly alleviated OIPN symptoms by relieving mechanical allodynia, preserving DRG integrity and reducing proinflammatory indicators lipopolysaccharide (LPS), IL-6 and TNF-α. Besides, DSD restored OXA induced intestinal barrier disruption, gut microbiota dysbiosis as well as systemic metabolic disorders. Correlation analysis revealed that DSD increased bacterial genera such as Faecalibaculum, Allobaculum, Dubosiella and Rhodospirillales_unclassified were closely associated with neuroinflammation related metabolites, including positively with short-chain fatty acids (SCFAs) and sphingomyelin (d18:1/16:0), and negatively with pi-methylimidazoleacetic acid, L-glutamine and homovanillic acid. Meanwhile, antibiotic intervention apparently relieved OIPN symptoms. Furthermore, fecal microbiota transplantation further confirmed the mediated effects of gut microbiota.

CONCLUSION: DSD alleviates OIPN by regulating gut microbiota and potentially relieving neuroinflammation related metabolic disorder.},
}

@article {pmid38582194,
year = {2024},
author = {Rook, GAW},
title = {Evolution and the critical role of the microbiota in the reduced mental and physical health associated with low socioeconomic status (SES).},
journal = {Neuroscience and biobehavioral reviews},
volume = {},
number = {},
pages = {105653},
doi = {10.1016/j.neubiorev.2024.105653},
pmid = {38582194},
issn = {1873-7528},
abstract = {The evolution of the gut-microbiota-brain axis in animals reveals that microbial inputs influence metabolism, the regulation of inflammation and the development of organs, including the brain. Inflammatory, neurodegenerative and psychiatric disorders are more prevalent in people of low socioeconomic status (SES). Many aspects of low SES reduce exposure to the microbial inputs on which we are in a state of evolved dependence, whereas the lifestyle of wealthy citizens maintains these exposures. This partially explains the health deficit of low SES, so focussing on our evolutionary history and on environmental and lifestyle factors that distort microbial exposures might help to mitigate that deficit. But the human microbiota is complex and we have poor understanding of its functions at the microbial and mechanistic levels, and in the brain. Perhaps its composition is more flexible than the microbiota of animals that have restricted habitats and less diverse diets? These uncertainties are discussed in relation to the encouraging but frustrating results of attempts to treat psychiatric disorders by modulating the microbiota.},
}

@article {pmid38579995,
year = {2024},
author = {Zeng, Z and Lv, B and Tang, YE and Sun, H and Li, S and He, Y and Wang, J and Wang, Z},
title = {Effects of dietary selenized glucose on intestinal microbiota and tryptophan metabolism in rats: Assessing skatole reduction potential.},
journal = {Environmental research},
volume = {},
number = {},
pages = {118874},
doi = {10.1016/j.envres.2024.118874},
pmid = {38579995},
issn = {1096-0953},
abstract = {3-Methylindole (Skatole), a degradation product of tryptophan produced by intestinal microbial activity, significantly contributes to odor nuisance. Its adverse effects on animal welfare, human health, and environmental pollution have been noted. However, it is still unclear whether the intestinal microbiota mediates the impact of selenium (Se) on skatole production and what the underlying mechanisms remain elusive. A selenized glucose (SeGlu) derivative is a novel organic selenium compound. In this study, a diverse range of dietary SeGlu-treated levels, including SeGlu-deficient (CK), SeGlu-adequate (0.15 mg Se per L), and SeGlu-supranutritional (0.4 mg Se per L) conditions, were used to investigate the complex interaction of SeGlu on intestinal microbiome and serum metabolome changes in male Sprague-Dawley (SD) rats. The study showed that SeGlu supplementation enhanced the antioxidant ability in rats, significantly manifested in the increases of the activity of catalase (CAT) and glutathione peroxidase (GSH-Px), while no change in the level of malonaldehyde (MDA). Metagenomic sequencing analysis verified that the SeGlu treatment group significantly increased the abundance of beneficial microorganisms such as Clostridium, Ruminococcus, Faecalibacterium, Lactobacillus, and Alloprevotella while reducing the abundance of opportunistic pathogens such as Bacteroides and Alistipes significantly. Further metabolomic analysis revealed phenylalanine, tyrosine, and tryptophan biosynthesis changes in the SeGlu treatment group. Notably, the biosynthesis of indole, a critical pathway, was affected by SeGlu treatment, with several crucial enzymes implicated. Correlation analysis demonstrated strong associations between specific bacterial species - Treponema, Bacteroides, and Ruminococcus, and changes in indole and derivative concentrations. Moreover, the efficacy of SeGlu-treated fecal microbiota was confirmed through fecal microbiota transplantation, leading to a decrease in the concentration of skatole in rats. Collectively, the analysis of microbiota and metabolome response to diverse SeGlu levels suggests that SeGlu is a promising dietary additive in modulating intestinal microbiota and reducing odor nuisance in the livestock and poultry industry.},
}

@article {pmid38578736,
year = {2024},
author = {Lin, L and Xu, S and Cai, M and Li, S and Chen, Y and Chen, L and Lin, Y},
title = {Effects of fecal microbiota transfer on blood pressure in animal models: A systematic review and meta-analysis.},
journal = {PloS one},
volume = {19},
number = {4},
pages = {e0300869},
pmid = {38578736},
issn = {1932-6203},
mesh = {Animals ; Blood Pressure ; *Fecal Microbiota Transplantation ; *Hypertension/therapy ; Feces ; Dysbiosis ; },
abstract = {BACKGROUND: Numerous recent studies have found a strong correlation between intestinal flora and the occurrence of hypertension. However, it remains unclear whether fecal microbiota transfer might affect the blood pressure of the host. This study aimed to quantify both associations.

METHODS: An electronic search was conducted in PubMed, EMBASE, Cochrane Library, Web of Science, China National Knowledge Infrastructure (CNKI), WanFang database, Weipu, Embase, and SinoMed to retrieve relevant studies. The final search was completed on August 22, 2022. Two authors independently applied the inclusion criteria, extracted data, and assessed the risk of bias assessment. All data were analyzed using RevMan 5.4.

RESULTS: A total of 5 articles were selected for final inclusion. All studies were assessed as having a high risk of bias according to the SYRCLE risk of bias tool. The meta-analysis results showed that transplantation of fecal bacteria from the hypertensive model can significantly improve the host's systolic pressure (MD = 18.37, 95%CI: 9.74~26.99, P<0.001), and diastolic pressure (MD = 17.65, 95%CI: 12.37~22.93, P<0.001). Subgroup analyses revealed that the increase in systolic pressure in the hypertension model subgroup (MD = 29.56, 95%CI = 23.55-35.58, P<0.001) was more pronounced than that in the normotensive model subgroup (MD = 12.48, 95%CI = 3.51-21.45, P<0.001).

CONCLUSION: This meta-analysis suggests a relationship between gut microbiota dysbiosis and increased blood pressure, where transplantation of fecal bacteria from the hypertensive model can cause a significant increase in systolic pressure and diastolic pressure in animal models.},
}

Animals
Blood Pressure
*Fecal Microbiota Transplantation
*Hypertension/therapy
Feces
Dysbiosis

@article {pmid38577203,
year = {2024},
author = {Koutromanos, I and Legaki, E and Gazouli, M and Vasilopoulos, E and Kouzoupis, A and Tzavellas, E},
title = {Gut microbiome in alcohol use disorder: Implications for health outcomes and therapeutic strategies-a literature review.},
journal = {World journal of methodology},
volume = {14},
number = {1},
pages = {88519},
pmid = {38577203},
issn = {2222-0682},
abstract = {Alcohol use disorder (AUD) represents a major public health issue which affects millions of people globally and consist a chronic relapsing condition associated with substantial morbidity and mortality. The gut microbiome plays a crucial role in maintaining overall health and has emerged as a significant contributor to the pathophysiology of various psychiatric disorders. Recent evidence suggests that the gut microbiome is intimately linked to the development and progression of AUD, with alcohol consumption directly impacting its composition and function. This review article aims to explore the intricate relationship between the gut microbiome and AUD, focusing on the implications for mental health outcomes and potential therapeutic strategies. We discuss the bidirectional communication between the gut microbiome and the brain, highlighting the role of microbiota-derived metabolites in neuroinflammation, neurotransmission, and mood regulation. Furthermore, we examine the influence of AUD-related factors, such as alcohol-induced gut dysbiosis and increased intestinal permeability, on mental health outcomes. Finally, we explore emerging therapeutic avenues targeting the gut microbiome in the management of AUD, including prebiotics, probiotics, and fecal microbiota transplantation. Understanding the complex interplay between the gut microbiome and AUD holds promise for developing novel interventions that could improve mental health outcomes in individuals with AUD.},
}

@article {pmid38575121,
year = {2024},
author = {Ren, J and Li, Y and Ni, H and Zhang, Y and Zhao, P and Xiao, Q and Hong, X and Zhang, Z and Yin, Y and Li, X and Zhang, Y and Yang, Y},
title = {Gut microbiota derived from fecal microbiota transplantation enhances body weight of Mimas squabs.},
journal = {Animal bioscience},
volume = {},
number = {},
pages = {},
doi = {10.5713/ab.23.0475},
pmid = {38575121},
issn = {2765-0189},
abstract = {OBJECTIVE: Compared to Mimas pigeons, Shiqi pigeons exhibit greater tolerance to coarse feeding because of their abundant gut microbiota. Here, to investigate the potential of utilizing intestinal flora derived from Shiqi pigeons, the intestinal flora and body indices of Mimas squabs were evaluated after fecal microbiota transplantation (FMT) from donors.

METHODS: A total of 90 one-day-old squabs were randomly divided into the control group (CON), the low-concentration group (LC) and the high-concentration group (HC): gavaged with 200 μL of bacterial solution at concentrations of 0, 0.1 and 0.2 g/15 mL, respectively.

RESULTS: The results suggested that FMT improved the body weight of Mimas squabs in the HC and LC groups (p < 0.01), and 0.1 g/15 mL was the optimal dose during FMT. After 16S rRNA sequencing was performed, compared to those in the CON group, the abundance levels of microflora, especially Lactobacillus, Muribaculaceae and Megasphaera (p < 0.05), in the FMT-treated groups were markedly greater. Random forest analysis indicated that the main functions of key microbes involve pathways associated with metabolism, further illustrating their important role in the host body.

CONCLUSION: FMT has been determined to be a viable method for augmenting the weight and intestinal microbiota of squabs, representing a unique avenue for enhancing the economic feasibility of squab breeding.},
}

@article {pmid38574899,
year = {2024},
author = {Stevens, LJ and van de Steeg, E and Doppenberg, JB and Alwayn, IPJ and Knibbe, CAJ and Dubbeld, J},
title = {Ex vivo Gut-Hepato-Biliary organ perfusion model to characterize oral absorption, gut-wall metabolism, pre-systemic hepatic metabolism and biliary excretion; application to midazolam.},
journal = {European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences},
volume = {},
number = {},
pages = {106760},
doi = {10.1016/j.ejps.2024.106760},
pmid = {38574899},
issn = {1879-0720},
abstract = {To date, characterization of the first-pass effect of orally administered drugs consisting of local intestinal absorption and metabolism, portal vein transport and hepatobiliary processes remains challenging. Aim of this study was to explore the applicability of a porcine ex-vivo perfusion model to study oral absorption, gut-hepatobiliary metabolism and biliary excretion of midazolam. Slaughterhouse procured porcine en bloc organs (n=4), were perfused via the aorta and portal vein. After 120min of perfusion, midazolam, atenolol, antipyrine and FD4 were dosed via the duodenum and samples were taken from the systemic- and portal vein perfusate, intestinal faecal effluent and bile to determine drug and metabolite concentrations. Stable arterial and portal vein flow was obtained and viability of the perfused organs was confirmed. After intraduodenal administration, midazolam was rapidly detected in the portal vein together with 1-OH midazolam (EG-pv of 0.16±0.1) resulting from gut wall metabolism through oxidation. In the intestinal faecal effluent, 1-OH midazolam and 1-OH midazolam glucuronide (EG-intestine 0.051±0.03) was observed resulting from local gut glucuronidation. Biliary elimination of midazolam (0.04±0.01%) and its glucuronide (0.01±0.01%) only minimally contributed to the enterohepatic circulation. More extensive hepatic metabolism (FH 0.35±0.07) over intestinal metabolism (FG 0.78±0.11) was shown, resulting in oral bioavailability of 0.27±0.05. Ex vivo perfusion demonstrated to be a novel approach to characterize pre-systemic extraction of midazolam by measuring intestinal as well as hepatic extraction. The model can generate valuable insights into the absorption and metabolism of new drugs.},
}

@article {pmid38574779,
year = {2024},
author = {Yan, G and Zhang, L and Wu, D and Jiang, S and Wu, Q and Dai, M},
title = {Paeonol attenuates nonalcoholic steatohepatitis by regulating intestinal flora and AhR/NLRP3/Caspase-1 metabolic pathway.},
journal = {Journal of ethnopharmacology},
volume = {},
number = {},
pages = {118147},
doi = {10.1016/j.jep.2024.118147},
pmid = {38574779},
issn = {1872-7573},
abstract = {Non-alcoholic steatohepatitis (NASH) is a common metabolic liver injury disease that is closely associated with obesity and metabolic disorders. Paeonol, an active ingredient found in Moutan Cortex, a traditional Chinese medicine which exhibits significant therapeutic effect on liver protection, has shown promising effects in treating liver diseases, particularly NASH. However, the specific intervention mechanism of paeonol on NASH is still unknown.

AIM OF THE STUDY: Our objective is to elucidate the pharmacological mechanism of paeonol in intervening NASH at the in vivo level, focusing on the impact on intestinal flora, tryptophan-related targeted metabolome, and related Aryl hydrocarbon receptor (AhR) pathways.

MATERIALS AND METHODS: Here, we explored the intervention effect of paeonol on NASH by utilizing the NASH mouse model. The Illumina highthroughput sequencing technology was preformed to determine the differences of gut microbiota of model and paeonol treatment group. The concentration of Indoleacetic acid is determined by ELISA. The intervention effect of NASH mouse and AhR/NLRP3/Caspase-1 metabolic pathway is analyzed by HE staining, oil red O staining, Immunohistochemistry, Immunofluorescence, Western blot and qRT-PCR assays. Fecal microbiota transplantation experiment also was performed to verify the intervention effect of paeonol on NASH by affecting gut microbiota.

RESULTS: Firstly, we discovered that paeonol effectively reduced liver pathology and blood lipid levels in NASH mice, thereby intervening in the progression of NASH. Subsequently, through 16S meta-analysis, we identified that paeonol can effectively regulate the composition of intestinal flora in NASH mice, transforming it to resemble that of normal mice. Specifically, paeonol decreased the abundance of certain Gram-negative tryptophan-metabolizing bacteria. Moreover, we discovered that paeonol significantly increased the levels of metabolites Indoleacetic acid, subsequently enhancing the expression of AhR-related pathway proteins. This led to the inhibition of the NOD-like receptor protein 3 (NLRP3) inflammasome production and inflammation generation in NASH. Lastly, we verified the efficacy of paeonol in intervening NASH by conducting fecal microbiota transplantation experiments, which confirmed its role in promoting the AhR/NLRP3/cysteinyl aspartate specific proteinase (Caspase-1) pathway.

CONCLUSIONS: Our findings suggest that paeonol can increase the production of Indoleacetic acid by regulating the gut flora, and promote the AhR/NLRP3/Caspase-1 metabolic pathway to intervene NASH.},
}

@article {pmid38574772,
year = {2024},
author = {Sottil, P and Lhomme, S and Saune, K and El Hayani, S and Oliveira-Mendes, K and Peron, JM and Kamar, N and Izopet, J and Abravanel, F},
title = {Evaluation of an automated platform for the detection of HEV RNA in plasma and stool.},
journal = {Journal of virological methods},
volume = {},
number = {},
pages = {114920},
doi = {10.1016/j.jviromet.2024.114920},
pmid = {38574772},
issn = {1879-0984},
abstract = {INTRODUCTION: We evaluated the performance of the automated Altostar HEV RNA platform for detecting HEV RNA.

METHODS AND RESULTS: Clinical performance was determined by testing 81 plasma samples and 10 fecal samples manually quantified previously with the Realstar RT-PCR assay using the Magnapure instrument for extraction. The assays were concordant for 79/81 plasma samples (97.5%) and 10/10 (100%) fecal samples. The two plasma samples that tested negative with the Altostar assay had a very low HEV RNA concentration (1.6 and 1.4 log10 IU/ml). Quantitative results obtained with the automated platform and the manual workflow were highly correlated (ρ= 0.98, p<0.01). The intra-run and inter-run standard deviation were 0.09 IU/ml and 0.13 IU/ml respectively. The assay was linear from 2 to 6log IU/ml. The limit of detection determined by Probit analysis with the WHO HEV RNA standard was 7.6 [95% CI: 4.4-52.5] IU/ml.

CONCLUSIONS: The Altostar platform enables highly accurate testing for the detection of HEV RNA in stool and the quantification of HEV RNA in plasma. This allowed us to shorten turnaround times and to save time for the technical staff.},
}

@article {pmid38572783,
year = {2024},
author = {Ren, S and Feng, L and Liu, H and Mao, Y and Yu, Z},
title = {Gut microbiome affects the response to immunotherapy in non-small cell lung cancer.},
journal = {Thoracic cancer},
volume = {},
number = {},
pages = {},
doi = {10.1111/1759-7714.15303},
pmid = {38572783},
issn = {1759-7714},
support = {ZR202102240880//Natural Science Foundation of Shandong Province/ ; 23-2-1-189-zyyd-jch//Natural Science Foundation of Qingdao Municipality/ ; 320.6750.2021-02-92//Wu Jieping Medical Foundation/ ; 82373170//National Natural Science Foundation of China/ ; Y-QL202101-0258//Chinese Society of Clinical Oncology/ ; Y-pierrefabre202101-0074//Chinese Society of Clinical Oncology/ ; YXH2022ZX02020//ShanDong Provincial Medical Association/ ; },
abstract = {BACKGROUND: Immunotherapy has revolutionized cancer treatment. Recent studies have suggested that the efficacy of immunotherapy can be further enhanced by the influence of gut microbiota. In this study, we aimed to investigate the impact of bacteria on the effectiveness of cancer immunotherapy by combining analysis of clinical samples with validation in animal models.

METHODS: In order to characterize the diversity and composition of microbiota and its relationship with response to immune checkpoint inhibitors (ICIs), 16S ribosomal RNA (rRNA) and GC-MS sequencing was performed on 71 stool samples from patients with advanced non-small cell lung cancer (NSCLC) prior to treatment with immune checkpoint blockade (ICB). Furthermore, fecal microbiota transplantation (FMT) was performed from different patients into mice and a subcutaneous tumor model established using the Lewis lung cancer cell line to evaluate the therapeutic effect of PD-1 on mice with varying gut microbiota.

RESULTS: The results demonstrated a significant association between elevated gut microbiota diversity and response to treatment with ICIs, p < 0.05. Faecalibacterium was markedly increased in the gut microbiota of responders (R), accompanied by increased short-chain fatty acid (SCFA) levels, especially butanoic acid, acetic acid and hexanoic acid, p < 0.05. Additionally, FMT from R and nonresponders (NR) could promote an anticancer effect and reduce the expression of Ki-67 cells in tumors in mice, p < 0.05. Moreover, R and NR FMT did not alter PD-L1 expression in the tumor tissues of mice, p > 0.05. The diversity of gut microbiota consistently correlated with an optimistic prognosis in NSCLC patients with immunotherapy, which could be functionally mediated by SCFAs.

CONCLUSION: The findings of the present study indicated that the diversity of gut microbiota and SCFAs is related to the efficacy of immunotherapy. FMT can effectively delay tumor progression, and enhance the effect of immunotherapy, thus providing evidence for improving the efficacy of immunotherapy in NSCLC patients.},
}

@article {pmid38572716,
year = {2024},
author = {van Lingen, E and Nooij, S and Terveer, E and Crossette, E and Prince, A and Bhattarai, S and Watson, A and Galazzo, G and Menon, R and Szabady, R and Bucci, V and Norman, J and van der Woude, J and van der Marel, S and Verspaget, H and van der Meulen-de Jong, A and Keller, J},
title = {Fecal Microbiota Transplantation engraftment after budesonide or placebo in patients with active ulcerative colitis using pre-selected donors: a randomized pilot study.},
journal = {Journal of Crohn's & colitis},
volume = {},
number = {},
pages = {},
doi = {10.1093/ecco-jcc/jjae043},
pmid = {38572716},
issn = {1876-4479},
abstract = {BACKGROUND: Fecal microbiota transplantation (FMT) shows some efficacy in treating patients with ulcerative colitis (UC), although variability has been observed among donors and treatment regimens. We investigated the effect of FMT using rationally selected donors after pretreatment with budesonide or placebo in active UC.

METHODS: Patients ≥ 18 years old with mild to moderate active UC were randomly assigned to three weeks budesonide (9 mg) or placebo followed by four weekly infusions of a donor feces suspension. Two donors were selected based on microbiota composition, Treg induction and SCFA production in mice. The primary endpoint was engraftment of donor microbiota after FMT. In addition, clinical efficacy was assessed.

RESULTS: In total, 24 patients were enrolled. Pretreatment with budesonide did not increase donor microbiota engraftment (p=0.56) nor clinical response, and engraftment was not associated with clinical response. At week 14, 10/24 (42%) of patients achieved (partial) remission. Remarkably, patients treated with FMT suspensions from one donor were associated with clinical response (80% of responders, p<0.05) but had lower overall engraftment of donor microbiota. Furthermore, differences in the taxonomic composition of the donors and the engraftment of certain taxa were associated with clinical response.

CONCLUSION: In this small study, pretreatment with budesonide did not significantly influence engraftment or clinical response after FMT. However, clinical response appeared donor-dependent. Response to FMT may be related to transfer of specific strains instead of overall engraftment, demonstrating the need to characterize mechanisms of actions of strains that maximize therapeutic benefit in ulcerative colitis.},
}

@article {pmid38571533,
year = {2024},
author = {Al Naser, Y and AlGashami, M and Aljashaami, L},
title = {Clostridioides difficile infection: a changing treatment paradigm.},
journal = {Przeglad gastroenterologiczny},
volume = {19},
number = {1},
pages = {1-5},
pmid = {38571533},
issn = {1895-5770},
abstract = {Clostridioides difficile infection (CDI) poses a persistent challenge in healthcare, with substantial morbidity and mortality implications. This comprehensive review explores current CDI management, emphasising guidelines from IDSA, SHEA, and ESCMID. Additionally, this study spotlights recent drug developments that have the potential to reshape CDI treatment paradigms. Within the current treatment landscape, fidaxomicin, vancomycin, bezlotoxumab, and faecal microbiota transplantation offer varied options, each with its unique strengths and limitations. Fidaxomicin, effective yet resource-constrained, presents a dilemma, with vancomycin emerging as a pragmatic alternative. Bezlotoxumab, though augmenting antibiotics, grapples with cost and safety concerns. Meanwhile, faecal microbiota transplantation, highly efficacious, confronts evolving safety considerations. The horizon of CDI treatment also features promising therapies such as SER-109 and Rebyota, epitomising the evolving paradigm. As CDI management advances, the critical role of standardised microbiome restoration therapies becomes evident, ensuring long-term safety and diversifying treatment strategies.},
}