@article {pmid39224076,
year = {2024},
author = {McMillan, AS and Theriot, CM},
title = {Bile acids impact the microbiota, host, and C. difficile dynamics providing insight into mechanisms of efficacy of FMTs and microbiota-focused therapeutics.},
journal = {Gut microbes},
volume = {16},
number = {1},
pages = {2393766},
pmid = {39224076},
issn = {1949-0984},
mesh = {*Bile Acids and Salts/metabolism ; Humans ; *Fecal Microbiota Transplantation ; *Clostridioides difficile/physiology ; *Gastrointestinal Microbiome ; *Clostridium Infections/therapy/microbiology ; Animals ; },
abstract = {Clostridioides difficile is a major nosocomial pathogen, causing significant morbidity and mortality worldwide. Antibiotic usage, a major risk factor for Clostridioides difficile infection (CDI), disrupts the gut microbiota, allowing C. difficile to proliferate and cause infection, and can often lead to recurrent CDI (rCDI). Fecal microbiota transplantation (FMT) and live biotherapeutic products (LBPs) have emerged as effective treatments for rCDI and aim to restore colonization resistance provided by a healthy gut microbiota. However, much is still unknown about the mechanisms mediating their success. Bile acids, extensively modified by gut microbes, affect C. difficile's germination, growth, and toxin production while also shaping the gut microbiota and influencing host immune responses. Additionally, microbial interactions, such as nutrient competition and cross-feeding, contribute to colonization resistance against C. difficile and may contribute to the success of microbiota-focused therapeutics. Bile acids as well as other microbial mediated interactions could have implications for other diseases being treated with microbiota-focused therapeutics. This review focuses on the intricate interplay between bile acid modifications, microbial ecology, and host responses with a focus on C. difficile, hoping to shed light on how to move forward with the development of new microbiota mediated therapeutic strategies to combat rCDI and other intestinal diseases.},
}

*Bile Acids and Salts/metabolism
Humans
*Fecal Microbiota Transplantation
*Clostridioides difficile/physiology
*Gastrointestinal Microbiome
*Clostridium Infections/therapy/microbiology
Animals

@article {pmid39222063,
year = {2024},
author = {Shiroma, H and Darzi, Y and Terajima, E and Nakagawa, Z and Tsuchikura, H and Tsukuda, N and Moriya, Y and Okuda, S and Goto, S and Yamada, T},
title = {Enteropathway: the metabolic pathway database for the human gut microbiota.},
journal = {Briefings in bioinformatics},
volume = {25},
number = {5},
pages = {},
pmid = {39222063},
issn = {1477-4054},
support = {JPMJCR19U3//JST AIP Acceleration Research/ ; JP16H06279//Japan Society for the Promotion of Science/ ; JP21ck0106546h0002//Japan Agency for Medical Research and Development/ ; 2020-A-7//National Cancer Center Research and Development Fund/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome ; *Metabolic Networks and Pathways ; *Databases, Factual ; Software ; Computational Biology/methods ; },
abstract = {The human gut microbiota produces diverse, extensive metabolites that have the potential to affect host physiology. Despite significant efforts to identify metabolic pathways for producing these microbial metabolites, a comprehensive metabolic pathway database for the human gut microbiota is still lacking. Here, we present Enteropathway, a metabolic pathway database that integrates 3269 compounds, 3677 reactions, and 876 modules that were obtained from 1012 manually curated scientific literature. Notably, 698 modules of these modules are new entries and cannot be found in any other databases. The database is accessible from a web application (https://enteropathway.org) that offers a metabolic diagram for graphical visualization of metabolic pathways, a customization interface, and an enrichment analysis feature for highlighting enriched modules on the metabolic diagram. Overall, Enteropathway is a comprehensive reference database that can complement widely used databases, and a tool for visual and statistical analysis in human gut microbiota studies and was designed to help researchers pinpoint new insights into the complex interplay between microbiota and host metabolism.},
}

Humans
*Gastrointestinal Microbiome
*Metabolic Networks and Pathways
*Databases, Factual
Software
Computational Biology/methods

@article {pmid39218555,
year = {2024},
author = {Zhang, M and Cui, Y and Liu, P and Mo, R and Wang, H and Li, Y and Wu, Y},
title = {Oat β-(1 → 3, 1 → 4)-d-glucan alleviates food allergy-induced colonic injury in mice by increasing Lachnospiraceae abundance and butyrate production.},
journal = {Carbohydrate polymers},
volume = {344},
number = {},
pages = {122535},
doi = {10.1016/j.carbpol.2024.122535},
pmid = {39218555},
issn = {1879-1344},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; Mice ; *Colon/pathology/drug effects/metabolism ; *Butyrates/metabolism ; *Food Hypersensitivity ; *Avena/chemistry ; Clostridiales ; beta-Glucans/pharmacology/chemistry ; Mice, Inbred BALB C ; Male ; Glucans/pharmacology/chemistry ; Fatty Acids, Volatile/metabolism ; Fecal Microbiota Transplantation ; },
abstract = {Oat β-(1 → 3, 1 → 4)-d-glucan (OBG), a linear polysaccharide primarily found in oat bran, has been demonstrated to possess immunomodulatory properties and regulate gut microbiota. This study aimed to investigate the impact of low molecular weight (Mw) OBG (155.2 kDa) on colonic injury and allergic symptoms induced by food allergy (FA), and to explore its potential mechanism. In Experiment 1, results indicated that oral OBG improved colonic inflammation and epithelial barrier, and significantly relieved allergy symptoms. Importantly, the OBG supplement altered the gut microbiota composition, particularly increasing the abundance of Lachnospiraceae and its genera, and promoted the production of short-chain fatty acids, especially butyrate. However, in Experiment 2, the gut microbial depletion eliminated these protective effects of OBG on the colon in allergic mice. Further, in Experiment 3, fecal microbiota transplantation and sterile fecal filtrate transfer directly validated the role of OBG-mediated gut microbiota and its metabolites in relieving FA and its induced colonic injury. Our findings suggest that low Mw OBG can alleviate FA-induced colonic damage by increasing Lachnospiraceae abundance and butyrate production, and provide novel insights into the health benefits and mechanisms of dietary polysaccharide intervention for FA.},
}

Animals
*Gastrointestinal Microbiome/drug effects
Mice
*Colon/pathology/drug effects/metabolism
*Butyrates/metabolism
*Food Hypersensitivity
*Avena/chemistry
Clostridiales
beta-Glucans/pharmacology/chemistry
Mice, Inbred BALB C
Male
Glucans/pharmacology/chemistry
Fatty Acids, Volatile/metabolism
Fecal Microbiota Transplantation

@article {pmid39217880,
year = {2024},
author = {Jin, Z and Liu, Z and Pan, J and Wang, S and Cui, M and He, C and Lin, M and Liu, X and Yu, X and Gong, F},
title = {FGF20 modulates gut microbiota to mitigate dextran sodium sulfate-induced ulcerative colitis in mouse models.},
journal = {International immunopharmacology},
volume = {142},
number = {Pt A},
pages = {113044},
doi = {10.1016/j.intimp.2024.113044},
pmid = {39217880},
issn = {1878-1705},
abstract = {Ulcerative colitis (UC), a prevalent form of inflammatory bowel disease (IBD), presents a significant clinical challenge due to the lack of optimal therapeutic strategies. Emerging evidence suggests that fibroblast growth factor 20 (FGF20) may play a crucial role in mitigating UC symptoms, though the mechanistic underpinnings remain elusive. In this study, a mouse model of UC was established using dextran sodium sulfate (DSS) to investigate the potential role of FGF20. Our findings revealed a marked reduction in FGF20 expression in the serum and colonic tissues of DSS-treated mice. Furthermore, FGF20 knockout did not exacerbate colonic damage in these mice. Conversely, overexpression of FGF20 via adeno-associated virus (AAV) significantly alleviated UC-associated symptoms. This alleviation was evidenced by attenuated intestinal shortening, mitigated weight loss, increased colonic goblet cell density and crypt formation, reduced inflammation severity and inflammatory cell infiltration, and enhanced expression of tight junction and mucin proteins. Moreover, FGF20 significantly ameliorated the dysbiosis of gut microbiota in DSS-treated mice by increasing the abundance of beneficial bacteria and decreasing the abundance of harmful bacteria. The beneficial effects of FGF20 were notably attenuated following gut microbiota depletion with an antibiotic regimen. Fecal microbiota transplantation experiments further supported the critical role of gut microbiota in mediating the effects of FGF20 on DSS-treated mice. In conclusion, these findings highlight the potential involvement of gut microbiota in the therapeutic effects of FGF20 in UC.},
}

@article {pmid39217582,
year = {2024},
author = {Yang, Q and Wang, Z and Liu, M and Gan, L},
title = {Causal Relationship Between Gut Microbiota and Leukemia: Future Perspectives.},
journal = {Oncology and therapy},
volume = {},
number = {},
pages = {},
pmid = {39217582},
issn = {2366-1089},
abstract = {The gut microbiota plays a crucial role in maintaining homeostasis in the human gastrointestinal tract. Numerous studies have shown a strong association between the gut microbiota and the emergence and progression of various diseases. Leukemia is one of the most common hematologic malignancies. Although standardized protocols and expert consensus have been developed for routine diagnosis and treatment, limitations remain due to individual differences. Nevertheless, a large number of studies have established a link between the gut microbiota and leukemia, with disturbances in the gut microbiota directly or indirectly affecting the development of leukemia. However, the causal relationship between the two remains unclear, and studying and exploring the causal relationship may open up entirely new avenues and protocols for use in the prevention and/or treatment of leukemia, offering new insights into diagnosis and treatment. In this review, the intricate relationship between the gut microbiota and leukemia is explored in depth, including causal associations, metabolite effects, therapeutic applications, and complications. Based on the characteristics of the gut microbiota, the future applications and prospects of gut microbiota are discussed to provide useful information for clinical treatment of leukemia.},
}

@article {pmid39217051,
year = {2024},
author = {Akhmedov, M and Espinoza, JL},
title = {Addressing the surge of infections by multidrug-resistant Enterobacterales in hematopoietic cell transplantation.},
journal = {Blood reviews},
volume = {},
number = {},
pages = {101229},
doi = {10.1016/j.blre.2024.101229},
pmid = {39217051},
issn = {1532-1681},
abstract = {Patients undergoing hematopoietic cell transplantation (HCT) have an increased risk of developing severe infections. In recent years, bloodstream infections caused by Gram-negative bacteria have been increasingly reported among HCT recipients, and many of these infections are caused by bacterial strains of the Enterobacterales order. Among these pathogens, particularly concerning are the multidrug-resistant Enterobacterales (MDRE), such as Extended Spectrum β-lactamase-producing Enterobacterales and Carbapenem-resistant Enterobacterales, since infections caused by these pathogens are difficult to treat due to the limited antimicrobial options and are associated with worse transplant outcomes. We summarized the evidence from studies published in PubMed and Scopus on the burden of MDRE infections in HCT recipients, and strategies for the management and prevention of these infections, including strict adherence to recommended infection control practices and multidisciplinary antimicrobial stewardship, the use of probiotics, and fecal microbiota transplantation, are also discussed.},
}

@article {pmid39214188,
year = {2024},
author = {Hensen, ADO and Vehreschild, MJGT and Gerding, DN and Krut, O and Chen, W and Young, VB and Tzipori, S and Solbach, P and Gibani, MM and Chiu, C and de Keersmaecker, SCJ and Dasyam, D and Morel, S and Devaster, JM and Corti, N and Kuijper, EJ and Roestenberg, M and Smits, WK},
title = {How to develop a Controlled Human Infection Model for Clostridioides difficile.},
journal = {Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cmi.2024.08.025},
pmid = {39214188},
issn = {1469-0691},
abstract = {BACKGROUND: Clostridioides difficile (C. difficile) remains the leading cause of healthcare-associated diarrhoea, posing treatment challenges due to antibiotic resistance and high relapse rates. Fecal microbiota transplantation (FMT) is a novel treatment strategy to prevent relapses of C. difficile infection (CDI), however the exact components conferring colonisation resistance are unknown, hampering its translation to a medicinal product. Development of novel products independent of antibiotics, which increase colonisation resistance or induce protective immune mechanisms are urgently needed.

OBJECTIVES: To establish a framework for a Controlled Human Infection Model (CHIM) for C. difficile, in which healthy volunteers are exposed to toxigenic C. difficile spores, offering the possibility to test novel approaches and identify microbiota and immunological targets. Whereas experimental exposure to non-toxigenic C. difficile (NTCD) has been done before, a toxigenic C. difficile CHIM faces ethical, scientific, logistical and biosafety challenges.

SOURCES: Specific challenges in developing a C. difficile CHIM were discussed by a group of international experts during a workshop organized by Inno4Vac, an IHI-funded consortium.

CONTENT: The experts agreed that the main challenges are: developing a clinically relevant CHIM which induces mild to moderate CDI symptoms but no severe CDI, determining optimal C. difficile inoculum dose and understanding the timing and duration of antibiotic pre-treatment in inducing susceptibility to CDI in healthy volunteers.

IMPLICATIONS: Should these challenges be tackled, a C. difficile CHIM not only provides a way forward for the testing of novel products but also offers a framework for better understanding of the pathophysiology, pathogenesis and immunology of C. difficile colonisation and infection.},
}

@article {pmid39212186,
year = {2024},
author = {Junker Mentzel, CM and Hui, Y and Hammerich, TMS and Klug-Dambmann, M and Liu, Y and Zachariassen, LF and Hansen, LH and Aslampaloglou, A and Kiersgaard, M and Nielsen, DS and Hansen, AK and Krych, L},
title = {Low-gainer diet-induced obese microbiota transplanted mice exhibit increased fighting.},
journal = {Clinical and translational science},
volume = {17},
number = {9},
pages = {e13906},
pmid = {39212186},
issn = {1752-8062},
support = {//LIFEPHARM/ ; //Novo Nordisk A/S/ ; //Center for Applied Laboratory Animal Research/ ; },
mesh = {Animals ; Male ; *Obesity/microbiology/etiology ; *Gastrointestinal Microbiome/physiology ; *Fecal Microbiota Transplantation ; *Mice, Inbred C57BL ; *Diet, High-Fat/adverse effects ; *Weight Gain ; Mice ; Disease Models, Animal ; Leptin/blood/metabolism ; Feces/microbiology ; },
abstract = {Weight gain variation is a great challenge in diet-induced obesity studies since low-gainer animals are of limited experimental value. The inbred C57BL/6 (B6) mice are frequently used models due to their genetic homogeneity and susceptibility to diet-induced obesity (DIO). The aim of this study is to investigate if the gut microbiota (GM) influences the fraction of low weight gainers in DIO studies. A total of 100 male B6 mice (donor population) were fed a high-fat diet for 14 weeks and divided into the study groups high gainer (HG) and low gainer (LG) based on their weight gain. Subsequently, fecal matter transplantation (FMT) was done on germ-free B6 mice with GM from HG and LG donors (FMT population). LG (13.35 ± 2.5 g) and HG (25.52 ± 2.0 g) animals were identified by the weight gain from week 1 to week 12. Interestingly, the start weight of the LG (20.36 ± 1.4 g) and HG (21.59 ± 0.7 g) groups differed significantly. Transplanting LG or HG fecal matter to germ-free mice resulted in significant differences in weight gain between HG and LG, as well as differences in serum leptin levels and epididymal fat pad weight. A clear LG-specific GM composition could not be distinguished by 16S rRNA gene amplicon sequencing. Surprisingly, significantly more fighting was recorded in LG groups of both donor populations and when transplanted to germ-free mice. The HG and LG phenotypes could be transferred to germ-free mice. The increased fighting in the LG group in both studies suggests not only that the tendency to fight can be transferred by FMT in these mice, but also that fighting should be prevented in DIO studies to minimize the number of LG animals.},
}

Animals
Male
*Obesity/microbiology/etiology
*Gastrointestinal Microbiome/physiology
*Fecal Microbiota Transplantation
*Mice, Inbred C57BL
*Diet, High-Fat/adverse effects
*Weight Gain
Mice
Disease Models, Animal
Leptin/blood/metabolism
Feces/microbiology

@article {pmid39214085,
year = {2024},
author = {Hayase, E and Hayase, T and Mukherjee, A and Stinson, SC and Jamal, MA and Ortega, MR and Sanchez, CA and Ahmed, SS and Karmouch, JL and Chang, CC and Flores, II and McDaniel, LK and Brown, AN and El-Himri, RK and Chapa, VA and Tan, L and Tran, BQ and Xiao, Y and Fan, C and Pham, D and Halsey, TM and Jin, Y and Tsai, WB and Prasad, R and Glover, IK and Enkhbayar, A and Mohammed, A and Schmiester, M and King, KY and Britton, RA and Reddy, P and Wong, MC and Ajami, NJ and Wargo, JA and Shelburne, S and Okhuysen, PC and Liu, C and Fowler, SW and Conner, ME and Katsamakis, Z and Smith, N and Burgos da Silva, M and Ponce, DM and Peled, JU and van den Brink, MRM and Peterson, CB and Rondon, G and Molldrem, JJ and Champlin, RE and Shpall, EJ and Lorenzi, PL and Mehta, RS and Martens, EC and Alousi, AM and Jenq, RR},
title = {Bacteroides ovatus alleviates dysbiotic microbiota-induced graft-versus-host disease.},
journal = {Cell host & microbe},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.chom.2024.08.004},
pmid = {39214085},
issn = {1934-6069},
abstract = {Acute lower gastrointestinal GVHD (aLGI-GVHD) is a serious complication of allogeneic hematopoietic stem cell transplantation. Although the intestinal microbiota is associated with the incidence of aLGI-GVHD, how the intestinal microbiota impacts treatment responses in aLGI-GVHD has not been thoroughly studied. In a cohort of patients with aLGI-GVHD (n = 37), we found that non-response to standard therapy with corticosteroids was associated with prior treatment with carbapenem antibiotics and a disrupted fecal microbiome characterized by reduced abundances of Bacteroides ovatus. In a murine GVHD model aggravated by carbapenem antibiotics, introducing B. ovatus reduced GVHD severity and improved survival. These beneficial effects of Bacteroides ovatus were linked to its ability to metabolize dietary polysaccharides into monosaccharides, which suppressed the mucus-degrading capabilities of colonic mucus degraders such as Bacteroides thetaiotaomicron and Akkermansia muciniphila, thus reducing GVHD-related mortality. Collectively, these findings reveal the importance of microbiota in aLGI-GVHD and therapeutic potential of B. ovatus.},
}

@article {pmid39213702,
year = {2024},
author = {Su, Y and Fan, X and Cai, X and Ning, J and Shen, M},
title = {Effects of fecal microbiota transplantation combined with selenium on intestinal microbiota in mice with colorectal cancer.},
journal = {Biochemical and biophysical research communications},
volume = {733},
number = {},
pages = {150580},
doi = {10.1016/j.bbrc.2024.150580},
pmid = {39213702},
issn = {1090-2104},
abstract = {Colorectal cancer (CRC) is the third most common cancer in the world. With the development of high-throughput gene sequencing technology, homeostasis imbalance of the intestinal microbiota has been proven to play a key role in the pathogenesis of CRC. Furthermore, fecal bacteria transplantation (FMT) has been shown to alter the intestinal microecology, and is potentially an effective treatment for CRC. Sodium selenite plays an important role in anticancer adjuvant therapy due to its high pro-oxidation characteristics. In this study, a murine CRC tumor model was induced by AOM/DSS, and CRC mice were treated by FMT, sodium selenite, and FMT combined with sodium selenite. The results showed that FMT, sodium selenite, and FMT combined with sodium selenite inhibited the occurrence of CRC in mice, increased the abundance of beneficial intestinal bacteria, produced different microorganisms, and changed the metabolic pathways of the intestinal microbiota. In summary, FMT, sodium selenite, and FMT combined with sodium selenite can inhibit the occurrence of CRC by increasing the abundance of beneficial bacteria and regulating phenotypes and metabolic pathways. Notably, the effect of FMT combined with sodium selenite in reducing the number of tumors, protecting intestinal tissues, and restoring the diversity and richness of the intestinal microbiota is superior to that of FMT alone or sodium selenite alone. The results of this study provide new ideas for the application of FMT and selenium in the treatment of CRC.},
}

@article {pmid39212377,
year = {2024},
author = {Pan, L and Yin, N and Duan, M and Mei, Q and Zeng, Y},
title = {The role of gut microbiome and its metabolites in pancreatitis.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0066524},
doi = {10.1128/msystems.00665-24},
pmid = {39212377},
issn = {2379-5077},
abstract = {Gut microbiome plays a vital role in the intestinal ecosystem and has close association with metabolites. Due to the development of metabolomics and microbiomics, recent studies have observed that alteration of either the gut microbiome or metabolites may have effects on the progression of pancreatitis. Several new treatments based on the gut microbiome or metabolites have been studied extensively in recent years. Gut microbes, such as Bifidobacterium, Akkermansia, and Lactobacillus, and metabolites, such as short-chain fatty acids, bile acids, vitamin, hydrogen sulfide, and alcohol, have different effects on pancreatitis. Some preliminary studies about new intervention measures were based on the gut microbiome and metabolites such as diet, prebiotic, herbal medicine, and fecal microbiota transplantation. This review aims to summarize the recent advances about the gut microbiome, metabolites, and pancreatitis in order to determine the potential beneficial role of the gut microbiome and metabolites in pancreatitis.},
}

@article {pmid39212113,
year = {2024},
author = {Liu, Z and Wang, M and Hu, Y and Li, J and Gong, W and Guo, X and Song, S and Zhu, B},
title = {Ulva lactuca polysaccharides combined with fecal microbiota transplantation ameliorated dextran sodium sulfate-induced colitis in C57BL/6J mice.},
journal = {Journal of the science of food and agriculture},
volume = {},
number = {},
pages = {},
doi = {10.1002/jsfa.13839},
pmid = {39212113},
issn = {1097-0010},
support = {2023YFD2100200//National Key Research and Development Program of China/ ; 32302148//National Natural Science Foundation of China/ ; ZDSYS20220117155800001//Shenzhen Science and Technology Program/ ; },
abstract = {BACKGROUND: Fecal microbiota transplantation (FMT) of healthy donors improves ulcerative colitis (UC) patients by restoring the balance of the gut microbiota. However, donors vary in microbial diversity and composition, often resulting in weak or even ineffective FMT. Improving the efficacy of FMT through combination treatment has become a promising strategy. Ulva lactuca polysaccharides (ULP) have been found to benefit host health by regulating gut microbiota. The effect of the combination of ULP and FMT in ameliorating UC has not yet been evaluated.

RESULTS: The present study found that supplementation with ULP combined with FMT showed better effects in ameliorating UC than supplementation with FMT alone. Results suggested that FMT or ULP combined with FMT alleviated the symptoms of UC in mice, as evidenced by prevention of body weight loss, improvement of disease activity index and protection of the intestinal mucus. Notably, ULP in combination with FMT was more effective than FMT in reducing levels of cytokines and related inflammatory enzymes. In addition, ULP combined with FMT effectively restored the dysbiosis induced by dextran sulfate sodium (DSS) and further enriched probiotics (such as Bifidobacterium). The production of short-chain fatty acids, especially acetic acid, was also significantly enriched by ULP combined with FMT.

CONCLUSION: Supplementation of ULP combined with FMT could significantly ameliorate DSS-induced colitis in mice by inhibiting inflammation and restoring dysbiosis of gut microbiota. These results suggested that ULP combined with FMT has potential application in ameliorating UC. © 2024 Society of Chemical Industry.},
}

@article {pmid39211181,
year = {2024},
author = {Kennedy, MS and Freiburger, A and Cooper, M and Beilsmith, K and St George, ML and Kalski, M and Cham, C and Guzzetta, A and Ng, SC and Chan, FK and Rubin, D and Henry, CS and Bergelson, J and Chang, EB},
title = {Diet outperforms microbial transplant to drive microbiome recovery post-antibiotics.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2024.08.01.606245},
pmid = {39211181},
issn = {2692-8205},
abstract = {High-fat, low-fiber Western-style diets (WD) induce microbiome dysbiosis characterized by reduced taxonomic diversity and metabolic breadth, which in turn increases risk for a wide array of metabolic, immune and systemic pathologies. Recent work has established that WD can impair microbiome resilience to acute perturbations like antibiotic treatment, although we know little about the mechanism of impairment and the specific host consequences of prolonged post-antibiotic dysbiosis. Here, we characterize the trajectory by which the gut microbiome recovers its taxonomic and functional profile after antibiotic treatment in mice on regular chow (RC) and WD, and find that only mice on RC undergo a rapid successional process of recovery. Metabolic modeling indicates that RC diet promotes the development of syntrophic cross-feeding interactions, while on WD, a dominant taxon monopolizes readily available resources without releasing syntrophic byproducts. Intervention experiments reveal that an appropriate dietary resource environment is both necessary and sufficient for rapid and robust microbiome recovery, whereas microbial transplant is neither. Furthermore, prolonged post-antibiotic dysbiosis in mice on WD renders them susceptible to infection by the intestinal pathogen Salmonella enterica serovar Typhimurium. Our data challenge widespread enthusiasm for fecal microbiota transplant (FMT) as a strategy to address dysbiosis and demonstrate that specific dietary interventions are, at minimum, an essential prerequisite for effective FMT, and may afford a safer, more natural, and less invasive alternative to FMT.},
}

@article {pmid39210613,
year = {2024},
author = {Xu, Y and Wu, X and Li, Y and Liu, X and Fang, L and Jiang, Z},
title = {Probiotics and the Role of Dietary Substrates in Maintaining the Gut Health: Use of Live Microbes and Their Products for Anticancer Effects against Colorectal Cancer.},
journal = {Journal of microbiology and biotechnology},
volume = {34},
number = {9},
pages = {1-14},
doi = {10.4014/jmb.2403.03056},
pmid = {39210613},
issn = {1738-8872},
abstract = {The gut microbiome is an important and the largest endocrine organ linked to the microbes of the GI tract. The bacterial, viral and fungal communities are key regulators of the health and disease status in a host at hormonal, neurological, immunological, and metabolic levels. The useful microbes can compete with microbes exhibiting pathogenic behavior by maintaining resistance against their colonization, thereby maintaining eubiosis. As diagnostic tools, metagenomic, proteomic and genomic approaches can determine various microbial markers in clinic for early diagnosis of colorectal cancer (CRC). Probiotics are live non-pathogenic microorganisms such as lactic acid bacteria, Bifidobacteria, Firmicutes and Saccharomyces that can help maintain eubiosis when administered in appropriate amounts. In addition, the type of dietary intake contributes substantially to the composition of gut microbiome. The use of probiotics has been found to exert antitumor effects at preclinical levels and promote the antitumor effects of immunotherapeutic drugs at clinical levels. Also, modifying the composition of gut microbiota by Fecal Microbiota Transplantation (FMT), and using live lactic acid producing bacteria such as Lactobacillus, Bifidobacteria and their metabolites (termed postbiotics) can contribute to immunomodulation of the tumor microenvironment. This can lead to tumor-preventive effects at early stages and antitumor effects after diagnosis of CRC. To conclude, probiotics are presumably found to be safe to use in humans and are to be studied further to promote their appliance at clinical levels for management of CRC.},
}

@article {pmid39206530,
year = {2024},
author = {Gupta, CL and Jaganathasamy, N and Madkaikar, M},
title = {Microbiome in sickle cell disease: Pathophysiology and therapeutic insights.},
journal = {British journal of haematology},
volume = {},
number = {},
pages = {},
doi = {10.1111/bjh.19736},
pmid = {39206530},
issn = {1365-2141},
abstract = {Sickle cell disease (SCD) is a complex genetic blood disorder characterized by abnormal haemoglobin, resulting in sickle-shaped red blood cells. While extensive research has concentrated on the genetic and physiological aspects of SCD, recent studies suggest a potential role of the human microbiome in SCD pathophysiology, adding new dimensions to its understanding. This review synthesizes current knowledge on the microbiome's involvement in SCD, focusing on alterations in the gut microbiome composition and diversity compared to healthy individuals, and their implications for disease pathogenesis. We explore how microbiome changes may contribute to vaso-occlusive crises and other complications, along with the possible associations of specific microbial taxa or markers with disease crises and clinical outcomes. Additionally, we discuss the potential of microbiome-targeted interventions, including probiotics, dietary modifications, and faecal microbiota transplantation, in managing SCD complications and improving patient outcomes. Understanding the intricate relationship between the microbiome and SCD could lead to innovative therapeutic strategies and personalized interventions for better managing the disease. This review underscores the importance of further microbiome research and its integration into holistic SCD care.},
}

@article {pmid39205822,
year = {2024},
author = {Hosseini-Asl, SMK and Mehrabani, G and Masoumi, SJ},
title = {Key Focus Areas in Pouchitis Therapeutic Status: A Narrative Review.},
journal = {Iranian journal of medical sciences},
volume = {49},
number = {8},
pages = {472-486},
pmid = {39205822},
issn = {1735-3688},
mesh = {Humans ; *Pouchitis/therapy/etiology/drug therapy ; Fecal Microbiota Transplantation/methods ; Probiotics/therapeutic use ; Anti-Bacterial Agents/therapeutic use ; },
abstract = {Pouchitis, as the most common complication after ileal pouch-anal anastomosis (IPAA), has an incidence from 7% to 46%. Pouchitis treatment still represents one of the biggest gaps of knowledge in the treatment of diseases. This review has focused on achievements and challenges in the treatment of pouchitis. A combined assessment of symptoms, endoscopic findings, histologic results, quick biomarkers, and fecal calprotectin test were determined to be valuable diagnostic criteria. Conventional therapy was described as a modification of bacterial flora, mainly with antibiotics and more recently with probiotics such as bifidobacteria, lactobacilli, and streptococci. Other therapeutic approaches such as anti-tumor necrosis factor, infliximab, adalimumab, vedolizumab, ustekinumab, tacrolimus, tofacitinib, thiopurines, corticosteroids, prolyl hydroxylase-containing enzymes, povidone-iodine, dextrose spray, fecal microbiota transplantation, herbal medicines, and leukocyte apheresis have been discussed. Changes in dietary components, and administration of complementary and alternative medicine, probiotics, and fecal transplantation in addition to conventional therapies were also shown to affect the outcome of disease. Due to the potential significant impairment in quality of life caused by pouchitis, it is essential to address the gaps in knowledge for both patients and physicians in its treatment. Therefore, well-designed and adequately powered studies should assess the optimal treatment for pouchitis.},
}

Humans
*Pouchitis/therapy/etiology/drug therapy
Fecal Microbiota Transplantation/methods
Probiotics/therapeutic use
Anti-Bacterial Agents/therapeutic use

@article {pmid39205654,
year = {2024},
author = {Wu, L and Zhou, J and Zhou, A and Lei, Y and Tang, L and Hu, S and Wang, S and Xiao, X and Chen, Q and Tu, D and Lu, C and Lai, Y and Li, Y and Zhang, X and Tang, B and Yang, S},
title = {Lactobacillus acidophilus ameliorates cholestatic liver injury through inhibiting bile acid synthesis and promoting bile acid excretion.},
journal = {Gut microbes},
volume = {16},
number = {1},
pages = {2390176},
doi = {10.1080/19490976.2024.2390176},
pmid = {39205654},
issn = {1949-0984},
mesh = {*Lactobacillus acidophilus ; *Bile Acids and Salts/metabolism ; Animals ; *Gastrointestinal Microbiome ; *Cholestasis/metabolism/microbiology ; Mice ; Humans ; Male ; *Probiotics/pharmacology/administration & dosage ; *Liver/metabolism ; *Mice, Inbred C57BL ; Feces/microbiology ; Cholesterol 7-alpha-Hydroxylase/metabolism/genetics ; Female ; Fibroblast Growth Factors/metabolism/genetics ; Fecal Microbiota Transplantation ; Dysbiosis/microbiology/therapy ; RNA, Ribosomal, 16S/genetics ; Middle Aged ; Adult ; Disease Models, Animal ; Ileum/microbiology/metabolism ; },
abstract = {Gut microbiota dysbiosis is involved in cholestatic liver diseases. However, the mechanisms remain to be elucidated. The purpose of this study was to examine the effects and mechanisms of Lactobacillus acidophilus (L. acidophilus) on cholestatic liver injury in both animals and humans. Bile duct ligation (BDL) was performed to mimic cholestatic liver injury in mice and serum liver function was tested. Gut microbiota were analyzed by 16S rRNA sequencing. Fecal bacteria transplantation (FMT) was used to evaluate the role of gut microbiota in cholestasis. Bile acids (BAs) profiles were analyzed by targeted metabolomics. Effects of L. acidophilus in cholestatic patients were evaluated by a randomized controlled clinical trial (NO: ChiCTR2200063330). BDL induced different severity of liver injury, which was associated with gut microbiota. 16S rRNA sequencing of feces confirmed the gut flora differences between groups, of which L. acidophilus was the most distinguished genus. Administration of L. acidophilus after BDL significantly attenuated hepatic injury in mice, decreased liver total BAs and increased fecal total BAs. Furthermore, after L. acidophilus treatment, inhibition of hepatic Cholesterol 7α-hydroxylase (CYP7α1), restored ileum Fibroblast growth factor 15 (FGF15) and Small heterodimer partner (SHP) accounted for BAs synthesis decrease, whereas enhanced BAs excretion was attributed to the increase of unconjugated BAs by enriched bile salt hydrolase (BSH) enzymes in feces. Similarly, in cholestasis patients, supplementation of L. acidophilus promoted the recovery of liver function and negatively correlated with liver function indicators, possibly in relationship with the changes in BAs profiles and gut microbiota composition. L. acidophilus treatment ameliorates cholestatic liver injury through inhibited hepatic BAs synthesis and enhances fecal BAs excretion.},
}

*Lactobacillus acidophilus
*Bile Acids and Salts/metabolism
Animals
*Gastrointestinal Microbiome
*Cholestasis/metabolism/microbiology
Mice
Humans
Male
*Probiotics/pharmacology/administration & dosage
*Liver/metabolism
*Mice, Inbred C57BL
Feces/microbiology
Cholesterol 7-alpha-Hydroxylase/metabolism/genetics
Female
Fibroblast Growth Factors/metabolism/genetics
Fecal Microbiota Transplantation
Dysbiosis/microbiology/therapy
RNA, Ribosomal, 16S/genetics
Middle Aged
Adult
Disease Models, Animal
Ileum/microbiology/metabolism

@article {pmid39204246,
year = {2024},
author = {Spigaglia, P},
title = {Clostridioides difficile and Gut Microbiota: From Colonization to Infection and Treatment.},
journal = {Pathogens (Basel, Switzerland)},
volume = {13},
number = {8},
pages = {},
pmid = {39204246},
issn = {2076-0817},
abstract = {Clostridioides difficile is the main causative agent of antibiotic-associated diarrhea (AAD) in hospitals in the developed world. Both infected patients and asymptomatic colonized individuals represent important transmission sources of C. difficile. C. difficile infection (CDI) shows a large range of symptoms, from mild diarrhea to severe manifestations such as pseudomembranous colitis. Epidemiological changes in CDIs have been observed in the last two decades, with the emergence of highly virulent types and more numerous and severe CDI cases in the community. C. difficile interacts with the gut microbiota throughout its entire life cycle, and the C. difficile's role as colonizer or invader largely depends on alterations in the gut microbiota, which C. difficile itself can promote and maintain. The restoration of the gut microbiota to a healthy state is considered potentially effective for the prevention and treatment of CDI. Besides a fecal microbiota transplantation (FMT), many other approaches to re-establishing intestinal eubiosis are currently under investigation. This review aims to explore current data on C. difficile and gut microbiota changes in colonized individuals and infected patients with a consideration of the recent emergence of highly virulent C. difficile types, with an overview of the microbial interventions used to restore the human gut microbiota.},
}

@article {pmid39203805,
year = {2024},
author = {Deleu, S and Jacobs, I and Vazquez Castellanos, JF and Verstockt, S and Trindade de Carvalho, B and Subotić, A and Verstockt, B and Arnauts, K and Deprez, L and Vissers, E and Lenfant, M and Vandermeulen, G and De Hertogh, G and Verbeke, K and Matteoli, G and Huys, GRB and Thevelein, JM and Raes, J and Vermeire, S},
title = {Effect of Mutant and Engineered High-Acetate-Producing Saccharomyces cerevisiae var. boulardii Strains in Dextran Sodium Sulphate-Induced Colitis.},
journal = {Nutrients},
volume = {16},
number = {16},
pages = {},
doi = {10.3390/nu16162668},
pmid = {39203805},
issn = {2072-6643},
support = {VR 2021 1712 DOC. 1492/4//Grand Challenges Program of VIB/ ; },
mesh = {Animals ; *Dextran Sulfate ; Female ; *Acetates ; Mice ; *Saccharomyces cerevisiae/genetics ; *Colitis/chemically induced/therapy ; *Probiotics ; Disease Models, Animal ; Colon/metabolism/microbiology/pathology ; Saccharomyces boulardii ; Colitis, Ulcerative/chemically induced/therapy/microbiology ; Mutation ; Gastrointestinal Microbiome ; Feces/microbiology ; Mice, Inbred C57BL ; },
abstract = {Acetate-producing Saccharomyces cerevisiae var. boulardii strains could exert improved effects on ulcerative colitis, which here, was preclinically evaluated in an acute dextran sodium sulphate induced model of colitis. Nine-week-old female mice were divided into 12 groups, receiving either drinking water or 2.75% dextran sodium sulphate for 7 days, combined with a daily gavage of various treatments with different levels of acetate accumulation: sham control (phosphate buffered saline, no acetate), non-probiotic control (Baker's yeast, no acetate), probiotic control (Enterol[®], transient acetate), and additionally several Saccharomyces cerevisiae var. boulardii strains with respectively no, high, and extra-high acetate accumulation. Disease activity was monitored daily, and feces samples were collected at different timepoints. On day 14, the mice were sacrificed, upon which blood and colonic tissue were collected for analysis. Disease activity in inflamed mice was lower when treated with the high-acetate-producing strain compared to sham and non-probiotic controls. The non-acetate-producing strain showed higher disease activity compared to the acetate-producing strains. Accordingly, higher histologic inflammation was observed in non- or transient-acetate-producing strains compared to the sham control, whereas this increase was not observed for high- and extra-high-acetate-producing strains upon induction of inflammation. These anti-inflammatory findings were confirmed by transcriptomic analysis of differentially expressed genes. Moreover, only the strain with the highest acetate production was superior in maintaining a stable gut microbial alpha-diversity upon inflammation. These findings support new possibilities for acetate-mediated management of inflammation in inflammatory bowel disease by administrating high-acetate-producing Saccharomyces cerevisae var. boulardii strains.},
}

Animals
*Dextran Sulfate
Female
*Acetates
Mice
*Saccharomyces cerevisiae/genetics
*Colitis/chemically induced/therapy
*Probiotics
Disease Models, Animal
Colon/metabolism/microbiology/pathology
Saccharomyces boulardii
Colitis, Ulcerative/chemically induced/therapy/microbiology
Mutation
Gastrointestinal Microbiome
Feces/microbiology
Mice, Inbred C57BL

@article {pmid39203583,
year = {2024},
author = {Yamada, CH and Ortis, GB and Buso, GM and Martins, TC and Zequinao, T and Telles, JP and Wollmann, LC and Montenegro, CO and Dantas, LR and Cruz, JW and Tuon, FF},
title = {Validation of Lyophilized Human Fecal Microbiota for the Treatment of Clostridioides difficile Infection: A Pilot Study with Pharmacoeconomic Analysis of a Middle-Income Country-Promicrobioma Project.},
journal = {Microorganisms},
volume = {12},
number = {8},
pages = {},
doi = {10.3390/microorganisms12081741},
pmid = {39203583},
issn = {2076-2607},
abstract = {BACKGROUND: Clostridioides difficile infection (CDI) represents a prevalent and potentially severe health concern linked to the usage of broad-spectrum antibiotics. The aim of this study was to evaluate a new lyophilized product based on human fecal microbiota for transplant, including cost-benefit analysis in the treatment of recurrent or refractory CDI.

METHODS: The product for fecal microbiota transplant was obtained from two donors. Microbiological, viability, and genomic analysis were evaluated. After validation, a clinical pilot study including recurrent or refractory CDI with 24 patients was performed. Clinical response and 4-week recurrence were the outcome. Cost-benefit analysis compared the fecal microbiota transplant with conventional retreatment with vancomycin or metronidazole.

RESULTS: The microbiota for transplant presented significant bacterial viability, with and adequate balance of Firmicutes and Bacteroidetes. The clinical response with the microbiota transplant was 92%. In financial terms, estimated expenditure for CDI solely related to recurrence, based on stochastic modeling, totals USD 222.8 million per year in Brazil.

CONCLUSIONS: The lyophilized human fecal microbiota for transplant is safe and can be an important step for a new product with low cost, even with genomic sequencing. Fecal microbiota transplantation emerges as a more cost-effective alternative compared to antimicrobials in the retreatment of CDI.},
}

@article {pmid39200335,
year = {2024},
author = {Zikou, E and Koliaki, C and Makrilakis, K},
title = {The Role of Fecal Microbiota Transplantation (FMT) in the Management of Metabolic Diseases in Humans: A Narrative Review.},
journal = {Biomedicines},
volume = {12},
number = {8},
pages = {},
doi = {10.3390/biomedicines12081871},
pmid = {39200335},
issn = {2227-9059},
abstract = {The gut microbiota represents a complex ecosystem of trillions of microorganisms residing in the human gastrointestinal tract, which is known to interact with the host physiology and regulate multiple functions. Alterations in gut microbial composition, diversity, and function are referred to as dysbiosis. Dysbiosis has been associated with a variety of chronic diseases, including Clostridioides difficile infections, but also cardiometabolic diseases, including obesity, metabolic syndrome, and type 2 diabetes mellitus (T2DM). The implication of gut microbiota dysbiosis in the pathogenesis of both obesity and T2DM has paved the way to implementing novel therapeutic approaches for metabolic diseases through gut microbial reconfiguration. These interventions include probiotics, prebiotics, and synbiotics, while a more innovative approach has been fecal microbiota transplantation (FMT). FMT is a procedure that delivers healthy human donor stool to another individual through the gastrointestinal tract, aiming to restore gut microbiota balance. Several studies have investigated this approach as a potential tool to mitigate the adverse metabolic effects of gut microbiota aberrations associated with obesity and T2DM. The aim of the present review was to critically summarize the existing evidence regarding the clinical applications of FMT in the management of obesity and T2DM and provide an update on the potential of this method to remodel the entire host microbiota, leading thus to weight loss and sustained metabolic benefits. Safety issues, long-term efficacy, limitations, and pitfalls associated with FMT studies are further discussed, emphasizing the need for further research and standardization in certain methodological aspects in order to optimize metabolic outcomes.},
}

@article {pmid39200203,
year = {2024},
author = {Kerstens, R and Joyce, P},
title = {The Gut Microbiome as a Catalyst and Emerging Therapeutic Target for Parkinson's Disease: A Comprehensive Update.},
journal = {Biomedicines},
volume = {12},
number = {8},
pages = {},
doi = {10.3390/biomedicines12081738},
pmid = {39200203},
issn = {2227-9059},
support = {2022-CF-EMCR-004-25314//Hospital Research Foundation/ ; },
abstract = {Parkinson's Disease is the second most prevalent neurological disorder globally, and its cause is still largely unknown. Likewise, there is no cure, and existing treatments do little more than subdue symptoms before becoming ineffective. It is increasingly important to understand the factors contributing to Parkinson's Disease aetiology so that new and more effective pharmacotherapies can be established. In recent years, there has been an emergence of research linking gut dysbiosis to Parkinson's Disease via the gut-brain axis. Advancements in microbial profiling have led to characterisation of a Parkinson's-specific microbial signature, where novel treatments that leverage and correct gut dysbiosis are beginning to emerge for the safe and effective treatment of Parkinson's Disease. Preliminary clinical studies investigating microbiome-targeted therapeutics for Parkinson's Disease have revealed promising outcomes, and as such, the aim of this review is to provide a timely and comprehensive update of the most recent advances in this field. Faecal microbiota transplantation has emerged as a novel and potential frontrunner for microbial-based therapies due to their efficacy in alleviating Parkinson's Disease symptomology through modulation of the gut-brain axis. However, more rigorous clinical investigation, along with technological advancements in diagnostic and in vitro testing tools, are critically required to facilitate the widespread clinical translation of microbiome-targeting Parkinson's Disease therapeutics.},
}

@article {pmid39199404,
year = {2024},
author = {Fu, Y and Cheng, HW},
title = {The Influence of Cecal Microbiota Transplantation on Chicken Injurious Behavior: Perspective in Human Neuropsychiatric Research.},
journal = {Biomolecules},
volume = {14},
number = {8},
pages = {},
doi = {10.3390/biom14081017},
pmid = {39199404},
issn = {2218-273X},
support = {2017-67015-26567//NIFA-AFRI, USDA/ ; },
mesh = {Animals ; *Chickens ; Humans ; *Gastrointestinal Microbiome ; Brain-Gut Axis ; Behavior, Animal ; Fecal Microbiota Transplantation ; Aggression ; Cecum/microbiology ; Mental Disorders/etiology/microbiology ; Stress, Psychological/microbiology ; Dysbiosis/microbiology ; },
abstract = {Numerous studies have evidenced that neuropsychiatric disorders (mental illness and emotional disturbances) with aggression (or violence) pose a significant challenge to public health and contribute to a substantial economic burden worldwide. Especially, social disorganization (or social inequality) associated with childhood adversity has long-lasting effects on mental health, increasing the risk of developing neuropsychiatric disorders. Intestinal bacteria, functionally as an endocrine organ and a second brain, release various immunomodulators and bioactive compounds directly or indirectly regulating a host's physiological and behavioral homeostasis. Under various social challenges, stress-induced dysbiosis increases gut permeability causes serial reactions: releasing neurotoxic compounds, leading to neuroinflammation and neuronal injury, and eventually neuropsychiatric disorders associated with aggressive, violent, or impulsive behavior in humans and various animals via a complex bidirectional communication of the microbiota-gut-brain (MGB) axis. The dysregulation of the MGB axis has also been recognized as one of the reasons for the prevalence of social stress-induced injurious behaviors (feather pecking, aggression, and cannibalistic pecking) in chickens. However, existing knowledge of preventing and treating these disorders in both humans and chickens is not well understood. In previous studies, we developed a non-mammal model in an abnormal behavioral investigation by rationalizing the effects of gut microbiota on injurious behaviors in chickens. Based on our earlier success, the perspective article outlines the possibility of reducing stress-induced injurious behaviors in chickens through modifying gut microbiota via cecal microbiota transplantation, with the potential for providing a biotherapeutic rationale for preventing injurious behaviors among individuals with mental disorders via restoring gut microbiota diversity and function.},
}

Animals
*Chickens
Humans
*Gastrointestinal Microbiome
Brain-Gut Axis
Behavior, Animal
Fecal Microbiota Transplantation
Aggression
Cecum/microbiology
Mental Disorders/etiology/microbiology
Stress, Psychological/microbiology
Dysbiosis/microbiology

@article {pmid39199231,
year = {2024},
author = {Mostafavi Abdolmaleky, H and Zhou, JR},
title = {Gut Microbiota Dysbiosis, Oxidative Stress, Inflammation, and Epigenetic Alterations in Metabolic Diseases.},
journal = {Antioxidants (Basel, Switzerland)},
volume = {13},
number = {8},
pages = {},
doi = {10.3390/antiox13080985},
pmid = {39199231},
issn = {2076-3921},
abstract = {Gut dysbiosis, resulting from an imbalance in the gut microbiome, can induce excessive production of reactive oxygen species (ROS), leading to inflammation, DNA damage, activation of the immune system, and epigenetic alterations of critical genes involved in the metabolic pathways. Gut dysbiosis-induced inflammation can also disrupt the gut barrier integrity and increase intestinal permeability, which allows gut-derived toxic products to enter the liver and systemic circulation, further triggering oxidative stress, inflammation, and epigenetic alterations associated with metabolic diseases. However, specific gut-derived metabolites, such as short-chain fatty acids (SCFAs), lactate, and vitamins, can modulate oxidative stress and the immune system through epigenetic mechanisms, thereby improving metabolic function. Gut microbiota and diet-induced metabolic diseases, such as obesity, insulin resistance, dyslipidemia, and hypertension, can transfer to the next generation, involving epigenetic mechanisms. In this review, we will introduce the key epigenetic alterations that, along with gut dysbiosis and ROS, are engaged in developing metabolic diseases. Finally, we will discuss potential therapeutic interventions such as dietary modifications, prebiotics, probiotics, postbiotics, and fecal microbiota transplantation, which may reduce oxidative stress and inflammation associated with metabolic syndrome by altering gut microbiota and epigenetic alterations. In summary, this review highlights the crucial role of gut microbiota dysbiosis, oxidative stress, and inflammation in the pathogenesis of metabolic diseases, with a particular focus on epigenetic alterations (including histone modifications, DNA methylomics, and RNA interference) and potential interventions that may prevent or improve metabolic diseases.},
}

@article {pmid39197065,
year = {2024},
author = {Xu, W and Liu, AX and Liu, KH and Zhang, S and Gong, ZH and Xiao, WJ},
title = {l-Theanine Alleviates Ulcerative Colitis by Regulating Colon Immunity via the Gut Microbiota in an MHC-II-Dependent Manner.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.4c04379},
pmid = {39197065},
issn = {1520-5118},
abstract = {Alterations to the gut microbiota are associated with ulcerative colitis (UC), whereas restoration of normobiosis can effectively alleviate UC. l-Theanine has been shown to reshape the gut microbiota and regulate gut immunity. To investigate the mechanisms by which l-theanine alleviates UC, we used l-theanine and l-theanine fecal microbiota solution to treat UC mice. In this study, we used l-theanine and l-theanine fecal microbiota solution to treat UC mice to explore the mechanism by which l-theanine alleviates UC. By reducing inflammation in the colon, we demonstrated that l-theanine alleviates symptoms of UC. Meanwhile, l-theanine can improve the abundance of microbiota related to short-chain fatty acid, bile acid, and tryptophan production. Single-cell sequencing results indicated that l-theanine-mediated suppression of UC was associated with immune cell changes, especially regarding macrophages and T and B cells, and validated the immune cell responses to the gut microbiota. Further, flow cytometry results showed that the ability of dendritic cells, macrophages, and monocytes to present microbiota antigens to colonic T cells in an MHC-II-dependent manner was reduced after treating normal mouse fecal donors with l-theanine. These results demonstrate that l-theanine modulates colon adaptive and innate immunity by regulating the gut microbiota in an MHC-II-dependent manner, thereby alleviating UC.},
}

@article {pmid39198444,
year = {2024},
author = {Chang, D and Gupta, VK and Hur, B and Cobo-López, S and Cunningham, KY and Han, NS and Lee, I and Kronzer, VL and Teigen, LM and Karnatovskaia, LV and Longbrake, EE and Davis, JM and Nelson, H and Sung, J},
title = {Gut Microbiome Wellness Index 2 enhances health status prediction from gut microbiome taxonomic profiles.},
journal = {Nature communications},
volume = {15},
number = {1},
pages = {7447},
pmid = {39198444},
issn = {2041-1723},
support = {UL1TR002377//U.S. Department of Health & Human Services | National Institutes of Health (NIH)/ ; },
mesh = {*Gastrointestinal Microbiome/genetics ; Humans ; *Feces/microbiology ; *Health Status ; Metagenome ; Bacteria/classification/genetics/isolation & purification ; Female ; },
abstract = {Recent advancements in translational gut microbiome research have revealed its crucial role in shaping predictive healthcare applications. Herein, we introduce the Gut Microbiome Wellness Index 2 (GMWI2), an enhanced version of our original GMWI prototype, designed as a standardized disease-agnostic health status indicator based on gut microbiome taxonomic profiles. Our analysis involves pooling existing 8069 stool shotgun metagenomes from 54 published studies across a global demographic landscape (spanning 26 countries and six continents) to identify gut taxonomic signals linked to disease presence or absence. GMWI2 achieves a cross-validation balanced accuracy of 80% in distinguishing healthy (no disease) from non-healthy (diseased) individuals and surpasses 90% accuracy for samples with higher confidence (i.e., outside the "reject option"). This performance exceeds that of the original GMWI model and traditional species-level α-diversity indices, indicating a more robust gut microbiome signature for differentiating between healthy and non-healthy phenotypes across multiple diseases. When assessed through inter-study validation and external validation cohorts, GMWI2 maintains an average accuracy of nearly 75%. Furthermore, by reevaluating previously published datasets, GMWI2 offers new insights into the effects of diet, antibiotic exposure, and fecal microbiota transplantation on gut health. Available as an open-source command-line tool, GMWI2 represents a timely, pivotal resource for evaluating health using an individual's unique gut microbial composition.},
}

*Gastrointestinal Microbiome/genetics
Humans
*Feces/microbiology
*Health Status
Metagenome
Bacteria/classification/genetics/isolation & purification
Female

@article {pmid39197710,
year = {2024},
author = {Vashishth, S and Ambasta, RK and Kumar, P},
title = {Deciphering the Microbial Map and its implications in the therapeutics of Neurodegenerative Disorder.},
journal = {Ageing research reviews},
volume = {},
number = {},
pages = {102466},
doi = {10.1016/j.arr.2024.102466},
pmid = {39197710},
issn = {1872-9649},
abstract = {Every facet of biological anthropology, including development, ageing, diseases, and even health maintenance, is influenced by gut microbiota's significant genetic and metabolic capabilities. With current advancements in sequencing technology and with new culture-independent approaches, researchers can surpass older correlative studies and develop mechanism-based studies on microbiome-host interactions. The microbiota-gut-brain axis (MGBA) regulates glial functioning, making it a possible target for the improvement of development and advancement of treatments for neurodegenerative diseases (NDDs). The gut-brain axis (GBA) is accountable for the reciprocal communication between the gastrointestinal and central nervous system, which plays an essential role in the regulation of physiological processes like controlling hunger, metabolism, and various gastrointestinal functions. Lately, studies have discovered the function of the gut microbiome for brain health-different microbiota through different pathways such as immunological, neurological and metabolic pathways. Additionally, we review the involvement of the neurotransmitters and the gut hormones related to gut microbiota. We also explore the MGBA in neurodegenerative disorders by focusing on metabolites. Further, targeting the blood-brain barrier (BBB), intestinal barrier, meninges, and peripheral immune system is investigated. Lastly, we discuss the therapeutics approach and evaluate the pre-clinical and clinical trial data regarding using prebiotics, probiotics, paraprobiotics, fecal microbiota transplantation, personalised medicine, and natural food bioactive in NDDs. A comprehensive study of the GBA will felicitate the creation of efficient therapeutic approaches for treating different NDDs.},
}

@article {pmid39194379,
year = {2024},
author = {Noguera-Fernández, N and Candela-González, J and Orenes-Piñero, E},
title = {Probiotics, Prebiotics, Fecal Microbiota Transplantation, and Dietary Patterns in Inflammatory Bowel Disease.},
journal = {Molecular nutrition & food research},
volume = {},
number = {},
pages = {e2400429},
doi = {10.1002/mnfr.202400429},
pmid = {39194379},
issn = {1613-4133},
support = {//Instituto Murciano de Investigaciones Biosanitarias Pascual Parrilla/ ; },
abstract = {SCOPE: Inflammatory bowel disease (IBD) is one of the most common chronic and debilitating functional bowel disorders affecting around 11% of the population across the world. IBD is associated with 3.6 million physician visits per year, being the most common reason visiting a gastroenterologist and the second most common reason to be absent from work, sharply increasing the health care costs.

METHODS AND RESULTS: Several treatments seem to be effective in IBD symptoms relief, such as probiotics, prebiotics, fecal microbiota transplantation (FMT), and dietary patterns. Probiotics (living microorganisms that can be supplemented) can protect against pathogenic bacteria due to their antimicrobial qualities. Prebiotics (nondigestible food ingredients) promote the growth of beneficial microbial strains in the gut, giving a health benefit to the host. FMT is supposed to directly change the recipient's microbial composition when a transfer of gastrointestinal microbiota from a healthy donor is carried out. And finally, dietary patterns are in the spotlight, due to the presence of certain nutrients in the gastrointestinal tract affecting gastrointestinal motility, sensitivity, barrier function, and gut microbiota.

CONCLUSION: It is particularly important to know what treatment options are available and which are the most efficient in relieving IBD symptoms and improving IBD patient's quality of life.},
}

@article {pmid39194187,
year = {2024},
author = {Wang, L and Xu, Y and Li, L and Yang, B and Zhao, D and Ye, C and Lin, Z and Cui, J and Liu, Y and Zhu, W and Li, N and Tian, H and Chen, Q},
title = {The impact of small intestinal bacterial overgrowth on the efficacy of fecal microbiota transplantation in patients with chronic constipation.},
journal = {mBio},
volume = {},
number = {},
pages = {e0202324},
doi = {10.1128/mbio.02023-24},
pmid = {39194187},
issn = {2150-7511},
abstract = {UNLABELLED: To investigate the impact of Small Intestinal Bacterial Overgrowth (SIBO) on the efficacy of Fecal Microbiota Transplantation (FMT) in patients with chronic constipation, our research team included 218 patients with chronic constipation treated with FMT. Based on the results of the SIBO breath test, the patients were divided into two groups: the constipation with SIBO group (SIBO) and the constipation without SIBO group (non-SIBO). The efficacy of the two groups was evaluated using constipation-related scoring scales. At the same time, feces and small intestinal fluid samples were collected from both groups before and after FMT to compare the changes in the intestinal microbiota through 16S rRNA sequencing. In this study, it was found that the clinical efficacy of FMT in the SIBO group was superior to that in the non-SIBO group. After FMT treatment, both groups showed a significant increase in bowel frequency and improvement in stool characteristics. Abdominal symptoms, rectal symptoms, and defecation symptoms were significantly alleviated (P < 0.05), and patients' quality of life was significantly enhanced (P < 0.05). After FMT, except for the Constipation Assessment Scale scores, other scale scores showed significant differences between the two groups, the SIBO group scoring significantly better than the non-SIBO group (P < 0.05). After FMT, there were minor changes in the colonic microbiota but more substantial changes in the small intestinal microbiota. At baseline, the SIBO group had a higher abundance of Veillonella, and lower abundances of Escherichia-Shigella and Acinetobacter compared to the non-SIBO group. Chronic constipation patients with SIBO have a better response to FMT than those without SIBO.

IMPORTANCE: Existing studies have rarely considered the impact of the small intestine's microbial state on the efficacy of fecal microbiota transplantation (FMT), nor have they extensively explored the effect of the small intestine's microbial state on the recovery of colonic motility. Therefore, this study investigates the influence of small intestinal bacterial overgrowth (SIBO) on the efficacy of FMT in treating constipation, specifically the impact of the microbial state of the small intestine on the restoration of colonic homeostasis, and consequently on the recovery of colonic motility.},
}

@article {pmid39193826,
year = {2024},
author = {Jelveh Moghaddam, E and Pourmand, G and Ahmadi Badi, S and Yarmohammadi, H and Soltanipur, M and Mahalleh, M and Rezaei, M and Mirhosseini, SM and Siadat, SD},
title = {Gut microbiota alterations in renal transplant recipients and the risk of urinary tract infection and delayed graft function: A preliminary prospective study.},
journal = {Urologia},
volume = {},
number = {},
pages = {3915603241276742},
doi = {10.1177/03915603241276742},
pmid = {39193826},
issn = {1724-6075},
abstract = {BACKGROUND: The implication of gut microbiota in the gut-kidney axis affects the pathophysiology of chronic kidney disease (CKD). Gut microbiota composition changes during CKD. We aimed to determine the relative frequency of important gut microbiota members in end-stage renal disease (ERSD) patients before and after renal transplantation compared to healthy subjects.

METHODS: Fifteen kidney transplant patients and 10 healthy subjects were recruited in this case-control prospective study. Fecal samples were taken sequentially from all patients before kidney transplantation, 1 week, and 1 month after it. The relative frequency of Lactobacillus spp., Bifidobacterium spp., Akkermansia muciniphila, Bacteroides fragilis, Escherichia coli, and Faecalibacterium pruasnitzii were determined through quantitative PCR. The obtained data was statistically analyzed by Stata software (Stata Corporation, USA).

RESULTS: The mean log number of all bacteria was significantly higher in healthy individuals than kidney transplant recipients (p < 0.001) except for Lactobacillus where the mean levels were almost identical in the two groups (p = 0.67). Moreover, 20% (3) of patients developed a urinary tract infection. Besides, 2 (13.33%) patients were diagnosed with delayed graft function. There were no statistically significant differences regarding changing trends in bacteria log number of Akkermansia muciniphila (p = 0.12), Bacteroid fragilis (p = 0.75), Bifidobacterium (p = 0.99), Escherichia coli (p = 0.5), Faecalibacterium (p = 0.98), and Lactobacilli (p = 0.93) between patients with and without delayed graft function (DGF).

CONCLUSION: Gut microbiota composition in patients with ESRD was significantly different from those without it. However, the microbiota profile did not significantly differ in patients with and without DGF.},
}

@article {pmid39193000,
year = {2024},
author = {Wu, Q and Yuan, LW and Yang, LC and Zhang, YW and Yao, HC and Peng, LX and Yao, BJ and Jiang, ZX},
title = {Role of gut microbiota in Crohn's disease pathogenesis: Insights from fecal microbiota transplantation in mouse model.},
journal = {World journal of gastroenterology},
volume = {30},
number = {31},
pages = {3689-3704},
pmid = {39193000},
issn = {2219-2840},
mesh = {*Crohn Disease/microbiology/therapy/pathology/metabolism ; Animals ; *Fecal Microbiota Transplantation ; *Gastrointestinal Microbiome ; Humans ; *Disease Models, Animal ; Mice ; Female ; Male ; Adult ; Feces/microbiology ; Trinitrobenzenesulfonic Acid ; Colon/microbiology/pathology/immunology ; Fibrosis ; Mesentery ; Intestinal Mucosa/microbiology/pathology ; Middle Aged ; Mice, Inbred C57BL ; Case-Control Studies ; Young Adult ; Permeability ; Adipose Tissue ; Adipokines/metabolism ; },
abstract = {BACKGROUND: Inflammatory bowel disease, particularly Crohn's disease (CD), has been associated with alterations in mesenteric adipose tissue (MAT) and the phenomenon termed "creeping fat". Histopathological evaluations showed that MAT and intestinal tissues were significantly altered in patients with CD, with these tissues characterized by inflammation and fibrosis.

AIM: To evaluate the complex interplay among MAT, creeping fat, inflammation, and gut microbiota in CD.

METHODS: Intestinal tissue and MAT were collected from 12 patients with CD. Histological manifestations and protein expression levels were analyzed to determine lesion characteristics. Fecal samples were collected from five recently treated CD patients and five control subjects and transplanted into mice. The intestinal and mesenteric lesions in these mice, as well as their systemic inflammatory status, were assessed and compared in mice transplanted with fecal samples from CD patients and control subjects.

RESULTS: Pathological examination of MAT showed significant differences between CD-affected and unaffected colons, including significant differences in gut microbiota structure. Fetal microbiota transplantation (FMT) from clinically healthy donors into mice with 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced CD ameliorated CD symptoms, whereas FMT from CD patients into these mice exacerbated CD symptoms. Notably, FMT influenced intestinal permeability, barrier function, and levels of proinflammatory factors and adipokines. Furthermore, FMT from CD patients intensified fibrotic changes in the colon tissues of mice with TNBS-induced CD.

CONCLUSION: Gut microbiota play a critical role in the histopathology of CD. Targeting MAT and creeping fat may therefore have potential in the treatment of patients with CD.},
}

*Crohn Disease/microbiology/therapy/pathology/metabolism
Animals
*Fecal Microbiota Transplantation
*Gastrointestinal Microbiome
Humans
*Disease Models, Animal
Mice
Female
Male
Adult
Feces/microbiology
Trinitrobenzenesulfonic Acid
Colon/microbiology/pathology/immunology
Fibrosis
Mesentery
Intestinal Mucosa/microbiology/pathology
Middle Aged
Mice, Inbred C57BL
Case-Control Studies
Young Adult
Permeability
Adipose Tissue
Adipokines/metabolism

@article {pmid39192045,
year = {2024},
author = {Nikdasti, A and Khodadadi, ES and Ferdosi, F and Dadgostar, E and Yahyazadeh, S and Heidari, P and Ehtiati, S and Vakili, O and Khatami, SH},
title = {Nutritional Strategies in Major Depression Disorder: From Ketogenic Diet to Modulation of the Microbiota-Gut-Brain Axis.},
journal = {Molecular neurobiology},
volume = {},
number = {},
pages = {},
pmid = {39192045},
issn = {1559-1182},
abstract = {Major depressive disorder (MDD) is a leading cause of disability worldwide. While traditional pharmacological treatments are effective for many cases, a significant proportion of patients do not achieve full remission or experience side effects. Nutritional interventions hold promise as an alternative or adjunctive approach, especially for treatment-resistant depression. This review examines the potential role of nutrition in managing MDD through addressing biological deficits and modulating pathways relevant to its pathophysiology. Specifically, it explores the ketogenic diet and gut microbiome modulation through various methods, including probiotics, prebiotics, synbiotics, postbiotics, and fecal microbiota transplantation. Numerous studies link dietary inadequacies to increased MDD risk and deficiencies in nutrients like omega-3 s, vitamins D and B, magnesium, and zinc. These deficiencies impact neurotransmitters, inflammation, and other biological factors in MDD. The gut-brain axis also regulates mood, stress response, and immunity, and disruptions are implicated in MDD. While medications aid acute symptoms, nutritional strategies may improve long-term outcomes by preventing relapse and promoting sustained remission. This comprehensive review aims to provide insights into nutrition's multifaceted relationship with MDD and its potential for developing more effective integrated treatment approaches.},
}

@article {pmid39191760,
year = {2024},
author = {Hartikainen, AK and Jalanka, J and Lahtinen, P and Ponsero, AJ and Mertsalmi, T and Finnegan, L and Crispie, F and Cotter, PD and Arkkila, P and Satokari, R},
title = {Fecal microbiota transplantation influences microbiota without connection to symptom relief in irritable bowel syndrome patients.},
journal = {NPJ biofilms and microbiomes},
volume = {10},
number = {1},
pages = {73},
pmid = {39191760},
issn = {2055-5008},
support = {316338//Academy of Finland (Suomen Akatemia)/ ; 323156//Academy of Finland (Suomen Akatemia)/ ; },
mesh = {*Irritable Bowel Syndrome/therapy/microbiology ; Humans ; *Fecal Microbiota Transplantation/methods ; *RNA, Ribosomal, 16S/genetics ; Female ; Male ; Adult ; Treatment Outcome ; *Gastrointestinal Microbiome ; Middle Aged ; Feces/microbiology ; Metagenomics/methods ; Bacteria/classification/genetics/isolation & purification ; },
abstract = {Imbalanced microbiota may contribute to the pathophysiology of irritable bowel syndrome (IBS), thus fecal microbiota transplantation (FMT) has been suggested as a potential treatment. Previous studies on the relationship between clinical improvement and microbiota after FMT have been inconclusive. In this study, we used 16S rRNA gene amplicon and shotgun metagenomics data from a randomized, placebo controlled FMT trial on 49 IBS patients to analyze changes after FMT in microbiota composition and its functional potential, and to identify connections between microbiota and patients' clinical outcome. As a result, we found that the successful modulation of microbiota composition and functional profiles by FMT from a healthy donor was not associated with the resolution of symptoms in IBS patients. Notably, a donor derived strain of Prevotella copri dominated the microbiota in those patients in the FMT group who had a low relative abundance of P. copri pre-FMT. The results highlight the multifactorial nature of IBS and the role of recipient's microbiota in the colonization of donor's strains.},
}

*Irritable Bowel Syndrome/therapy/microbiology
Humans
*Fecal Microbiota Transplantation/methods
*RNA, Ribosomal, 16S/genetics
Female
Male
Adult
Treatment Outcome
*Gastrointestinal Microbiome
Middle Aged
Feces/microbiology
Metagenomics/methods
Bacteria/classification/genetics/isolation & purification

@article {pmid39189608,
year = {2024},
author = {Tejada, JN and Walters, WA and Wang, Y and Kordahi, M and Chassaing, B and Pickard, J and Nunez, G and Ley, R and Gewirtz, AT},
title = {Prevention and cure of murine C. difficile infection by a Lachnospiraceae strain.},
journal = {Gut microbes},
volume = {16},
number = {1},
pages = {2392872},
pmid = {39189608},
issn = {1949-0984},
support = {R01 DK083890/DK/NIDDK NIH HHS/United States ; R01 DK095782/DK/NIDDK NIH HHS/United States ; R01 DK099071/DK/NIDDK NIH HHS/United States ; },
mesh = {Animals ; Mice ; *Clostridioides difficile/genetics/growth & development/physiology/pathogenicity ; *Clostridium Infections/microbiology/prevention & control ; *Gastrointestinal Microbiome/drug effects ; *Germ-Free Life ; *Clostridiales/genetics/growth & development ; Mice, Inbred C57BL ; Disease Models, Animal ; Feces/microbiology ; Female ; Anti-Bacterial Agents/pharmacology ; },
abstract = {We sought to better understand how intestinal microbiota confer protection against Clostridioides difficile (C. difficile) infection (CDI). We utilized gnotobiotic altered Schaedler flora (ASF) mice, which lack the abnormalities of germfree (GF) mice as well as the complexity and heterogeneity of antibiotic-treated mice. Like GF mice, ASF mice were highly prone to rapid lethal CDI, without antibiotics, while very low infectious doses resulted in chronic CDI. Administering such chronic CDI mice an undefined preparation of Clostridia lowered C. difficile levels by several logs. Importantly, such resolution of CDI was associated with colonization of Lachnospiraceae. Fractionation of the Clostridia population to enrich for Lachnospiraceae led to the appreciation that its CDI-impeding property strongly associated with a specific Lachnospiraceae strain, namely uncultured bacteria and archaea (UBA) 3401. UBA3401 was recalcitrant to being propagated as a pure culture but could be maintained in ASF mice, wherein it comprised up to about 50% of the intestinal microbiota, which was sufficient to generate a high-quality genomic sequence of this bacterium. Sequence analysis and ex vivo study of UBA3401 indicated that it had the ability to secrete substance(s) that directly impeded C. difficile growth. Moreover, in vivo administration of UBA3401/ASF feces provided strong protection to C. difficile challenge. Thus, UBA3401 may contribute to and/or provide a means to study microbiota-mediated CDI resistance.},
}

Animals
Mice
*Clostridioides difficile/genetics/growth & development/physiology/pathogenicity
*Clostridium Infections/microbiology/prevention & control
*Gastrointestinal Microbiome/drug effects
*Germ-Free Life
*Clostridiales/genetics/growth & development
Mice, Inbred C57BL
Disease Models, Animal
Feces/microbiology
Female
Anti-Bacterial Agents/pharmacology

@article {pmid39189041,
year = {2024},
author = {Haussmann, AJ and McMahan, ZH and Volkmann, ER},
title = {Understanding the gastrointestinal microbiome in systemic sclerosis: methodological advancements and emerging research.},
journal = {Current opinion in rheumatology},
volume = {},
number = {},
pages = {},
doi = {10.1097/BOR.0000000000001048},
pmid = {39189041},
issn = {1531-6963},
abstract = {PURPOSE OF REVIEW: This review highlights the role of the gastrointestinal (GI) microbiome in systemic sclerosis (SSc). We describe techniques for evaluating the GI microbiome in humans, and emerging research linking GI microbiome alterations (i.e., dysbiosis) and distinct SSc clinical manifestations. We also address the evolving treatment landscape targeting dysbiosis in SSc.

RECENT FINDINGS: Recent literature brings into focus the complex relationship between the GI microbiome and SSc pathogenesis. Advanced techniques (e.g., shotgun metagenomics, meta-transcriptomics) provide deeper insights into microbial taxonomy and active gene expression, exposing dysbiosis as a potential driver of SSc. New studies demonstrate that SSc patients who possess specific SSc clinical features, (e.g., interstitial lung disease), have unique GI microbiome profiles.

SUMMARY: Dysbiosis is associated with specific clinical features in patients with SSc. New tools for studying the GI microbiome have furthered our understanding of the relationship between dysbiosis and SSc complications. Therapeutic avenues such as dietary adjustments, probiotics, antibiotics, mindfulness practices, and fecal transplants offer potential for managing SSc and preventing its progression through GI microbiome modulation. By clarifying what is known about the relationship between the GI dysbiosis, GI dysfunction, and SSc, this review enhances our understanding of SSc pathogenesis and proposes targeted interventions.},
}

@article {pmid39188602,
year = {2024},
author = {Soldera, J},
title = {Navigating treatment resistance: Janus kinase inhibitors for ulcerative colitis.},
journal = {World journal of clinical cases},
volume = {12},
number = {24},
pages = {5468-5472},
pmid = {39188602},
issn = {2307-8960},
abstract = {The management of refractory ulcerative colitis (UC) and acute severe UC (ASUC) is challenging due to the lack of standardized approaches in cases resistant to multiple treatments. In this editorial, I investigate the efficacy and safety of Janus kinase inhibitors, particularly upadacitinib and tofacitinib, in controlling severe and refractory disease. I highlight a notable case report by Xu et al, which explores the case of a patient with primary nonresponse to two classes of biologics and two fecal microbiota transplants who exhibited a remarkable response to upadacitinib. Furthermore, I discuss the use of tofacitinib in refractory UC and ASUC, either as monotherapy or in combination with biologics, which has shown promising response rates. Additionally, emerging evidence of upadacitinib efficacy in ASUC is presented. Overall, these cases emphasize the complex nature of managing refractory ASUC and the potential of small-molecule therapies to achieve remission. Further research is needed to refine treatment strategies for patients with treatment-resistant UC.},
}

@article {pmid39188104,
year = {2024},
author = {Naik, A and Godbole, MS},
title = {Elucidating the Intricate Roles of Gut and Breast Microbiomes in Breast Cancer Metastasis to the Bone.},
journal = {Cancer reports (Hoboken, N.J.)},
volume = {7},
number = {8},
pages = {e70005},
pmid = {39188104},
issn = {2573-8348},
mesh = {Humans ; *Breast Neoplasms/pathology/microbiology/therapy ; Female ; *Gastrointestinal Microbiome ; *Bone Neoplasms/secondary/microbiology/therapy ; *Tumor Microenvironment/immunology ; Breast/pathology/microbiology ; Microbiota ; Animals ; },
abstract = {BACKGROUND: Breast cancer is the most predominant and heterogeneous cancer in women. Moreover, breast cancer has a high prevalence to metastasize to distant organs, such as the brain, lungs, and bones. Patients with breast cancer metastasis to the bones have poor overall and relapse-free survival. Moreover, treatment using chemotherapy and immunotherapy is ineffective in preventing or reducing cancer metastasis.

RECENT FINDINGS: Microorganisms residing in the gut and breast, termed as the resident microbiome, have a significant influence on the formation and progression of breast cancer. Recent studies have identified some microorganisms that induce breast cancer metastasis to the bone. These organisms utilize multiple mechanisms, including induction of epithelial-mesenchymal transition, steroid hormone metabolism, immune modification, bone remodeling, and secretion of microbial products that alter tumor microenvironment, and enhance propensity of breast cancer cells to metastasize. However, their involvement makes these microorganisms suitable as novel therapeutic targets. Thus, studies are underway to prevent and reduce breast cancer metastasis to distant organs, including the bone, using chemotherapeutic or immunotherapeutic drugs, along with probiotics, antibiotics or fecal microbiota transplantation.

CONCLUSIONS: The present review describes association of gut and breast microbiomes with bone metastases. We have elaborated on the mechanisms utilized by breast and gut microbiomes that induce breast cancer metastasis, especially to the bone. The review also highlights the current treatment options that may target both the microbiomes for preventing or reducing breast cancer metastases. Finally, we have specified the necessity of maintaining a diverse gut microbiome to prevent dysbiosis, which otherwise may induce breast carcinogenesis and metastasis especially to the bone. The review may facilitate more detailed investigations of the causal associations between these microbiomes and bone metastases. Moreover, the potential treatment options described in the review may promote discussions and research on the modes to improve survival of patients with breast cancer by targeting the gut and breast microbiomes.},
}

Humans
*Breast Neoplasms/pathology/microbiology/therapy
Female
*Gastrointestinal Microbiome
*Bone Neoplasms/secondary/microbiology/therapy
*Tumor Microenvironment/immunology
Breast/pathology/microbiology
Microbiota
Animals

@article {pmid39187939,
year = {2024},
author = {Wan, L and Wang, H and Liang, Y and Zhang, X and Yao, X and Zhu, G and Cai, J and Liu, G and Liu, X and Niu, Q and Li, S and Zhang, B and Gao, J and Wang, J and Shi, X and Hu, L and Liu, X and Zou, Z and Yang, G},
title = {Effect of oral faecal microbiota transplantation intervention for children with autism spectrum disorder: A randomised, double-blind, placebo-controlled trial.},
journal = {Clinical and translational medicine},
volume = {14},
number = {9},
pages = {e70006},
pmid = {39187939},
issn = {2001-1326},
support = {2023YFC2706405//National Key Research and Development Program of China/ ; 2022YFC2705301//National Key Research and Development Program of China/ ; 7222187//Beijing Natural Science Foundation/ ; qzx-2023-1//Seventh Medical Center of Chinese PLA General Hospital/ ; 22JSZ20//Seventh Medical Center of Chinese PLA General Hospital/ ; 82170302//National Natural Science Foundation of China/ ; },
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; *Autism Spectrum Disorder/therapy ; Double-Blind Method ; Child ; Male ; Female ; Treatment Outcome ; Child, Preschool ; Placebos ; },
}

Humans
*Fecal Microbiota Transplantation/methods
*Autism Spectrum Disorder/therapy
Double-Blind Method
Child
Male
Female
Treatment Outcome
Child, Preschool
Placebos

@article {pmid39187483,
year = {2024},
author = {Li, H and Du, Y and Cheng, K and Chen, Y and Wei, L and Pei, Y and Wang, X and Wang, L and Zhang, Y and Hu, X and Lu, Y and Zhu, X},
title = {Gut microbiota-derived indole-3-acetic acid suppresses high myopia progression by promoting type I collagen synthesis.},
journal = {Cell discovery},
volume = {10},
number = {1},
pages = {89},
pmid = {39187483},
issn = {2056-5968},
support = {82122017//National Natural Science Foundation of China (National Science Foundation of China)/ ; 82271069//National Natural Science Foundation of China (National Science Foundation of China)/ ; 81870642//National Natural Science Foundation of China (National Science Foundation of China)/ ; 81470613//National Natural Science Foundation of China (National Science Foundation of China)/ ; 81670835//National Natural Science Foundation of China (National Science Foundation of China)/ ; },
abstract = {High myopia (HM) is a leading cause of blindness worldwide with currently no effective interventions available. A major hurdle lies in its often isolated perception as a purely ocular morbidity, disregarding potential systemic implications. Recent evidence suggests the existence of a gut-eye axis; however, the role of gut microbiota in the pathogenesis of HM remains largely unexplored. Herein, we provide a potential crosstalk among HM's gut dysbiosis, microbial metabolites, and scleral remodeling. Utilizing 16S rRNA gene sequencing, we observed an altered gut microbiota profile in HM patients with a significant reduction in probiotic abundance compared with healthy controls. Subsequent targeted metabolic profiling revealed a notable decrease in plasma levels of the gut microbiota-derived metabolite indole-3-acetic acid (3-IAA) among HM patients, which is closely associated with the reduced probiotics, both negatively correlated with HM severity. Genetic analyses determined that gut microbiota are causally associated with myopia risk. Importantly, when mice subjected to HM modeling receive fecal microbiota transplantation from healthy donors, there is an increase in 3-IAA plasma levels and simultaneous retardation of HM progression along with better maintenance of collagen type I alpha 1 (COL1A1) expression in the sclera. Furthermore, 3-IAA gavage achieves similar effects. Mechanistic investigations confirm the transcriptional activation of COL1A1 by 3-IAA via promoting the enrichment of SP1 to its promoter. Together, our findings provide novel insights into the gut microbiota-eye axis in the pathogenesis of HM and propose new strategies for HM intervention by remodeling the gut microbiota and indole supplementation.},
}

@article {pmid39187454,
year = {2024},
author = {Lu, M and Xie, L and Yin, S and Zhou, J and Yi, L and Ye, L},
title = {The Gut Microbial Lipid Metabolite 14(15)- EpETE Inhibits Substance P Release by Targeting GCG/PKA Signaling to Relieve Cisplatin-Induced Nausea and Vomiting in Rats.},
journal = {Journal of microbiology and biotechnology},
volume = {34},
number = {9},
pages = {1-9},
doi = {10.4014/jmb.2403.03044},
pmid = {39187454},
issn = {1738-8872},
abstract = {Chemotherapy-induced nausea and vomiting (CINV) is a debilitating side effect related to activation of substance P (SP). SP activation can result from dysregulation of the gut-brain axis, and also from activation of protein kinase A signaling (PKA) signaling. In this study, we connected these factors in an attempt to unveil the mechanisms underlying CINV and develop new therapeutic strategies. Female rats were injected with cisplatin to induce pica. Fecal samples were collected before/after injection, and subjected to lipid metabolomics analysis. In another portion of pica rats, the PKA inhibitor KT5720 was applied to investigate the involvement of PKA signaling in CINV, while fecal microbiota transplantation (FMT) was implemented to verify the therapeutic effect of the lipid metabolite 14(15)-EpETE. Pica symptoms were recorded, followed by ileal histological examination. The targeting relationship between 14(15)-EpETE and glucagon was determined by bioinformatics. SP and glucagon/PKA signaling in rat ileum, serum, and/or brain substantia nigra were detected by immunohistochemistry, enzyme-linked immunosorbent assay, and/or western blot. The results showed a significantly lower level of 14(15)-EpETE in rat feces after cisplatin injection. KT5720 treatment alleviated cisplatin-induced pica symptoms, ileal injury, SP content increase in the ileum, serum, and brain substantia nigra, and ileal PKA activation in rats. The ileal level of glucagon was elevated by cisplatin in rats. FMT exerted an effect similar to that of KT5720 treatment, relieving the cisplatin-induced changes, including ileal glucagon/PKA activation in rats. Our findings demonstrate that FMT restores 14(15)-EpETE production, which inhibits SP release by targeting GCG/PKA signaling, ultimately mitigating CINV.},
}

@article {pmid39187187,
year = {2024},
author = {Zhang, H and Wei, H and Qin, X and Song, H and Yang, M and Zhang, L and Liu, Y and Wang, Z and Zhang, Y and Lai, Y and Yang, J and Chen, Y and Chen, Z and Zeng, J and Wang, X and Liu, R},
title = {Is anxiety and depression transmissible? - Depressed mother rats transmit anxiety- and depression-like phenotypes to cohabited rat pups through gut microbiota assimilation.},
journal = {Journal of affective disorders},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jad.2024.08.164},
pmid = {39187187},
issn = {1573-2517},
abstract = {OBJECTIVE: This study is to investigate the role of gut microbiota transmission in the development of anxiety/depression in offspring exposed to maternal depression.

METHOD: Offspring rats were cohabitated with their depressed mother or father rats (which exposed to chronic unpredictable mild stress (CUMS)) for 2, 4, and 6 months, the anxiety- and depression-like behaviors, and interaction/caring activities between mother/father and their pups were detected. The gut microbiota composition and its relationship with behaviors were analyzed. Fecal microbiota transplantation (FMT) was performed to establish the gut microbiota of depressed/normal mother rats in the offspring rats to further confirm the role of "depressive gut microbiota" transmission in mediating the anxiety/depression in the pups.

RESULTS: Anxiety and depression phenotypes can be transmitted from depressed mother rats to their cohabited offspring. Frequent interaction and gut microbiota assimilation were observed between rat mothers and pups. Remodeling of the gut microbiota in pups by FMT could induce or attenuate anxiety- and depression-like phenotypes depending on the origin of the fecal microbiota. By comparison, the pups cohabitated with depressed father rats showed slighter anxiety and depression.

CONCLUSIONS: These data together support that depressed mother can transmit anxiety/depression to their pups through gut microbiota assimilation, which is related to frequent interaction. Our study reinforces the importance of mental health of mothers in preventing the occurrence of childhood anxiety and depression, and pointing out the possibility of remodeling intestinal microbiota as an effective therapy for treating anxiety/depression in children.},
}

@article {pmid39184689,
year = {2024},
author = {Smith, B and Smith, H and Machini, M},
title = {Novel Pharmaceuticals and Therapeutics for Tumor Necrosis Factor-Alpha-Resistant Crohn's Disease: A Narrative Review.},
journal = {Cureus},
volume = {16},
number = {7},
pages = {e65357},
pmid = {39184689},
issn = {2168-8184},
abstract = {Inflammatory bowel disease (IBD) is a medical condition that causes persistent, relapsing inflammation of the gastrointestinal tract. It is an umbrella term encompassing two different conditions: ulcerative colitis (UC) and Crohn's disease (CD). The standard treatment for patients with moderate to severe CD is tumor necrosis factor-α (TNF-α) inhibitors; however, a subset of CD patients face challenges in regard to this disease's treatment. Certain populations of patients with CD may exhibit resistance or develop tolerance to TNF-α inhibitor therapy over time. The recurrent gastrointestinal inflammation associated with CD can severely impact the quality of life and lead to complications for those suffering from this condition. The symptomatic flare-ups these subpopulations continue to experience underscores why such a need for alternative therapies is desperately needed. These alternative therapies not only offer potential benefits for those with TNF-α resistance, but CD may also serve as a superior therapy option for those trying to avoid the adverse effects of CD treatments available today. This review aims to explore and investigate the novel drugs and therapies that are being investigated for the treatment of TNF-α resistant CD, such as upadacitinib, risankizumab, vedolizumab, synbiotics, fecal microbiota transplantation (FMT), and stem cell therapy. Upadacitinib is a Janus kinase inhibitor, Risankizumab is a monoclonal antibody targeting interleukin-23, and Vedolizumab is an integrin receptor antagonist. The latest advancements in CD management have shown encouraging results. Some of these novel drugs and therapies not only offer a potential solution for CD patients exhibiting resistance to TNF-α inhibitors but may also provide a superior alternative for individuals prone to opportunistic infections.},
}

@article {pmid39184030,
year = {2024},
author = {Shera, S and Katzka, W and Yang, JC and Chang, C and Arias-Jayo, N and Lagishetty, V and Balioukova, A and Chen, Y and Dutson, E and Li, Z and Mayer, EA and Pisegna, JR and Sanmiguel, C and Pawar, S and Zhang, D and Leitman, M and Hernandez, L and Jacobs, JP and Dong, TS},
title = {Bariatric-induced microbiome changes alter MASLD development in association with changes in the innate immune system.},
journal = {Frontiers in microbiology},
volume = {15},
number = {},
pages = {1407555},
pmid = {39184030},
issn = {1664-302X},
abstract = {INTRODUCTION: Metabolic dysfunction-associated steatotic liver disease (MASLD) affects nearly 25% of the population and is the leading cause for liver-related mortality. Bariatric surgery is a well-known treatment for MASLD and obesity. Understanding the fundamental mechanisms by which bariatric surgery can alter MASLD can lead to new avenues of therapy and research. Previous studies have identified the microbiome's role in bariatric surgery and in inflammatory immune cell populations. The host innate immune system modulates hepatic inflammation and fibrosis, and thus the progression of MASLD. The precise role of immune cell types in the pathogenesis of MASLD remains an active area of investigation. The aim of this study was to understand the interplay between microbiota composition post-bariatric surgery and the immune system in MASLD.

METHODS: Eighteen morbidly obese females undergoing sleeve gastrectomy were followed pre-and post-surgery. Stool from four patients, showing resolved MASLD post-surgery with sustained weight loss, was transplanted into antibiotic treated mice. Mice received pre-or post-surgery stool and were fed a standard or high-fat diet. Bodyweight, food intake, and physiological parameters were tracked weekly. Metabolic parameters were measured post-study termination.

RESULTS: The human study revealed that bariatric surgery led to significant weight loss (p > 0.05), decreased inflammatory markers, and improved glucose levels six months post-surgery. Patients with weight loss of 20% or more showed distinct changes in blood metabolites and gut microbiome composition, notably an increase in Bacteroides. The mouse model confirmed surgery-induced microbiome changes to be a major factor in the reduction of markers and attenuation of MASLD progression. Mice receiving post-surgery fecal transplants had significantly less weight gain and liver steatosis compared to pre-surgery recipients. There was also a significant decrease in inflammatory cytokines interferon gamma, interleukin 2, interleukin 15, and mig. This was accompanied by alterations in liver immunophenotype, including an increase in natural killer T cells and reduction of Kupfer cells in the post-surgery transplant group.

DISCUSSION: Our findings suggest surgery induced microbial changes significantly reduce inflammatory markers and fatty liver progression. The results indicate a potential causal link between the microbiome and the host immune system, possibly mediated through modulation of liver NKT and Kupffer cells.},
}

@article {pmid39183943,
year = {2024},
author = {Fitzjerrells, RL and Ollberding, NJ and Mangalam, AK},
title = {Looking at the full picture, using topic modeling to observe microbiome communities associated with disease.},
journal = {Gut microbes reports},
volume = {1},
number = {1},
pages = {1-11},
pmid = {39183943},
issn = {2993-3935},
abstract = {The microbiome, a complex micro-ecosystem, helps the host with various vital physiological processes. Alterations of the microbiome (dysbiosis) have been linked with several diseases, and generally, differential abundance testing between the healthy and patient groups is performed to identify important bacteria. However, providing a singular species of bacteria to an individual as treatment has not been as successful as fecal microbiota transplant therapy, where the entire microbiome of a healthy individual is transferred. These observations suggest that a combination of bacteria might be crucial for the beneficial effects. Here we provide the framework to utilize topic modeling, an unsupervised machine learning approach, to identify a community of bacteria related to health or disease. Specifically, we used our previously published gut microbiome data of patients with multiple sclerosis (MS), a neurodegenerative disease linked to a dysbiotic gut microbiome. We identified communities of bacteria associated with MS, including genera previously discovered, but also others that would have been overlooked by differential abundance testing. This method can be a useful tool for analyzing the microbiome, and it should be considered along with the commonly utilized differential abundance tests to better understand the role of the gut microbiome in health and disease.},
}

@article {pmid39182245,
year = {2024},
author = {Luo, X and Yang, X and Tan, S and Zhang, Y and Liu, Y and Tian, X and Huang, Y and Zhou, Y and He, C and Yin, K and Xu, D and Li, X and Sun, F and Tang, R and Cao, J and Zheng, K and Yu, Y and Pan, W},
title = {Gut microbiota mediates anxiety-like behaviors induced by chronic infection of Toxoplasma gondii in mice.},
journal = {Gut microbes},
volume = {16},
number = {1},
pages = {2391535},
pmid = {39182245},
issn = {1949-0984},
mesh = {Animals ; *Gastrointestinal Microbiome ; Mice ; *Anxiety/microbiology ; *Mice, Inbred C57BL ; *Toxoplasma/physiology ; Male ; Fecal Microbiota Transplantation ; Dysbiosis/microbiology ; Amygdala/metabolism ; Behavior, Animal ; Toxoplasmosis/physiopathology/psychology/parasitology/microbiology ; Chronic Disease ; Brain-Gut Axis/physiology ; Disease Models, Animal ; Colon/microbiology/parasitology ; },
abstract = {BACKGROUND: Chronic infection with the neurotropic parasite Toxoplasma gondii (T. gondii) can cause anxiety and gut microbiota dysbiosis in hosts. However, the potential role of gut microbiota in anxiety induced by the parasite remains unclear.

METHODS: C57BL/6J mice were infected with 10 cysts of T. gondii. Antibiotic depletion of gut microbiota and fecal microbiota transplantation experiments were utilized to investigate the causal relationship between gut microbiota and anxiety. Anxiety-like behaviors were examined by the elevated plus maze test and the open field test; blood, feces, colon and amygdala were collected to evaluate the profiles of serum endotoxin (Lipopolysaccharide, LPS) and serotonin (5-hydroxytryptamine, 5-HT), gut microbiota composition, metabolomics, global transcriptome and neuroinflammation in the amygdala. Furthermore, the effects of Diethyl butylmalonate (DBM, an inhibitor of mitochondrial succinate transporter, which causes the accumulation of endogenous succinate) on the disorders of the gut-brain axis were evaluated.

RESULTS: Here, we found that T. gondii chronic infection induced anxiety-like behaviors and disturbed the composition of the gut microbiota in mice. In the amygdala, T. gondii infection triggered the microglial activation and neuroinflammation. In the colon, T. gondii infection caused the intestinal dyshomeostasis including elevated colonic inflammation, enhanced bacterial endotoxin translocation to blood and compromised intestinal barrier. In the serum, T. gondii infection increased the LPS levels and decreased the 5-HT levels. Interestingly, antibiotics ablation of gut microbiota alleviated the anxiety-like behaviors induced by T. gondii infection. More importantly, transplantation of the fecal microbiota from T. gondii-infected mice resulted in anxiety and the transcriptomic alteration in the amygdala of the antibiotic-pretreated mice. Notably, the decreased abundance of succinate-producing bacteria and the decreased production of succinate were observed in the feces of the T. gondii-infected mice. Moreover, DBM administration ameliorated the anxiety and gut barrier impairment induced by T. gondii infection.

CONCLUSIONS: The present study uncovers a novel role of gut microbiota in mediating the anxiety-like behaviors induced by chronic T. gondii infection. Moreover, we show that DBM supplementation has a beneficial effect on anxiety. Overall, these findings provide new insights into the treatment of T. gondii-related mental disorders.},
}

Animals
*Gastrointestinal Microbiome
Mice
*Anxiety/microbiology
*Mice, Inbred C57BL
*Toxoplasma/physiology
Male
Fecal Microbiota Transplantation
Dysbiosis/microbiology
Amygdala/metabolism
Behavior, Animal
Toxoplasmosis/physiopathology/psychology/parasitology/microbiology
Chronic Disease
Brain-Gut Axis/physiology
Disease Models, Animal
Colon/microbiology/parasitology

@article {pmid39182099,
year = {2024},
author = {Zheng, H and Zhang, X and Li, C and Wang, D and Shen, Y and Lu, J and Zhao, L and Li, X and Gao, H},
title = {BCAA mediated microbiota-liver-heart crosstalk regulates diabetic cardiomyopathy via FGF21.},
journal = {Microbiome},
volume = {12},
number = {1},
pages = {157},
pmid = {39182099},
issn = {2049-2618},
support = {22074106//National Natural Science Foundation of China/ ; 21974096//National Natural Science Foundation of China/ ; },
mesh = {Animals ; *Fibroblast Growth Factors/metabolism ; Mice ; *Gastrointestinal Microbiome ; *Diabetic Cardiomyopathies/metabolism/microbiology ; *Liver/metabolism ; *Amino Acids, Branched-Chain/metabolism ; Signal Transduction ; Diabetes Mellitus, Type 1/microbiology/metabolism ; Male ; Myocardium/metabolism/pathology ; PPAR alpha/metabolism ; Mice, Inbred C57BL ; Diabetes Mellitus, Experimental/metabolism/microbiology ; },
abstract = {BACKGROUND: Diabetic cardiomyopathy (DCM) is one of leading causes of diabetes-associated mortality. The gut microbiota-derived branched-chain amino acids (BCAA) have been reported to play a central role in the onset and progression of DCM, but the potential mechanisms remain elusive.

RESULTS: We found the type 1 diabetes (T1D) mice had higher circulating BCAA levels due to a reduced BCAA degradation ability of the gut microbiota. Excess BCAA decreased hepatic FGF21 production by inhibiting PPARα signaling pathway and thereby resulted in a higher expression level of cardiac LAT1 via transcription factor Zbtb7c. High cardiac LAT1 increased the levels of BCAA in the heart and then caused mitochondrial damage and myocardial apoptosis through mTOR signaling pathway, leading to cardiac fibrosis and dysfunction in T1D mice. Additionally, transplant of faecal microbiota from healthy mice alleviated cardiac dysfunction in T1D mice, but this effect was abolished by FGF21 knockdown.

CONCLUSIONS: Our study sheds light on BCAA-mediated crosstalk among the gut microbiota, liver and heart to promote DCM and FGF21 serves as a key mediator. Video Abstract.},
}

Animals
*Fibroblast Growth Factors/metabolism
Mice
*Gastrointestinal Microbiome
*Diabetic Cardiomyopathies/metabolism/microbiology
*Liver/metabolism
*Amino Acids, Branched-Chain/metabolism
Signal Transduction
Diabetes Mellitus, Type 1/microbiology/metabolism
Male
Myocardium/metabolism/pathology
PPAR alpha/metabolism
Mice, Inbred C57BL
Diabetes Mellitus, Experimental/metabolism/microbiology

@article {pmid39180723,
year = {2024},
author = {Jiang, L and Hao, Y and Han, D and Dong, W and Yang, A and Sun, Z and Ge, Y and Duan, S and Zhang, X and Dai, Z},
title = {Gut microbiota dysbiosis deteriorates immunoregulatory effects of tryptophan via colonic indole and LBP/HTR2B-mediated macrophage function.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrae166},
pmid = {39180723},
issn = {1751-7370},
abstract = {Tryptophan (Trp) has been shown to regulate immune function by modulating gut serotonin (5-HT) metabolism and signaling. However, the mechanisms underlying the microbial modulation of gut 5-HT signaling in gut inflammation with gut microbiota dysbiosis require further investigation. Here, we investigated the effects of Trp supplementation on the composition and metabolism of the gut microbiome and 5-HT signaling-related gut immune function using a dextran sodium sulfate (DSS)-induced colitis mouse model coupled with antibiotic exposure. The results showed that antibiotic treatment before but not during DSS treatment decreased the immunoregulatory effects of Trp and aggravated gut inflammation and body weight loss in mice. Metagenomic analysis revealed that the fecal microbiota transplantation (FMT) of Trp-enriched gut microbiota to recipient mice subject to antibiotic preexposure and DSS treatment aggravated inflammation by increasing the relative abundances of Lactobacillus and Parabacteroides and the microbial production of indole coupled with the activation of the 5-HT receptor HTR2B in the colon. Transcriptomic analysis showed that HTR2B agonist administration strengthened the beneficial effects of Trp in DSS-induced colitis mice with antibiotic exposure by reducing gut lipopolysaccharide-binding protein (LBP) production, IκB-α/nuclear factor-κB signaling, and M1 macrophage polarization. Indole treatment reduced LBP production and M1 macrophage polarization both in mice with DSS-induced colitis and in lipopolysaccharide-treated mouse macrophages; however, the HTR2B antagonist reversed the effects of indole. Our findings provide the basis for developing new dietary and therapeutic interventions to improve gut microbiota dysbiosis-associated inflammatory gut disorders and diseases.},
}

@article {pmid39180442,
year = {2024},
author = {Wang, Z and Yang, L and Feng, Y and Duan, B and Zhang, H and Tang, Y and Zhang, C and Yang, J},
title = {Isoorientin Alleviates DSS-Treated Acute Colitis in Mice by Regulating Intestinal Epithelial P-Glycoprotein (P-gp) Expression.},
journal = {DNA and cell biology},
volume = {},
number = {},
pages = {},
doi = {10.1089/dna.2024.0101},
pmid = {39180442},
issn = {1557-7430},
abstract = {Isoorientin (ISO) is a naturally occurring flavonoid with diverse functional properties that mitigate the risk of diseases stemming from oxidation, inflammation, and cancer cell proliferation. P-glycoprotein (P-gp) is a vital component of the intestinal epithelium and may play a role in the onset of intestinal inflammatory conditions, such as inflammatory bowel disease (IBD). Recent studies have suggested that short-chain fatty acids (SCFAs) and secondary bile acids (SBAs) produced by the gut microbiota stimulate the increase of P-gp expression, alleviating excessive inflammation and thereby preservation of intestinal homeostasis. ISO has been shown to improve colon health and modulate the gut microbiota. In this study, we aimed to explore whether ISO can modulate the microbes and their metabolites to influence P-gp expression to alleviate IBD. First, the impact of ISO on dextran sulfate sodium (DSS)-treated colitis in mice was investigated. Second, 16S rRNA gene sequencing was conducted. The present study indicated that ISO mitigated the symptoms and pathological damage associated with DSS-treated colitis in mice. Western blot analysis revealed ISO upregulated P-gp in colon tissues, suggesting the critical role of P-gp protein in intestinal epithelial cells. 16S microbial diversity sequencing revealed ISO restored the richness and variety of intestinal microorganisms in colitis-bearing mice and enriched SCFA-producing bacteria, such as Lachnospiraceae_NK4A136_group. The experiments also revealed that the ISO fecal microbiota transplantation (FMT) inoculation of DSS-treated mice had similarly beneficial results. FMT mice showed a reduction in colitis symptoms, which was more pronounced in ISO-FMT than in CON-FMT mice. Meanwhile, ISO-FMT expanded the abundance of beneficial microorganisms, increased the expression of metabolites, such as SCFAs and total SBAs, and significantly upregulated the expression of P-gp protein. In addition, Spearman's correlation analysis demonstrated a positive correlation between the production of SCFAs and SBAs and the expression of P-gp. The present study identified that ISO increases the expression of P-gp in the intestinal epithelium by regulating intestinal microorganisms and their metabolites, which maintains colonic homeostasis, improves the integrity of the colonic epithelium, and alleviates colitis.},
}

@article {pmid39180286,
year = {2024},
author = {Jin, X and Sheng, W and Liu, X and Zhu, D},
title = {Optimizing Colonoscopy Preparation in Autistic Children: A Comparative Study of Hypertonic Sugar Saline and Normal Saline Enemas.},
journal = {Clinical pediatrics},
volume = {},
number = {},
pages = {99228241275054},
doi = {10.1177/00099228241275054},
pmid = {39180286},
issn = {1938-2707},
abstract = {OBJECTIVE: This study evaluates the effectiveness of combining oral polyethylene glycol electrolyte solution with hypertonic sugar saline enema for colonoscopy preparation in autistic children.

METHODS: Clinical data of 58 children with autism who underwent fecal bacteria transplantation and transendoscopic enteral tubing (TET) catheterization at the hospital were retrospectively analyzed. Participants were allocated into 2 groups: a control group (26 children) and an observation group (32 children), differentiated by their intestinal preparation protocols. The control group was administered oral polyethylene glycol combined with normal saline enema, whereas the observation group was given oral polyethylene glycol combined with hypertonic sugar saline enema. The Boston Bowel Preparation Scale (BBPS) was used to score intestinal cleanliness. Differences in intestinal cleanliness and colonoscopy duration between the 2 groups were compared.

RESULTS: The group treated with hypertonic sugar saline enema exhibited significantly higher BBPS scores (6.78 ± 0.83) and an intestinal passage rate of 96.86%, which were statistically significant compared with the control group (P < 0.05). In addition, the colonoscopy duration was notably shorter in the observation group (14.03 ± 4.86 minutes) compared with the control group (P < 0.05).

CONCLUSION: Our findings suggest that an oral polyethylene glycol electrolyte solution combined with a hypertonic sugar saline enema is a more effective preparation method for colonoscopy in autistic children.},
}

@article {pmid39179176,
year = {2024},
author = {Ngo, VL and Wang, Y and Wang, Y and Shi, Z and Britton, R and Zou, J and Ramani, S and Jiang, B and Gewirtz, AT},
title = {Select gut microbiota impede rotavirus vaccine efficacy.},
journal = {Cellular and molecular gastroenterology and hepatology},
volume = {},
number = {},
pages = {101393},
doi = {10.1016/j.jcmgh.2024.101393},
pmid = {39179176},
issn = {2352-345X},
abstract = {BACKGROUND& AIMS: The protection provided by rotavirus (RV) vaccines is highly heterogeneous amongst individuals. We hypothesized that microbiota composition might influence RV vaccine efficacy.

METHODS: First, we examined the potential of segmented filamentous bacteria (SFB) colonization to influence RV vaccine efficacy in mice. Next, we probed the Influence of human microbiomes on RV vaccination via administering mice fecal microbial transplants (FMT) from children with robust or minimal RV vaccine responsiveness. Post-FMT, mice were subjected to RV vaccination followed by RV challenge.

RESULTS: SFB colonization induced a phenotype that was reminiscent of RV vaccine failure, i.e. failure to generate RV antigens and, consequently, anti-RV antibodies following RV vaccination resulting in proneness to RV challenge after SFB levels diminished. FMT from children to mice recapitulated donor vaccination phenotype. Specifically, mice receiving FMT from high-responsive vaccinees copiously shed RV antigens and robustly generated anti-RV antibodies following RV vaccination. Concomitantly, such mice were impervious to RV challenge. In contrast, mice receiving FMT from children who had not responded to RV vaccination exhibited only modest responses to RV vaccination and, concomitantly, remained prone to RV challenge. Microbiome analysis ruled out a role for SFB but suggested involvement of Clostridium perfringens. Oral administration of cultured C. perfringens to gnotobiotic mice partially recapitulated the RV vaccine non-responder phenotype. Analysis of published microbiome data found C. perfringens abundance in children modestly associated with RV vaccine failure.

CONCLUSION: Microbiota composition influences RV vaccine efficacy with C. perfringens being one, perhaps of many, potential contributing taxa.},
}

@article {pmid39178987,
year = {2024},
author = {Shukla, V and Singh, S and Verma, S and Verma, S and Rizvi, AA and Abbas, M},
title = {Targeting the Microbiome to Improve Human Health with the Approach of Personalized Medicine: Latest Aspects and Current Updates.},
journal = {Clinical nutrition ESPEN},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.clnesp.2024.08.005},
pmid = {39178987},
issn = {2405-4577},
abstract = {The intricate ecosystem of microorganisms residing within and on the human body, collectively known as the microbiome, significantly influences human health. Imbalances in this microbiome, referred to as dysbiosis, have been associated with various diseases, prompting the exploration of novel therapeutic approaches. Personalized medicine, Tailors treatments to individual patient characteristics, offers a promising avenue for addressing microbiome-related health issues. This review highlights recent developments in utilizing personalized medicine to target the microbiome, aiming to enhance health outcomes. Noteworthy strategies include fecal microbiota transplantation (FMT), where healthy donor microbes are transferred to patients, showing promise in treating conditions such as recurrent Clostridium difficile infection. Additionally, probiotics, which are live microorganisms similar to beneficial gut inhabitants, and prebiotics, non-digestible compounds promoting microbial growth, are emerging as tools to restore microbiome balance. The integration of these approaches, known as synbiotics, enhances microbial colonization and therapeutic effects. Advances in metagenomics and sequencing technologies provide the means to understand individual microbiome profiles, enabling tailored interventions. This paper aims to present the latest insights in leveraging personalized medicine to address microbiome-related health concerns, envisioning a future where microbiome-based therapies reshape disease management and promote human health.},
}

@article {pmid39176325,
year = {2024},
author = {Nilofar, F and Babu, N and Kumar, M and Palanisamy, S and T, G},
title = {From Hemorrhage to Diarrhea: The Comprehensive Clinical Journey of a Patient With Pseudomembranous Colitis.},
journal = {Cureus},
volume = {16},
number = {7},
pages = {e65176},
pmid = {39176325},
issn = {2168-8184},
abstract = {Pseudomembranous colitis (PC) is an inflammation of the colon primarily caused by the bacterium Clostridium difficile (C. difficile), often following antibiotic use. This case report describes the intricate clinical course of a 48-year-old male farmer with a history of chronic alcoholism, tobacco use, and seizure disorder, who presented with acute onset of left-sided weakness. CT brain revealed an intra-axial hemorrhage in the right gangliocapsular region with significant edema and midline shift. The patient's condition necessitated mechanical ventilation due to a low Glasgow Coma Scale (GCS) score. Complications ensued with the onset of ventilator-associated pneumonia (VAP) on day six, attributed to multi-drug resistant Acinetobacter baumannii, which was managed with meropenem and polymyxin. Following successful weaning from the ventilator, he experienced severe watery diarrhea, high-grade fever, and diffuse abdominal pain on day 13. Subsequent stool tests confirmed PC caused by C. difficile, characterized by diffuse colonic wall-thickening with a water target sign on contrast-enhanced CT (CECT) abdomen. Initial treatment with oral vancomycin and metronidazole was followed by symptomatic treatment. Two weeks later, the patient had a relapse of PC, presenting with multiple episodes of loose stools, which was managed with oral metronidazole alone. Colonoscopy and biopsy confirmed the relapse, showing inflamed colonic mucosa with pseudomembranes. This case highlights the importance of strict infection control, prudent antibiotic use, and close monitoring for these patients. It also suggests the potential role of fecal microbiota transplantation (FMT) for recurrent cases. The patient's recovery demonstrates the effectiveness of meticulous medical management and adherence to infection control protocols in achieving optimal outcomes.},
}

@article {pmid39173982,
year = {2024},
author = {Ding, FF and Zhou, NN and Wang, T and Bao, MY and Qiao, F and Du, ZY and Zhang, ML},
title = {Fish gut-derived probiotic Pediococcus pentosaceus alleviates gossypol-induced intestinal inflammation by inhibiting NLRC3/NF-κB/IL-1β signal pathway in Nile tilapia.},
journal = {Fish & shellfish immunology},
volume = {153},
number = {},
pages = {109852},
doi = {10.1016/j.fsi.2024.109852},
pmid = {39173982},
issn = {1095-9947},
abstract = {Cottonseed meal (CSM) and cottonseed protein concentrate (CPC) serve as protein alternatives to fish meal and soybean meal in the feed industry. However, the presence of gossypol residue in CSM and CPC can potentially trigger severe intestinal inflammation, thereby restricting the widespread utilization of these two protein sources. Probiotics are widely used to prevent or alleviate intestinal inflammation, but their efficacy in protecting fish against gossypol-induced enteritis remains uncertain. Here, the protective effect of Pediococcus pentosaceus, a strain isolated from the gut of Nile tilapia (Oreochromis niloticus), was evaluated. Three diets, control diet (CON), gossypol diet (GOS) and GOS supplemented with P. pentosaceus YC diet (GP), were used to feed Nile tilapia for 10 weeks. After the feeding trial, P. pentosaceus YC reduced the activity of myeloperoxidase (MPO) in the proximal intestine (PI) and distal intestine (DI). Following a 7-day exposure to Aeromonas hydrophila, the addition of P. pentosaceus YC was found to increase the survival rate of the fish. P. pentosaceus YC significantly inhibited the oxidative stress caused by gossypol, which was evidenced by lower reactive oxygen species (ROS) and malondialdehyde (MDA), as well as higher activities of glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) in PI and DI. Addition of P. pentosaceus YC significantly inhibited enteritis, with the lower expression of pro-inflammatory cytokines (il-1β, il-6, il-8) and higher expression of anti-inflammatory cytokines tgf-β. RNA-seq analysis indicated that P. pentosaceus YC supplementation significantly inhibited nlrc3 and promoted nf-κb expression in PI and DI, and the siRNA interference experiment in vivo demonstrated that intestinal inflammation was mediated by NLRC3/NF-κB/IL-1β signaling pathway. Fecal bacteria transplantation experiment demonstrated that gut microbiota mediated the protective effect of P. pentosaceus YC. These findings offer valuable insights into the application of P. pentosaceus YC for alleviating gossypol-induced intestinal inflammation in fish.},
}

@article {pmid39173885,
year = {2024},
author = {MacGibeny, MA and Adjei, S and Pyle, H and Bunick, CG and Ghannoum, M and Grada, A and Harris-Tryon, T and Tyring, SK and Kong, HH},
title = {Alterations in the Skin Microbiome in Dermatologic Diseases and with External Exposures: CME Part 2.},
journal = {Journal of the American Academy of Dermatology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jaad.2024.07.1499},
pmid = {39173885},
issn = {1097-6787},
abstract = {In Part I of our CME we reviewed the skin microbiome in healthy individuals. Part II reviews the evolving understanding of alterations in the skin microbiome in specific human diseases. We also discuss how the skin microbiome can change with environmental exposures and medications such as antibiotics as well as ongoing research on microbiome-based interventions.},
}

@article {pmid39173756,
year = {2024},
author = {Liu, J and Zhang, Z and Zhong, S and Zhang, X and Yang, J and Zhou, Q and Wang, D and Chang, X and Wang, H},
title = {Fecal microbiome transplantation alleviates manganese-induced neurotoxicity by altering the composition and function of the gut microbiota via the cGAS-STING/NLRP3 pathway.},
journal = {The Science of the total environment},
volume = {951},
number = {},
pages = {175681},
doi = {10.1016/j.scitotenv.2024.175681},
pmid = {39173756},
issn = {1879-1026},
abstract = {Manganese (Mn) is an environmental pollutant, and overexposure can cause neurodegenerative disorders similar to Alzheimer's disease and Parkinson's disease that are characterized by β-amyloid (Aβ) overexpression, Tau hyperphosphorylation and neuroinflammation. However, the mechanisms of Mn neurotoxicity are not clearly defined. In our study, a knockout mouse model of Mn exposure combined with gut flora-induced neurotoxicity was constructed to investigate the effect of gut flora on Mn neurotoxicity. The results showed that the levels of Tau, p-Tau and Aβ in the hippocampus of C57BL/6 mice were greater than those in the hippocampus of control mice after 5 weeks of continuous exposure to manganese chloride (Mn content of 200 mg/L). Transplanted normal and healthy fecal microbiota from mice significantly downregulated Tau, p-Tau and Aβ expression and ameliorated brain pathology. Moreover, Mn exposure activated the cGAS-STING pathway and altered the cecal microbiota profile, characterized by an increase in Clostridiales, Pseudoflavonifractor, Ligilactobacillus and Desulfovibrio, and a decrease in Anaerotruncus, Eubacterium_ruminantium_group, Fusimonas and Firmicutes, While fecal microbiome transplantation (FMT) treatment inhibited this pathway and restored the microbiota profile. FMT alleviated Mn exposure-induced neurotoxicity by inhibiting activation of the NLRP3 inflammasome triggered by overactivation of the cGAS-STING pathway. Deletion of the cGAS and STING genes and FMT altered the gut microbiota composition and its predictive function. Phenotypic prediction revealed that FMT markedly decreased the abundances of anaerobic and stress-tolerant bacteria and significantly increased the abundances of facultative anaerobic bacteria and biofilm-forming bacteria after blocking the cGAS-STING pathway compared to the Mn-exposed group. FMT from normal and healthy mice ameliorated the neurotoxicity of Mn exposure, possibly through alterations in the composition and function of the microbiome associated with the cGAS-STING/NLRP3 pathway. This study provides a prospective direction for future research on the mechanism of Mn neurotoxicity.},
}

@article {pmid39172643,
year = {2024},
author = {Offersen, SM and Mao, X and Spiegelhauer, MR and Larsen, F and Li, VR and Sandris Nielsen, D and Aunsholt, L and Thymann, T and Brunse, A},
title = {Fecal virus-like particles are sufficient to reduce necrotizing enterocolitis.},
journal = {Gut microbes},
volume = {16},
number = {1},
pages = {2392876},
doi = {10.1080/19490976.2024.2392876},
pmid = {39172643},
issn = {1949-0984},
mesh = {*Enterocolitis, Necrotizing/prevention & control/therapy ; Animals ; *Feces/virology/microbiology ; *Gastrointestinal Microbiome ; *Fecal Microbiota Transplantation/methods ; Swine ; Humans ; Bacteria/classification/isolation & purification/genetics ; Animals, Newborn ; Disease Models, Animal ; Virome ; Clostridium perfringens ; Bacteriophages/genetics/physiology ; Diarrhea/therapy/virology/prevention & control/microbiology ; },
abstract = {Fecal filtrate transfer (FFT) is emerging as a safer alternative to traditional fecal microbiota transplantation (FMT) - particularly in the context of necrotizing enterocolitis (NEC), a severe gastrointestinal condition affecting preterm infants. Using a preterm piglet model, FFT has demonstrated superiority over FMT in safety and NEC prevention. Since FFT is virtually devoid of bacteria, prokaryotic viruses (bacteriophages) are assumed to mediate the beneficial effects. However, this assumption remains unproven. To address this gap, we separated virus-like particles (30 kDa to 0.45 µm) of donor feces from the residual postbiotic fluid. We then compared clinical and gut microbiota responses to these fractions with the parent FFT solution after transferring them to NEC-susceptible preterm piglets. Virome transfer was equally effective as FFT in reducing the severity of NEC-like pathology. The bacterial compositional data corroborated clinical findings as virome transfer reduced the relative abundance of several NEC-associated pathogens e.g. Klebsiella pneumoniae and Clostridium perfringens. Virome transfer diversified gut viral communities with concomitant constraining effects on the bacterial composition. Unexpectedly, virome transfer, but not residual postbiotic fluid, led to earlier diarrhea. While diarrhea may be a minor concern in human infants, future work should identify ways of eliminating this side effect without losing treatment efficacy.},
}

*Enterocolitis, Necrotizing/prevention & control/therapy
Animals
*Feces/virology/microbiology
*Gastrointestinal Microbiome
*Fecal Microbiota Transplantation/methods
Swine
Humans
Bacteria/classification/isolation & purification/genetics
Animals, Newborn
Disease Models, Animal
Virome
Clostridium perfringens
Bacteriophages/genetics/physiology
Diarrhea/therapy/virology/prevention & control/microbiology

@article {pmid39172216,
year = {2024},
author = {Xu, X and Jin, H and Li, X and Yan, C and Zhang, Q and Yu, X and Liu, Z and Liu, S and Zhu, F},
title = {Fecal Microbiota Transplantation Regulates Blood Pressure by Altering Gut Microbiota Composition and Intestinal Mucosal Barrier Function in Spontaneously Hypertensive Rats.},
journal = {Probiotics and antimicrobial proteins},
volume = {},
number = {},
pages = {},
pmid = {39172216},
issn = {1867-1314},
abstract = {Hypertension is accompanied by gut microbiota imbalance, but the role of bacteria in the pathogenesis of hypertension requires further study. In this study, we used fecal microbiota transplantation to determine the impact of microbiota composition on blood pressure in spontaneous hypertensive rats (SHRs), using normotensive Wistar Kyoto (WKY) rats as controls. SHRs were randomly divided into two groups (n = 10/group), SHR and SHR-T (SHR plus fecal transplantation) and WKY into WKY and WKY-T (WKY plus fecal transplantation). SHR-T received fecal transplantation from WKY, while WKY-T received fecal transplantation from SHR. Blood pressure was measured from the tail artery in conscious rats. 16S rDNA gene amplicon sequencing was used to analyze bacterial composition. Circulating levels of diamine oxidase, D-lactate, FITC-Dextrans, and lipopolysaccharide were determined. Hematoxylin and eosin (H&E) staining was used to observe structural changes in the intestinal mucosa. Immunofluorescence, Western blot, and RT-PCR were utilized to determine changes in the expression of tight junction proteins. Following cross fecal transplantation, blood pressure decreased in SHR and increased in WKY. Significant differences in gut microbial composition were found between hypertensive and normotensive rats, specifically regarding the relative abundance of lactic and butyric acid-producing bacteria. Changes in gut microbiota composition also impacted the intestinal mucosal barrier integrity. Moreover, fecal transplantation affected the expression of tight junction proteins that may impact intestinal mucosal permeability and structural integrity. Blood pressure may be associated with butyric acid-producing intestinal microbiota and its function in regulating the integrity of intestinal mucosal barrier.},
}

@article {pmid39170992,
year = {2024},
author = {Sanchez Cruz, C and Rojas Huerta, A and Lima Barrientos, J and Rodriguez, C and Devani, A and Boosahda, V and Rasagna Mareddy, NS and Briceno Silva, G and Del Castillo Miranda, JC and Reyes Gochi, KA and Reyes Gochi, MD and Alvarez, S and Ghattas Hasbun, PE},
title = {Inflammatory Bowel Disease and Cardiovascular Disease: An Integrative Review With a Focus on the Gut Microbiome.},
journal = {Cureus},
volume = {16},
number = {7},
pages = {e65136},
pmid = {39170992},
issn = {2168-8184},
abstract = {Inflammatory bowel disease (IBD), which includes Crohn's disease and ulcerative colitis, is a chronic inflammatory condition of the gastrointestinal tract. Recent research indicates a significant link between IBD and cardiovascular disease (CVD), the leading cause of global morbidity and mortality. This review examines the association between IBD and CVD, emphasizing the role of the gut microbiome in this relationship. IBD patients have a higher risk of cardiovascular events, such as coronary artery disease, heart failure, and cerebrovascular incidents, primarily due to chronic systemic inflammation, genetic factors, and gut microbiota imbalance (dysbiosis). Dysbiosis in IBD increases intestinal permeability, allowing bacterial products to enter the bloodstream, which promotes inflammation and endothelial dysfunction, contributing to CVD. Understanding the gut microbiome's role in IBD and CVD suggests new therapeutic interventions. Modulating the microbiome through diet, probiotics, and fecal microbiota transplantation (FMT) are promising research avenues. These interventions aim to restore a healthy gut microbiota balance, potentially reducing inflammation and improving cardiovascular outcomes. Additionally, the review emphasizes the importance of regular cardiovascular risk assessments and personalized preventive measures in managing IBD patients. Such measures include routine monitoring of cardiovascular health, tailored lifestyle modifications, and early intervention strategies to mitigate cardiovascular risk. By integrating current knowledge, this review aims to improve understanding and management of the interconnected pathophysiology of IBD and CVD. This approach will ultimately enhance patient outcomes and provide a foundation for future research and clinical practice guidelines in this area.},
}

@article {pmid39170985,
year = {2024},
author = {Zou, X and Zou, X and Gao, L and Zhao, H},
title = {Gut microbiota and psoriasis: pathogenesis, targeted therapy, and future directions.},
journal = {Frontiers in cellular and infection microbiology},
volume = {14},
number = {},
pages = {1430586},
pmid = {39170985},
issn = {2235-2988},
mesh = {*Psoriasis/therapy/microbiology/drug therapy ; Humans ; *Gastrointestinal Microbiome ; *Medicine, Chinese Traditional ; *Fecal Microbiota Transplantation ; *Probiotics/therapeutic use ; Prebiotics ; Cytokines/metabolism ; Interleukin-17/metabolism ; },
abstract = {BACKGROUND: Psoriasis is one of the most common autoimmune skin diseases. Increasing evidence shows that alterations in the diversity and function of microbiota can participate in the pathogenesis of psoriasis through various pathways and mechanisms.

OBJECTIVE: To review the connection between microbial changes and psoriasis, how microbial-targeted therapy can be used to treat psoriasis, as well as the potential of prebiotics, probiotics, synbiotics, fecal microbiota transplantation, diet, and Traditional Chinese Medicine as supplementary and adjunctive therapies.

METHODS: Literature related to the relationship between psoriasis and gut microbiota was searched in PubMed and CNKI.

RESULTS: Adjunct therapies such as dietary interventions, traditional Chinese medicine, and probiotics can enhance gut microbiota abundance and diversity in patients with psoriasis. These therapies stimulate immune mediators including IL-23, IL-17, IL-22, and modulate gamma interferon (IFN-γ) along with the NF-kB pathway, thereby suppressing the release of pro-inflammatory cytokines and ameliorating systemic inflammatory conditions.

CONCLUSION: This article discusses the direction of future research and clinical treatment of psoriasis from the perspective of intestinal microbiota and the mechanism of traditional Chinese medicine, so as to provide clinicians with more comprehensive diagnosis and treatment options and bring greater hope to patients with psoriasis.},
}

*Psoriasis/therapy/microbiology/drug therapy
Humans
*Gastrointestinal Microbiome
*Medicine, Chinese Traditional
*Fecal Microbiota Transplantation
*Probiotics/therapeutic use
Prebiotics
Cytokines/metabolism
Interleukin-17/metabolism

@article {pmid39166878,
year = {2024},
author = {Lu, Q and Zhu, R and Zhou, L and Zhang, R and Li, Z and Xu, P and Wang, Z and Wu, G and Ren, J and Jiao, D and Song, Y and Li, J and Wang, W and Liang, R and Ma, X and Sun, Y},
title = {Gut dysbiosis contributes to the development of Budd-Chiari syndrome through immune imbalance.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0079424},
doi = {10.1128/msystems.00794-24},
pmid = {39166878},
issn = {2379-5077},
abstract = {UNLABELLED: Budd-Chiari syndrome (B-CS) is a rare and lethal condition characterized by hepatic venous outflow tract blockage. Gut microbiota has been linked to numerous hepatic disorders, but its significance in B-CS pathogenesis is uncertain. First, we performed a case-control study (Ncase = 140, Ncontrol = 63) to compare the fecal microbiota of B-CS and healthy individuals by metagenomics sequencing. B-CS patients' gut microbial composition and activity changed significantly, with a different metagenomic makeup, increased potentially pathogenic bacteria, including Prevotella, and disease-linked microbial function. Imbalanced cytokines in patients were demonstrated to be associated with gut dysbiosis, which led us to suspect that B-CS is associated with gut microbiota and immune dysregulation. Next, 16S ribosomal DNA sequencing on fecal microbiota transplantation (FMT) mice models examined the link between gut dysbiosis and B-CS. FMT models showed damaged liver tissues, posterior inferior vena cava, and increased Prevotella in the disturbed gut microbiota of FMT mice. Notably, B-CS-FMT impaired the morphological structure of colonic tissues and increased intestinal permeability. Furthermore, a significant increase of the same cytokines (IL-5, IL-6, IL-9, IL-10, IL-17A, IL-17F, and IL-13) and endotoxin levels in B-CS-FMT mice were observed. Our study suggested that gut microbial dysbiosis may cause B-CS through immunological dysregulation.

IMPORTANCE: This study revealed that gut microbial dysbiosis may cause Budd-Chiari syndrome (B-CS). Gut dysbiosis enhanced intestinal permeability, and toxic metabolites and imbalanced cytokines activated the immune system. Consequently, the escalation of causative factors led to their concentration in the portal vein, thereby compromising both the liver parenchyma and outflow tract. Therefore, we proposed that gut microbial dysbiosis induced immune imbalance by chronic systemic inflammation, which contributed to the B-CS development. Furthermore, Prevotella may mediate inflammation development and immune imbalance, showing potential in B-CS pathogenesis.},
}

@article {pmid39166867,
year = {2024},
author = {Sintes, R and McLellan, P and Navelli, G and Landman, C and Delage, S and Truong, S and Benech, N and Kapel, N and Moreino Sabater, A and Schnuriger, A and Eckert, C and Bleibtreu, A and Joly, A-C and Sokol, H},
title = {Use of frozen native feces for fecal microbiota transplantation in recurrent Clostridioides difficile infection: a simple way to improve the efficiency of donor feces preparation.},
journal = {Antimicrobial agents and chemotherapy},
volume = {},
number = {},
pages = {e0073424},
doi = {10.1128/aac.00734-24},
pmid = {39166867},
issn = {1098-6596},
abstract = {Preparing fecal microbiota transplants immediately after donation is resource-intensive, and a proportion are destroyed following abnormal screening results. We retrospectively compared two processes, frozen fecal preparation (FFP) and fresh native frozen preparation (FNFP), for clinical efficacy in the treatment of recurrent Clostridioides difficile infection (rCDI). FFP and FNFP were similarly effective with clinical success rates of 76.7% and 86.7% (P = 0.32), respectively. FNFP is an efficient procedure that saves resources while maintaining clinical efficacy in rCDI.},
}

@article {pmid39165355,
year = {2024},
author = {Huang, J and Zhang, J and Wang, F and Tang, X},
title = {Modified Gegen Qinlian Decoction modulated the gut microbiome and bile acid metabolism and restored the function of goblet cells in a mouse model of ulcerative colitis.},
journal = {Frontiers in immunology},
volume = {15},
number = {},
pages = {1445838},
pmid = {39165355},
issn = {1664-3224},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Colitis, Ulcerative/microbiology/drug therapy/metabolism/therapy ; Mice ; *Disease Models, Animal ; *Drugs, Chinese Herbal/pharmacology/therapeutic use ; *Goblet Cells/drug effects/metabolism ; *Bile Acids and Salts/metabolism ; Male ; Fecal Microbiota Transplantation ; Mice, Inbred C57BL ; Colon/pathology/metabolism/drug effects/microbiology ; },
abstract = {OBJECTIVE: Modified Gegen Qinlian Decoction (MGQD) has been shown to effectively relieve ulcerative colitis (UC) without a known pharmacological mechanism. In this study, the anti-colitis efficaciousness of MGQD and its underlying mechanisms in UC were evaluated.

METHODS: Mice with colitis were administered MGQD for 7 days. Following the evaluation of clinical symptoms, gut microbiota in the feces of UC mice was examined using 16S rRNA sequencing and bile acids (BAs) were examined using LC/MS. Gut microbiota consumption and fecal microbiota transplantation (FMT) were used to explore the involvement of gut microbiota in the anti-UC action of MGQD.

RESULTS: MGQD relieved colitis as shown by weight loss protection, a lower disease activity index (DAI), restoration of intestinal length reduction, and lower histopathologic scores. MGQD also restored crypt stem cell proliferation and function of colonic goblet cells, and promoted MUC2 protein secretion. Interestingly, investigations using gut bacterial depletion and FMT showed that MGQD attenuated colonic damage in a gut-dependent way. The modulation of the gut microbiota by MGQD might be attributed to a decrease in Odoribacter and an increase in norank_f_Muribaculaceae. In addition, MGQD modulated the metabolism of BAs while restoring the structure of the gut microbiota.

CONCLUSION: MGQD significantly alleviated colitis in mice, which may be associated with the modulation of gut microbiota and BA metabolism and restoration of function of goblet cells. However, factors other than the gut microbiota may also be involved in the amelioration of UC by MGQD.},
}

Animals
*Gastrointestinal Microbiome/drug effects
*Colitis, Ulcerative/microbiology/drug therapy/metabolism/therapy
Mice
*Disease Models, Animal
*Drugs, Chinese Herbal/pharmacology/therapeutic use
*Goblet Cells/drug effects/metabolism
*Bile Acids and Salts/metabolism
Male
Fecal Microbiota Transplantation
Mice, Inbred C57BL
Colon/pathology/metabolism/drug effects/microbiology

@article {pmid39165756,
year = {2023},
author = {Hosseini, PSK and Wang, B and Luan, Y and Sun, F and Michail, S},
title = {Gut metabolomic profiles in paediatric ulcerative colitis patients prior to and after receiving faecal microbiota transplants.},
journal = {Gut microbiome (Cambridge, England)},
volume = {4},
number = {},
pages = {},
pmid = {39165756},
issn = {2632-2897},
support = {R01 HD081197/HD/NICHD NIH HHS/United States ; UL1 TR000130/TR/NCATS NIH HHS/United States ; UL1 TR001855/TR/NCATS NIH HHS/United States ; },
abstract = {Ulcerative colitis (UC) is an immune-mediated inflammation of the colonic mucosa. Gut microbiota dysbiosis may play a significant role in disease pathogenesis by causing shifts in metabolomic profiles within the gut. To identify differences and trends in the metabolomic profile of paediatric UC patients pre- and post-faecal microbiota transplants (FMT). Forty-six paediatric patients with mild-to-moderate UC and 30 healthy paediatric patients were enrolled in this study. Baseline stool samples were collected prior to FMT initiation and at months 1, 3, 6, and 12 post-FMT. Pediatric Ulcerative Colitis Activity Index (PUCAI) scores were calculated at baseline and months 1, 3, 6, and 12 after FMT. The average Bray-Curtis dissimilarities to healthy subjects decreased after FMT. In principal coordinate analysis plots, UC patients' centroids drew nearer to healthy individuals. The variance explained by phenotype (Healthy versus UC) reduced and remained significant. From 1 to 3 months after FMT, PUCAI trends were statistically significant and decreasing. PUCAI scores remain flat starting 6 months after FMT. This study concludes that paediatric UC patients have a significantly different baseline metabolite profile than healthy controls. Although being time limited, FMT significantly altered these metabolite profiles and shifted them towards that of healthy controls.},
}

@article {pmid39163753,
year = {2024},
author = {Wang, Z and Wang, X and Fu, L and Xu, S and Wang, X and Liao, Q and Zhuang, T and Liu, L and Zhang, H and Li, W and Xiong, A and Gu, L and Wang, Z and Wang, R and Tao, F and Yang, L and Ding, L},
title = {Shengmai San formula alleviates high-fat diet-induced obesity in mice through gut microbiota-derived bile acid promotion of M2 macrophage polarization and thermogenesis.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {133},
number = {},
pages = {155938},
doi = {10.1016/j.phymed.2024.155938},
pmid = {39163753},
issn = {1618-095X},
abstract = {BACKGROUND: Shengmai San Formula (SMS) is a traditional Chinese medicine (TCM) that has been used to treat wasting-thirst regarded as diabetes mellitus, which occurs disproportionately in obese patients. Therefore, we investigated whether SMS could be used to treat obesity, and explored possible mechanisms by which it might improve glucose and fat metabolism.

METHODS: To investigate the effects of SMS on a high-fat diet (HFD)-induced obesity (DIO) model, we studied glucose metabolism via glucose tolerance testing (GTT) and insulin tolerance testing (ITT). Browning of white adipose tissue (WAT) was evaluated using H&E staining, along with browning-related gene and protein expression. Changes in bile acid (BA) levels in serum, liver, ileum, and inguinal white adipose tissue were detected by Ultra performance liquid chromatography tandem quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS). In addition, antimicrobial mixture (ABX) and fecal microbial transplantation (FMT) experiments were used to verify the role of gut flora in the effects produced by SMS on HFD-induced obesity model.

RESULTS: SMS ameliorated diet-induced dyslipidemia in a dose-dependent manner and reduced glucose intolerance and insulin resistance in DIO mice, helping to restore energy metabolism homeostasis. SMS significantly altered the structure of intestinal microbiome composition, decreasing the abundance of Lactobacillus carrying bile salt hydrolase (BSH) enzymes and thereby increasing the level of conjugated BAs in the blood, ileum, and iWAT. Increased TCA content promoted the secretion of Slit3 from M2 macrophages in iWAT, which activates the protein kinase A/calmodulin-dependent protein kinase II (PKA/CaMKII) signaling pathway in sympathetic neurons via the roundabouts receptor 1(ROBO1). This pathway promotes the synthesis and release of norepinephrine (NE), inducing cyclic adenosine monophosphate (cAMP) release in adipose tissue that activates the cyclic adenosine monophosphate/protein kinase A/phosphorylated hormone-sensitive lipase (cAMP/PKA/pHSL) pathway and enhances WAT browning. ABX treatment eliminated SMS effects on glucose and lipid metabolism in DIO mice, whereas glucose and lipid metabolism in obese mice improved following SMS-FMT and increased the level of serum bile acids.

CONCLUSION: SMS affects intestinal flora and bile acid composition in vivo and increased TCA promotes M2 macrophage polarization and Slit3 release in adipose tissue. This induces NE release and increases WAT browning in obese mice, which may be a mechanism by which SMS could be used to treat obesity.},
}

@article {pmid39163678,
year = {2024},
author = {Wang, X and Peng, J and Cai, P and Xia, Y and Yi, C and Shang, A and Akanyibah, FA and Mao, F},
title = {The emerging role of the gut microbiota and its application in inflammatory bowel disease.},
journal = {Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie},
volume = {179},
number = {},
pages = {117302},
doi = {10.1016/j.biopha.2024.117302},
pmid = {39163678},
issn = {1950-6007},
abstract = {Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, is a complex disorder with an unknown cause. However, the dysbiosis of the gut microbiome has been found to play a role in IBD etiology, including exacerbated immune responses and defective intestinal barrier integrity. The gut microbiome can also be a potential biomarker for several diseases, including IBD. Currently, conventional treatments targeting pro-inflammatory cytokines and pathways in IBD-associated dysbiosis do not yield effective results. Other therapies that directly target the dysbiotic microbiome for effective outcomes are emerging. We review the role of the gut microbiome in health and IBD and its potential as a diagnostic, prognostic, and therapeutic target for IBD. This review also explores emerging therapeutic advancements that target gut microbiome-associated alterations in IBD, such as nanoparticle or encapsulation delivery, fecal microbiota transplantation, nutritional therapies, microbiome/probiotic engineering, phage therapy, mesenchymal stem cells (MSCs), gut proteins, and herbal formulas.},
}

@article {pmid39163526,
year = {2024},
author = {van der Vossen, EWJ and Davids, M and Voermans, B and Wortelboer, K and Hartstra, AV and Koopen, AM and de Groot, P and Levin, E and Nieuwdorp, M},
title = {Disentangle beneficial effects of strain engraftment after fecal microbiota transplantation in subjects with MetSyn.},
journal = {Gut microbes},
volume = {16},
number = {1},
pages = {2388295},
pmid = {39163526},
issn = {1949-0984},
mesh = {*Fecal Microbiota Transplantation ; Humans ; *Gastrointestinal Microbiome ; Male ; Middle Aged ; *Metabolic Syndrome/therapy/microbiology ; Female ; Feces/microbiology ; Bacteria/classification/isolation & purification/metabolism/genetics ; Adult ; Blood Pressure ; Treatment Outcome ; },
abstract = {Fecal Microbiota Transplantation (FMT) has emerged as a potential modality for mitigating microbiome-associated diseases. Despite this potential, the precise causal pathways by which specific gut microbiota strains induce remission remain inadequately elucidated. In this study, we aimed to discern the impact of engraftment of donor-infused strains on alterations in plasma metabolites, subsequently contributing to the amelioration of clinical parameters involved in subjects with metabolic syndrome (MetSyn) receiving an FMT. We observed that a higher fraction of donor strains engrafted in the recipient is correlated to a reduction in diastolic blood pressure and found specific strain associations through canonical correlation analysis. Integrating the metabolomics profile shows that engraftment of Collinsella aerofaciens and Fusocatenibacter saccharovorans was related to a reduction in 2-oxoarginine in plasma, which was subsequently correlated to a reduction in diastolic blood pressure. In conclusion, we applied a novel framework to elucidate on the complex and heterogenous FMT intervention, establishing a connection between engrafted microbiota and clinical outcome parameters. Our findings underscore the potential therapeutic efficacy of FMT in ameliorating MetSyn, demonstrating a potential contribution of microbial strain engraftment to the improvement of MetSyn via modulation of circulating metabolites.},
}

*Fecal Microbiota Transplantation
Humans
*Gastrointestinal Microbiome
Male
Middle Aged
*Metabolic Syndrome/therapy/microbiology
Female
Feces/microbiology
Bacteria/classification/isolation & purification/metabolism/genetics
Adult
Blood Pressure
Treatment Outcome

@article {pmid39163273,
year = {2024},
author = {Zhu, X and Dai, X and Zhao, L and Li, J and Zhu, Y and He, W and Guan, X and Wu, T and Liu, L and Song, H and Lei, L},
title = {Quercetin activates energy expenditure to combat metabolic syndrome through modulating gut microbiota-bile acids crosstalk in mice.},
journal = {Gut microbes},
volume = {16},
number = {1},
pages = {2390136},
pmid = {39163273},
issn = {1949-0984},
mesh = {*Quercetin/pharmacology ; Animals ; *Gastrointestinal Microbiome/drug effects ; Mice ; *Energy Metabolism/drug effects ; *Metabolic Syndrome/metabolism/microbiology/drug therapy ; Male ; *Bile Acids and Salts/metabolism ; *Mice, Inbred C57BL ; *Thermogenesis/drug effects ; *Adipose Tissue, Brown/metabolism/drug effects ; Adipose Tissue, White/metabolism/drug effects ; Receptors, G-Protein-Coupled/metabolism/genetics ; Disease Models, Animal ; Fecal Microbiota Transplantation ; },
abstract = {Abdominal obesity-related metabolic syndrome (MetS) has emerged as a significant global public health issue that affects human health. Flavonoids, such as quercetin, have been reported to exert obvious anti-obesity and lipid-lowering effects in both humans and animal models. However, the precise underlying mechanism remains elusive. In this study, we investigated the potential roles of gut microbiota-bile acids (BAs) interactions in quercetin-induced anti-obesity effects and metabolic benefits. Oral administration of quercetin significantly enhanced energy metabolism through activating thermogenesis of brown adipose tissues (BAT) and browning of white adipose tissues (WAT), thus mitigating metabolic dysfunctions in an abdominal obesity-related MetS mouse model. Further mechanistic studies demonstrated that quercetin treatment substantially promoted the generation of non-12α-hydroxylated BAs (non-12OH BAs), particularly ursodeoxycholic acid (UDCA) and lithocholic acid (LCA), in serum via regulating the overall structure of gut microbiota and enriching Lactobacillus. High level of non-12OH BAs bind to Takeda G protein-coupled receptor 5 (TGR5) on adipocytes to stimulate thermogenesis. Remarkably, fecal microbiota transplantation (FMT) from quercetin-treated mice replicated the effects of quercetin on non-12OH BAs generation and energy expenditure, which suggested gut microbiota reshape and concomitant BAs regulation were responsible for the benefits on energy metabolism of quercetin in the MetS mouse model. Our findings not only highlighted the critical role of gut microbiota-BAs crosstalk in mediating quercetin-induced energy expenditure, but also enriched the pharmacological mechanisms of quercetin in ameliorating MetS-related diseases.},
}

*Quercetin/pharmacology
Animals
*Gastrointestinal Microbiome/drug effects
Mice
*Energy Metabolism/drug effects
*Metabolic Syndrome/metabolism/microbiology/drug therapy
Male
*Bile Acids and Salts/metabolism
*Mice, Inbred C57BL
*Thermogenesis/drug effects
*Adipose Tissue, Brown/metabolism/drug effects
Adipose Tissue, White/metabolism/drug effects
Receptors, G-Protein-Coupled/metabolism/genetics
Disease Models, Animal
Fecal Microbiota Transplantation

@article {pmid39163019,
year = {2024},
author = {Manithody, C and Denton, C and Mehta, S and Carter, J and Kurashima, K and Bagwe, A and Syn, M and Guzman, M and Besmer, S and Jain, S and McHale, M and Qureshi, K and Nazzal, M and Caliskan, Y and Long, J and Lin, CJ and Hutchinson, C and Ericsson, AC and Jain, AK},
title = {Intraduodenal Fecal Microbiota Transplantation Ameliorates Gut Atrophy and Cholestasis in a Novel Parenteral Nutrition Piglet Model.},
journal = {American journal of physiology. Gastrointestinal and liver physiology},
volume = {},
number = {},
pages = {},
doi = {10.1152/ajpgi.00012.2024},
pmid = {39163019},
issn = {1522-1547},
support = {NIH-1R01DK131136-01//HHS | National Institutes of Health (NIH)/ ; NIH-R21AI169487-01//HHS | National Institutes of Health (NIH)/ ; NIH-1R03 DK121046-01//HHS | National Institutes of Health (NIH)/ ; NIH-P01AG078106-01//HHS | National Institutes of Health (NIH)/ ; NIH-1U01 AI163064-01//HHS | National Institutes of Health (NIH)/ ; },
abstract = {BACKGROUND: Total parenteral nutrition (TPN) provides lifesaving nutritional support intravenously; however it is associated with significant side effects. Given gut microbial alterations noted with TPN, we hypothesized that transferring fecal microbiota from healthy controls would restore gut-systemic signaling in TPN and mitigate injury.

METHODS: Using our novel ambulatory model (US Patent: US 63/136,165), 31 piglets were randomly allocated to enteral nutrition (EN), TPN only, TPN + antibiotics (TPN-A) or TPN + intraduodenal fecal microbiota transplant (TPN-FMT) for 14 days. Gut, liver, and serum were assessed through histology, biochemistry, and qPCR. Stool samples underwent 16s rRNA sequencing. PERMANOVA, Jaccard and Bray-Curtis metrics were performed.

RESULTS: Significant bilirubin elevation in TPN and TPN-A vs EN (p<0.0001) was prevented with FMT. IFN-G, TNF-alpha, IL-beta, IL-8 and LPS were significantly higher in TPN (p=0.009/0.001/0.043/0.011/<0.0001), with preservation upon FMT. Significant gut-atrophy by villous/crypt ratio in TPN (p<0.0001) and TPN-A (p=0.0001) vs EN was prevented by FMT (p=0.426 vs EN). Microbiota profiles using Principal Coordinate Analysis demonstrated significant FMT and EN overlap, with the largest separation in TPN-A followed by TPN, driven primarily by Firmicutes and Fusobacteria. TPN altered gut barrier was preserved upon FMT. Upregulated CYP7A1 and BSEP in TPN and TPN-A, and downregulatedFGFR4, EGF, FXR and TGR5 vs EN was prevented by FMT.

CONCLUSION: This study provides novel evidence of prevention of gut atrophy, liver injury and microbial dysbiosis with intraduodenal FMT, challenging current paradigms into TPN injury mechanisms and underscores importance of gut microbes as prime targets for therapeutics and drug discovery.},
}

@article {pmid39162553,
year = {2024},
author = {Yang, S and Tong, L and Li, X and Zhang, Y and Chen, H and Zhang, W and Zhang, H and Chen, Y and Chen, R},
title = {A novel clinically relevant human fecal microbial transplantation model in humanized mice.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0043624},
doi = {10.1128/spectrum.00436-24},
pmid = {39162553},
issn = {2165-0497},
abstract = {The intact immune system of mice exhibits resistance to colonization by exogenous microorganisms, but the gut microbiota profiles of the humanized mice and the patterns of human fecal microbiota colonization remain unexplored. Humanized NCG (huNCG) mice were constructed by injected CD34 +stem cells. 16S rRNA sequencing and fecal microbiota transplantation (FMT) technologies were used to detect the differences in microbiota and selective colonization ability for exogenous community colonization among three mice cohorts (C57BL/6J, NCG, and huNCG). Flow cytometry analysis showed that all huNCG mice had over 25% hCD45 +in peripheral blood. 16S rRNA gene sequence analysis showed that compared with NCG mice, the gut microbiota of huNCG mice were significantly altered. After FMT, the principal coordinates analysis (PCoA) showed that the gut microbial composition of huNCG mice (huNCG-D9) was similar to that of donors. The relative abundance of Firmicutes and Bacteroidetes were significantly increased in huNCG mice compared to NCG mice. Further comparison of ASV sequences revealed that Bacteroides plebeius, Bacteroides finegoldii, Escherichia fergusonii, Escherichia albertii, Klebsiella pneumoniae, and Klebsiella variicola exhibited higher abundance and stability in huNCG mice after FMT. Furthermore, PICRUSt2 analysis showed that huNCG mice had significantly enhanced metabolism and immunity. This study demonstrated that humanized mice are more conducive to colonization within the human gut microbiota, which provides a good method for studying the association between human diseases and microbiota.IMPORTANCEThe gut microbiota and biomarkers of humanized mice are systematically revealed for the first time. The finding that human fecal microbiota colonize humanized mice more stably provides new insights into the study of interactions between immune responses and gut microbiota.},
}

@article {pmid39162211,
year = {2024},
author = {Zhang, H and Xiao, Y and Wen, Q and Zhang, S and Li, P and Marcella, C and Hu, B and Liu, H and Zhang, F and Cui, B},
title = {Washed microbiota transplantation improved the level of serum vitamin D in ulcerative colitis.},
journal = {Journal of gastroenterology and hepatology},
volume = {},
number = {},
pages = {},
doi = {10.1111/jgh.16717},
pmid = {39162211},
issn = {1440-1746},
support = {81600417//National Natural Science Foundation of China/ ; BK20211384//Natural Science Foundation of Jiangsu Province/ ; YKK23284//Nanjing Health Technology Development Project/ ; //Nanjing Medical University Fan Daiming Research Funds for Holistic Integrative Medicine/ ; },
abstract = {BACKGROUND AND AIM: Vitamin D (VD) deficiency was reported to correlate with ulcerative colitis (UC) activity, which might be closely related to gut microbiota dysbiosis. This study aims to investigate the effects of washed microbiota transplantation (WMT) on VD metabolism in UC.

METHODS: The serum levels of 25-hdroxyvitamin D [25(OH)D] in 121 patients with UC and 53 healthy controls (HC) were detected. Subsequently, a non-randomized control trial (non-RCT) was conducted. Patients with UC were non-randomly assigned to undergo WMT (n = 28) vs. conventional treatment (5-aminosalicylic acid, 5-ASA, n = 10). Serum levels of 25(OH)D, fecal microbiota, and the expression of vitamin D receptor (VDR) in patients with UC were evaluated with a 3-month follow-up.

RESULTS: Serum VD levels collected in the clinic practice indicated that patients with UC had significantly lower VD levels than HC (P < 0.001). In the non-RCT, serum 25(OH)D level and VDR expression significantly increased (P = 0.011, 0.026, respectively) in the WMT group, while no noticeable changes were observed in the non-WMT group. Microbiome profiling revealed that the increase in VD levels after WMT was positively associated with the abundances of Adlercreutzia_equolifaciens, Ruminococcus_obeum, and Dorea but negatively correlated with Escherichia.

CONCLUSIONS: The study suggested that WMT increases the levels of VD with characteristic changes of specific microbiota, which indicated the association between the VD and the activity of UC might be regulated by gut microbiota.},
}

@article {pmid39161885,
year = {2024},
author = {Wang, J and Yuan, ZY and Wang, XY and Zhu, JX and Huang, WF and Xu, GH and Yi, LT},
title = {Anthocyanins-rich cranberry extract attenuates DSS-induced IBD in an intestinal flora independent manner.},
journal = {Current research in food science},
volume = {9},
number = {},
pages = {100815},
pmid = {39161885},
issn = {2665-9271},
abstract = {Cranberry is abundantly rich in anthocyanins, a type of flavonoid with potent antioxidant properties and the resistance against certain diseases. In this study, anthocyanin-rich cranberry extract was extracted, purified, and its components were analyzed. 92.18 % of anthocyanins was obtained and the total content of anthocyanins was 302.62 mg/g after AB-8 resin purification. Quantification analysis showed that the extract mainly contained cyanidin-3-galactoside, procyanidin B2 and procyanidin B4. Then we explored its effects on dextran sulfate sodium (DSS)-induced inflammatory bowel disease (IBD) in mice. The supplementation of cranberry extract resulted in an alleviation of IBD symptoms, evidenced by improvements in the disease activity index (DAI), restoration of colon length and colonic morphology. Cranberry extract reversed the elevated iron and malondialdehyde (MDA) levels and restored glutathione (GSH) levels in IBD mice. Further analysis revealed that cranberry modulated ferroptosis-associated genes and reduced expression of pro-inflammatory cytokines. Although cranberry influenced the intestinal flora balance by reducing Proteobacteria and Escherichia-Shigella, and increasing Lactobacillus, as well as enhancing SCFAs content, these effects were not entirely dependent on intestinal flora modulation, as indicated by antibiotic intervention and fecal microbiota transplantation (FMT) experiments. In conclusion, our findings suggest that the beneficial impact of cranberry extract on IBD may primarily involve the regulation of colonic ferroptosis, independent of significant alterations in intestinal flora.},
}

@article {pmid39096665,
year = {2024},
author = {Garg, P and Bhasin, SL and Malhotra, P and Rana, SS and Singh, S and Sethi, J and Sehgal, R and Khurana, S and Datta, P},
title = {Multiplex PCR for gastrointestinal parasites in stool: Benchmarking against direct microscopy and simplex PCR.},
journal = {Diagnostic microbiology and infectious disease},
volume = {110},
number = {2},
pages = {116475},
doi = {10.1016/j.diagmicrobio.2024.116475},
pmid = {39096665},
issn = {1879-0070},
mesh = {Humans ; *Feces/parasitology ; *Multiplex Polymerase Chain Reaction/methods ; *Sensitivity and Specificity ; *Microscopy/methods ; *Giardia lamblia/genetics/isolation & purification ; Adult ; *Entamoeba histolytica/genetics/isolation & purification ; Female ; Male ; Middle Aged ; Cryptosporidium/genetics/isolation & purification ; Child ; Young Adult ; Child, Preschool ; Intestinal Diseases, Parasitic/diagnosis/parasitology ; Adolescent ; Benchmarking ; Coinfection/parasitology/diagnosis ; Aged ; Diarrhea/parasitology/diagnosis ; Giardiasis/diagnosis/parasitology ; Molecular Diagnostic Techniques/methods ; Infant ; },
abstract = {PURPOSE: To develop and validate a multiplex conventional PCR assay to simultaneously detect Cryptosporidium spp., Entamoeba histolytica, and Giardia lamblia in diarrheal samples as a rapid, cost-effective, and sensitive diagnostic tool for prevalent co-infections for improved diagnostic accuracy and efficiency in resource-limited settings.

METHODS: Stool samples collected from patients with gastrointestinal symptoms after taking written consent, processed via wet mount, iodine mount, and PCR assays. Cohen's kappa statistical analysis was done to test agreement.

RESULT: Among 240 patients, 28.75% showed intestinal protozoa via Microscopy; Single-plex and multiplex PCR demonstrated 100% concordance, detecting 27.9%; confirmed by sequencing. Highest parasite positivity was observed in transplant and immunocompromised patients, with moderate to almost perfect agreement between microscopy and molecular methods.

CONCLUSION: Multiplex-conventional PCR offers superior sensitivity and specificity over microscopy and 100% concordance with single-plex PCR, enabling rapid, cost-effective diagnosis of multiple parasites from single stool sample. Its adoption could revolutionize parasitic infection management in routine diagnostics.},
}

Humans
*Feces/parasitology
*Multiplex Polymerase Chain Reaction/methods
*Sensitivity and Specificity
*Microscopy/methods
*Giardia lamblia/genetics/isolation & purification
Adult
*Entamoeba histolytica/genetics/isolation & purification
Female
Male
Middle Aged
Cryptosporidium/genetics/isolation & purification
Child
Young Adult
Child, Preschool
Intestinal Diseases, Parasitic/diagnosis/parasitology
Adolescent
Benchmarking
Coinfection/parasitology/diagnosis
Aged
Diarrhea/parasitology/diagnosis
Giardiasis/diagnosis/parasitology
Molecular Diagnostic Techniques/methods
Infant

@article {pmid39161797,
year = {2024},
author = {Taha, AM and Abouelmagd, K and Nada, SA and Mahmoud, AM and Nguyen, D and Sharma, S and Elewa, M},
title = {Impact of fecal microbiota transplantation in severe alcoholic hepatitis: A systematic review and meta-analysis.},
journal = {JGH open : an open access journal of gastroenterology and hepatology},
volume = {8},
number = {8},
pages = {e70007},
pmid = {39161797},
issn = {2397-9070},
abstract = {BACKGROUND AND AIM: Severe alcoholic hepatitis (SAH) is a serious condition with few treatments. By modifying the gut-liver axis, fecal microbiota transplantation (FMT) was proposed as a treatment for SAH. The purpose of this meta-analysis was to evaluate the efficacy of FMT versus the standard of care (SOC) in improving SAH patient survival rates.

METHODS: A thorough search of electronic databases was conducted till September 2023. The survival rates of SAH patients undergoing FMT versus SOC were compared. Using Review Manager 5.4, odds ratios (ORs) with 95% confidence intervals (CIs) were calculated.

RESULTS: The meta-analysis consisted of six studies with a total of 371 patients with SAH. Patients who received FMT had significantly higher survival rates at 1 and 3 months compared to those who received SOC, with pooled OR of 2.91 (95% CI: 1.56-5.42, P = 0.0008) and 3.07 (95% CI: 1.81-5.20, P < 0.0001), respectively. However, the survival advantage disappeared after 6 months (OR: 2.96, 95% CI: 0.99-8.85, P = 0.05) and 1 year of follow-up (OR: 1.81, 95% CI: 0.44-7.46, P = 0.41).

CONCLUSION: This meta-analysis highlights the potential of FMT to significantly improve short-term survival rates in SAH patients. However, the survival benefit did not last 6-12 months. These findings call for additional research into the effectiveness of FMT over the long term, along with strategies for extending the survival benefit.},
}

@article {pmid39161161,
year = {2024},
author = {Yang, H and Shao, Y and Hu, Y and Qian, J and Wang, P and Tian, L and Ni, Y and Li, S and Al-Nusaif, M and Liu, C and Le, W},
title = {Fecal microbiota from patients with Parkinson's disease intensifies inflammation and neurodegeneration in A53T mice.},
journal = {CNS neuroscience & therapeutics},
volume = {30},
number = {8},
pages = {e70003},
pmid = {39161161},
issn = {1755-5949},
support = {YDZX20213100001002//Shanghai Municipal Central Government Funds for Guiding Local Scientific and Technological Development/ ; 32220103006//National Nature Science Foundation of China/ ; 82271524//National Nature Science Foundation of China/ ; },
mesh = {Animals ; Mice ; *Parkinson Disease/microbiology/metabolism ; Humans ; *Fecal Microbiota Transplantation ; *Gastrointestinal Microbiome/physiology ; Male ; Inflammation/metabolism/microbiology ; Feces/microbiology ; Mice, Transgenic ; Mice, Inbred C57BL ; Female ; alpha-Synuclein/metabolism ; Brain/metabolism/pathology ; },
abstract = {AIMS: We evaluated the potential of Parkinson's disease (PD) fecal microbiota transplantation to initiate or exacerbate PD pathologies and investigated the underlying mechanisms.

METHODS: We transplanted the fecal microbiota from PD patients into mice by oral gavage and assessed the motor and intestinal functions, as well as the inflammatory and pathological changes in the colon and brain. Furthermore, 16S rRNA gene sequencing combined with metabolomics analysis was conducted to assess the impacts of fecal delivery on the fecal microbiota and metabolism in recipient mice.

RESULTS: The fecal microbiota from PD patients increased intestinal inflammation, deteriorated intestinal barrier function, intensified microglia and astrocyte activation, abnormal deposition of α-Synuclein, and dopaminergic neuronal loss in the brains of A53T mice. A mechanistic study revealed that the fecal microbiota of PD patients stimulated the TLR4/NF-κB/NLRP3 pathway in both the brain and colon. Additionally, multiomics analysis found that transplantation of fecal microbiota from PD patients not only altered the composition of the gut microbiota but also influenced the fecal metabolic profile of the recipient mice.

CONCLUSION: The fecal microbiota from PD patients intensifies inflammation and neurodegeneration in A53T mice. Our findings demonstrate that imbalance and dysfunction in the gut microbiome play significant roles in the development and advancement of PD.},
}

Animals
Mice
*Parkinson Disease/microbiology/metabolism
Humans
*Fecal Microbiota Transplantation
*Gastrointestinal Microbiome/physiology
Male
Inflammation/metabolism/microbiology
Feces/microbiology
Mice, Transgenic
Mice, Inbred C57BL
Female
alpha-Synuclein/metabolism
Brain/metabolism/pathology

@article {pmid39161102,
year = {2024},
author = {Fasano, A and Chassaing, B and Haller, D and Flores Ventura, E and Carmen-Collado, M and Pastor, N and Koren, O and Berni Canani, R},
title = {Microbiota during pregnancy and early life: role in maternal-neonatal outcomes based on human evidence.},
journal = {Gut microbes},
volume = {16},
number = {1},
pages = {2392009},
doi = {10.1080/19490976.2024.2392009},
pmid = {39161102},
issn = {1949-0984},
mesh = {Humans ; Pregnancy ; Female ; Infant, Newborn ; *Gastrointestinal Microbiome ; Milk, Human/microbiology ; Fecal Microbiota Transplantation ; Infant ; Host Microbial Interactions ; },
abstract = {Here, we explored the vast potential of microbiome-based interventions in preventing and managing non-communicable diseases including obesity, diabetes, allergies, celiac disease, inflammatory bowel diseases, malnutrition, and cardiovascular diseases across different life stages. We discuss the intricate relationship between microbiome and non-communicable diseases, emphasizing on the "window of opportunity" for microbe-host interactions during the first years after birth. Specific biotics and also live biotherapeutics including fecal microbiota transplantation emerge as pivotal tools for precision medicine, acknowledging the "one size doesn't' fit all" aspect. Challenges in implementation underscore the need for advanced technologies, scientific transparency, and public engagement. Future perspectives advocate for understanding maternal-neonatal microbiome, exploring the maternal exposome and delving into human milk's role in the establishment and restoration of the infant microbiome and its influence over health and disease. An integrated scientific approach, employing multi-omics and accounting for inter-individual variance in microbiome composition and function appears central to unleash the full potential of early-life microbiome interventions in revolutionizing healthcare.},
}

Humans
Pregnancy
Female
Infant, Newborn
*Gastrointestinal Microbiome
Milk, Human/microbiology
Fecal Microbiota Transplantation
Infant
Host Microbial Interactions

@article {pmid39159270,
year = {2024},
author = {Romaní-Pérez, M and Líebana-García, R and Flor-Duro, A and Bonillo-Jiménez, D and Bullich-Vilarrubias, C and Olivares, M and Sanz, Y},
title = {Obesity and the gut microbiota: implications of neuroendocrine and immune signaling.},
journal = {The FEBS journal},
volume = {},
number = {},
pages = {},
doi = {10.1111/febs.17249},
pmid = {39159270},
issn = {1742-4658},
support = {//The European Commission - NextGeneration EU/ ; CEX2021-001189-S//Spanish Ministry of Science and Innovation/ ; PID2020-119536RB-I00//Spanish Ministry of Science and Innovation/ ; },
abstract = {Obesity is a major health challenge due to its high prevalence and associated comorbidities. The excessive intake of a diet rich in fat and sugars leads to a persistent imbalance between energy intake and energy expenditure, which increases adiposity. Here, we provide an update on relevant diet-microbe-host interactions contributing to or protecting from obesity. In particular, we focus on how unhealthy diets shape the gut microbiota and thus impact crucial intestinal neuroendocrine and immune system functions. We describe how these interactions promote dysfunction in gut-to-brain neuroendocrine pathways involved in food intake control and postprandial metabolism and elevate the intestinal proinflammatory tone, promoting obesity and metabolic complications. In addition, we provide examples of how this knowledge may inspire microbiome-based interventions, such as fecal microbiota transplants, probiotics, and biotherapeutics, to effectively combat obesity-related disorders. We also discuss the current limitations and gaps in knowledge of gut microbiota research in obesity.},
}

@article {pmid39158846,
year = {2024},
author = {Chen, J and Song, YU and Zeng, W and Wang, L and Qin, J and Fang, L and Ding, Y},
title = {Research progress on the role of gut microbiota and its metabolites in the occurrence and development of septic-associated liver injury.},
journal = {Shock (Augusta, Ga.)},
volume = {},
number = {},
pages = {},
doi = {10.1097/SHK.0000000000002441},
pmid = {39158846},
issn = {1540-0514},
abstract = {Sepsis is a life-threatening organ dysfunction that occurs due to a dysregulated host response to infection. Septic-associated liver injury (SALI) has been closely linked to the prognosis and mortality of sepsis. Recent investigations have delved into the gut-liver axis and its association with SALI, identifying its pivotal role in the gut microbiota. Bacterial translocation and the onset of SALI can occur due to an imbalance in the gut microbiota, impairing the function of the gut barrier. Moreover, their metabolites might exacerbate or initiate SALI by modulating immune responses. Nevertheless, interventions to restore the balance of the gut microbiota, such as the administration of probiotics, fecal microbiota transplantation, or dietary adjustments, may ameliorate SALI and enhance the prognosis and survival rates of septic patients. This review aimed to elucidate the function of the gut microbiota in the genesis and procession of SALI and its potential therapeutic value, offering a deeper understanding of the pathogenesis and therapeutic avenues for SALI.},
}

@article {pmid39158277,
year = {2024},
author = {Cabirol, A and Chhun, A and Liberti, J and Kesner, L and Neuschwander, N and Schaerli, Y and Engel, P},
title = {Fecal transplant allows transmission of the gut microbiota in honey bees.},
journal = {mSphere},
volume = {},
number = {},
pages = {e0026224},
doi = {10.1128/msphere.00262-24},
pmid = {39158277},
issn = {2379-5042},
abstract = {UNLABELLED: The study of the fecal microbiota is crucial for unraveling the pathways through which gut symbionts are acquired and transmitted. While stable gut microbial communities are essential for honey bee health, their modes of acquisition and transmission are yet to be confirmed. The gut of honey bees is colonized by symbiotic bacteria within 5 days after emergence from their wax cells as adults. Few studies have suggested that bees could be colonized in part via contact with fecal matter in the hive. However, the composition of the fecal microbiota is still unknown. It is particularly unclear whether all bacterial species can be found viable in the feces and can therefore be transmitted to newborn nestmates. Using 16S rRNA gene amplicon sequencing, we revealed that the composition of the honey bee fecal microbiota is strikingly similar to the microbiota of entire guts. We found that fecal transplantation resulted in gut microbial communities similar to those obtained from feeding gut homogenates. Our study shows that fecal sampling and transplantation are viable tools for the non-invasive analysis of bacterial community composition and host-microbe interactions. It also implies that contact of young bees with fecal matter in the hive is a plausible route for gut microbiota acquisition.

IMPORTANCE: Honey bees are crucial pollinators for many crops and wildflowers. They are also powerful models for studying microbiome-host interactions. However, current methods rely on gut tissue disruption to analyze microbiota composition and use gut homogenates to inoculate microbiota-deprived bees. Here, we provide two new and non-invasive approaches that will open doors to longitudinal studies: fecal sampling and transplantation. Furthermore, our findings provide insights into gut microbiota transmission in social insects by showing that ingestion of fecal matter can result in gut microbiota acquisition.},
}

@article {pmid39157730,
year = {2024},
author = {Ceccon, M and Kantsjö, JB and Ronchi, F},
title = {Personalized Paths: Unlocking Alzheimer's via the Gut-Brain Axis.},
journal = {Visceral medicine},
volume = {40},
number = {4},
pages = {194-209},
pmid = {39157730},
issn = {2297-4725},
abstract = {BACKGROUND: Alzheimer's disease (AD) is characterised by abnormal protein aggregates in the brain that lead to cognitive decline. While current therapies only treat symptoms, disease-modifying treatments are urgently needed. Studies suggest that the composition of the microbiota is altered in people with AD, suggesting a link between gut bacteria and AD-related brain changes.

SUMMARY: In our narrative review, we explore various microbial interventions, such as faecal microbiota transplantation, probiotics, and diet, as powerful potential treatments. Studies suggest changes in microbiota composition following these interventions, with some beneficial effects on cognitive function. However, the mechanism of action of these microbial interventions is still unknown.

KEY MESSAGE: Our aim was to highlight the importance of personalised approaches, taking into account individual metabolic and microbiome profiles. We try to address gaps in current research and emphasise the need for microbiota analysis at different stages of the disease and its integration with clinical parameters and lifestyle information for a comprehensive understanding of AD progression (summarised in online suppl. Fig. 1; for all online suppl. material, see https://doi.org/10.1159/000535869).},
}

@article {pmid39155775,
year = {2024},
author = {Jarasvaraparn, C and Rodrigo, M and Hartley, C and Karnsakul, W},
title = {Exploring Odevixibat's efficacy in alagille syndrome: insights from recent clinical trials and IBAT Inhibitor Experiences.},
journal = {Expert opinion on pharmacotherapy},
volume = {},
number = {},
pages = {},
doi = {10.1080/14656566.2024.2392873},
pmid = {39155775},
issn = {1744-7666},
abstract = {INTRODUCTION: Alagille syndrome (ALGS) is a rare, genetic, multisystem disorder commonly associated with cholestatic liver disease; patients with ALGS may experience elevated serum bile acids and severe pruritus with associated impaired sleep. The ileal bile acid transporter (IBAT) is located on the luminal surface of enterocytes in the terminal ileum; this transport protein mediates resorption of conjugated bile acids for recirculation back to the liver. Inhibition of IBAT disrupts the enterohepatic circulation and leads to fecal elimination of bile acids.

AREAS COVERED: Here, the role of odevixibat as a novel, nonsurgical approach to interrupting the enterohepatic circulation from the intestine by inhibition of IBAT is reviewed, specifically in reference to currently available data on pharmacologic IBAT inhibition. IBAT inhibition has been shown to reduce serum bile acids and pruritus in trials of cholestatic liver diseases in children including ALGS.

EXPERT OPINION: Odevixibat or IBAT inhibitor should be considered as a first-line treatment for ALGS to improve pruritis, quality of life and liver-related outcomes including absence of liver transplant, surgical biliary diversion, hepatic decompensation, and death.},
}

@article {pmid39154362,
year = {2024},
author = {Feng, R and Yang, W and Feng, W and Huang, X and Cen, M and Peng, G and Wu, W and Wang, Z and Jing, Y and Long, T and Liu, Y and Li, Z and Chang, G and Huang, K},
title = {Time-restricted feeding ameliorates non-alcoholic fatty liver disease through modulating hepatic nicotinamide metabolism via gut microbiota remodeling.},
journal = {Gut microbes},
volume = {16},
number = {1},
pages = {2390164},
pmid = {39154362},
issn = {1949-0984},
mesh = {Animals ; *Non-alcoholic Fatty Liver Disease/metabolism/microbiology ; *Gastrointestinal Microbiome ; Mice ; *Liver/metabolism ; *Diet, High-Fat/adverse effects ; Male ; *Niacinamide/metabolism ; *Mice, Inbred C57BL ; Disease Models, Animal ; Lipid Metabolism ; Aldehyde Oxidase/metabolism ; Lipogenesis ; Hepatocytes/metabolism ; Humans ; },
abstract = {Non-alcoholic fatty liver disease (NAFLD) has emerged as a global health concern, lacking specific therapeutic strategies. Time-restricted feeding (TRF) regimen demonstrated beneficial effects in NAFLD; however, the underlying mechanisms remain unclear. In this study, we established a NAFLD mouse model through a high-fat diet (HFD) and implemented the 16:8 TRF regimen for a duration of 6 weeks. We demonstrated that TRF remarkably alleviated hepatic steatosis in HFD mice. Of note, aldehyde oxidase 1 (AOX1), a key enzyme in hepatic nicotinamide (NAM) catabolism, exhibited apparent upregulation in response to HFD, leading to abnormal accumulation of N-Methyl-6-pyridone-3-carboxamide (N-Me-6-PY, also known as 2PY) and N-Methyl-4-pyridone-5-carboxamide (N-Me-4-PY, also known as 4PY), whereas it was almost restored by TRF. Both N-Me-6-PY and N-Me-4-PY promoted de novo lipogenesis and fatty acid uptake capacities in hepatocyte, and aggravated hepatic steatosis in mice either fed chow diet or HFD. In contrast, pharmacological inhibition of AOX1 was sufficient to ameliorate the hepatic steatosis and lipid metabolic dysregulation induced by HFD. Moreover, transplantation of fecal microbiota efficiently mimicked the modulatory effect of TRF on NAM metabolism, thus mitigating hepatic steatosis and lipid metabolic disturbance, suggesting a gut microbiota-dependent manner. In conclusion, our study reveals the intricate relationship between host NAM metabolic modification and gut microbiota remodeling during the amelioration of NAFLD by TRF, providing promising insights into the prevention and treatment of NAFLD.},
}

Animals
*Non-alcoholic Fatty Liver Disease/metabolism/microbiology
*Gastrointestinal Microbiome
Mice
*Liver/metabolism
*Diet, High-Fat/adverse effects
Male
*Niacinamide/metabolism
*Mice, Inbred C57BL
Disease Models, Animal
Lipid Metabolism
Aldehyde Oxidase/metabolism
Lipogenesis
Hepatocytes/metabolism
Humans

@article {pmid39153277,
year = {2024},
author = {Huang, Y and Chen, H and Chen, J and Wu, Q and Zhang, W and Li, D and Lu, Y and Chen, Y},
title = {Yellow tea polysaccharides protect against non-alcoholic fatty liver disease via regulation of gut microbiota and bile acid metabolism in mice.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {133},
number = {},
pages = {155919},
doi = {10.1016/j.phymed.2024.155919},
pmid = {39153277},
issn = {1618-095X},
abstract = {BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is a major clinical and global public health issue, with no specific pharmacological treatment available. Currently, there is a lack of approved drugs for the clinical treatment of NAFLD. Large-leaf yellow tea polysaccharides (YTP) is a natural biomacromolecule with excellent prebiotic properties and significant therapeutic effects on multiple metabolic diseases. However, the specific mechanisms by which YTP regulates NAFLD remain unclear.

PURPOSE: This study aims to explore the prebiotic effects of YTP and the potential mechanisms by which it inhibits hepatic cholesterol accumulation in NAFLD mice.

METHODS: The effects of YTP on lipid accumulation were evaluated in NAFLD mice through obesity trait analysis and bile acids (BAs) metabolism assessment. Additionally, fecal microbiota transplantation (FMT) was performed, and high-throughput sequencing was employed to investigate the mechanisms underlying YTP's regulatory effects on gut microbiota and BA metabolism.

RESULTS: Our study demonstrated that YTP altered the constitution of colonic BA, particularly increasing the levels of conjugated BA and non-12OH BA, which suppressed ileum FXR receptors and hepatic BA reabsorption, facilitated BA synthesis, and fecal BA excretion. The modifications were characterized by a decrease in the levels of FXR, FGF15, FGFR4, and ASBT proteins, and an increase in the levels of Cyp7a1 and Cyp27a1 proteins. YTP might affect enterohepatic circulation and by the activated the hepatic FXR-SHP pathway. Meanwhile, YTP reshaped the intestinal microbiome structure by decreasing BSH-producing genera and increasing taurine metabolism genera. The correlation analysis implied that Muribaculaceae, Pseudomonas, acterium_coprostanoligenes_group, Clostridiales, Lachnospiraceae_NK4A136_group, Delftia, Dubosiella, and Romboutsia were strongly correlated with specific BA monomers.

CONCLUSIONS: YTP modulates bile salt hydrolase-related microbial genera to activate alternative bile acid synthesis pathways, thereby inhibiting NAFLD progression. These results suggest that YTP may serve as a potential probiotic formulation, offering a feasible dietary intervention for NAFLD.},
}

@article {pmid39152200,
year = {2024},
author = {Han, Z and Sun, J and Jiang, B and Chen, K and Ge, L and Sun, Z and Wang, A},
title = {Fecal microbiota transplantation accelerates restoration of florfenicol-disturbed intestinal microbiota in a fish model.},
journal = {Communications biology},
volume = {7},
number = {1},
pages = {1006},
pmid = {39152200},
issn = {2399-3642},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Thiamphenicol/analogs & derivatives/pharmacology ; *Fecal Microbiota Transplantation ; *Dysbiosis/therapy/microbiology ; *Anti-Bacterial Agents/pharmacology/adverse effects ; Carps/microbiology ; Bacteria/metabolism/drug effects ; },
abstract = {Antibiotic-induced dysbiosis in the fish gut causes significant adverse effects. We use fecal microbiota transplantation (FMT) to accelerate the restoration of florfenicol-perturbed intestinal microbiota in koi carp, identifying key bacterial populations and metabolites involved in the recovery process through microbiome and metabolome analyses. We demonstrate that florfenicol disrupts intestinal microbiota, reducing beneficial genera such as Lactobacillus, Bifidobacterium, Bacteroides, Romboutsia, and Faecalibacterium, and causing mucosal injuries. Key metabolites, including aromatic amino acids and glutathione-related compounds, are diminished. We show that FMT effectively restores microbial populations, repairs intestinal damage, and normalizes critical metabolites, while natural recovery is less effective. Spearman correlation analyses reveal strong associations between the identified bacterial genera and the levels of aromatic amino acids and glutathione-related metabolites. This study underscores the potential of FMT to counteract antibiotic-induced dysbiosis and maintain fish intestinal health. The restored microbiota and normalized metabolites provide a basis for developing personalized probiotic therapies for fish.},
}

Animals
*Gastrointestinal Microbiome/drug effects
*Thiamphenicol/analogs & derivatives/pharmacology
*Fecal Microbiota Transplantation
*Dysbiosis/therapy/microbiology
*Anti-Bacterial Agents/pharmacology/adverse effects
Carps/microbiology
Bacteria/metabolism/drug effects

@article {pmid39150086,
year = {2024},
author = {Di Stefano, M},
title = {Fecal Microbiota Transplantation in the Treatment of Severe Constipation in Children: Is It the Future?.},
journal = {The American journal of gastroenterology},
volume = {},
number = {},
pages = {},
pmid = {39150086},
issn = {1572-0241},
}

@article {pmid39147234,
year = {2024},
author = {Li, Z and Sun, T and He, Z and Li, Z and Xiong, J and Xiang, H},
title = {Intestinal dysbacteriosis contributes to persistent cognitive impairment after resolution of acute liver failure.},
journal = {The American journal of pathology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ajpath.2024.07.014},
pmid = {39147234},
issn = {1525-2191},
abstract = {Regulating the gut microbiota alleviates hepatic encephalopathy (HE). It remains unclear whether it is imperative to withhold treatment for microbial imbalance after liver functional recovery. This work aims to elucidate the alterations in cognitive behavior, liver function, synaptic transmission, and brain metabolites in acute liver failure(ALF) mice before and after hepatic function recovery. Here, thioacetamide was injected intraperitoneally to establish an ALF mouse model, which induced HE. By performing hierarchical clustering analysis, we found that the liver functions normalized, but cognitive dysfunction and intestinal dysbacteriosis were found in the ALF mice 14 days after thioacetamide injection. Additionally, fecal microbiota transplant from the ALF mice with liver function recovery could induce liver injury and cognitive impairment. Moreover, we found alterations in synaptic transmission in the ALF mice with liver function improvement, and the correlations between the gut bacteria and synaptic transmission in the cortex were significant. Finally, we detected apparent alterations in the brain metabolic profiles of the ALF mice after liver function improvement by performing [1]H nuclear magnetic resonance spectroscopy, suggesting a risk of HE. These results showed that intestinal dysbacteriosis in ALF mice with liver function recovery is sufficient to induce liver injury and cognitive impairment. These results indicated continuous care may be necessary for monitoring microbial imbalance even in ALF-induced HE patients whose liver function has recovered significantly.},
}

@article {pmid39146793,
year = {2024},
author = {Sartor, RB},
title = {Microbiome modification for personalized treatment of dysbiotic diseases.},
journal = {Cell host & microbe},
volume = {32},
number = {8},
pages = {1219-1224},
doi = {10.1016/j.chom.2024.07.023},
pmid = {39146793},
issn = {1934-6069},
support = {P01 DK094779/DK/NIDDK NIH HHS/United States ; P30 DK034987/DK/NIDDK NIH HHS/United States ; },
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; *Dysbiosis/therapy ; *Precision Medicine/methods ; *Gastrointestinal Microbiome ; Clostridium Infections/therapy/microbiology ; Inflammation ; Clostridioides difficile ; Biomarkers ; },
abstract = {Fecal microbial transplantation (FMT) for inflammatory diseases or refractory immune checkpoint inhibitor therapy is less effective than for preventing recurrent Clostridioides difficile infection. This commentary outlines strategies to use biomarkers of successful FMT to guide newer approaches to restore microbial homeostasis in individuals with dysbiosis-mediated inflammation.},
}

Humans
*Fecal Microbiota Transplantation/methods
*Dysbiosis/therapy
*Precision Medicine/methods
*Gastrointestinal Microbiome
Clostridium Infections/therapy/microbiology
Inflammation
Clostridioides difficile
Biomarkers

@article {pmid39146792,
year = {2024},
author = {Chambers, L and Grencewicz, D and Spakowicz, D},
title = {From poo to promise: Fecal microbiota transplants support immunotherapy re-sensitization in solid tumors.},
journal = {Cell host & microbe},
volume = {32},
number = {8},
pages = {1217-1218},
doi = {10.1016/j.chom.2024.07.015},
pmid = {39146792},
issn = {1934-6069},
mesh = {*Fecal Microbiota Transplantation/methods ; Humans ; *Immunotherapy/methods ; Immune Checkpoint Inhibitors/therapeutic use ; Gastrointestinal Microbiome/immunology ; Melanoma/therapy/immunology ; Neoplasms/therapy/immunology ; Esophageal Neoplasms/therapy/immunology/microbiology ; Carcinoma, Hepatocellular/therapy/immunology/microbiology ; Liver Neoplasms/therapy/immunology ; Animals ; Feces/microbiology ; },
abstract = {Fecal microbiota transplants (FMTs) recently entered the cancer therapeutics field as a method to resensitize treatment-resistant melanoma patients to immune checkpoint inhibitors (ICIs). In this issue of Cell Host & Microbe, Kim and colleagues extend its utility to other solid tumors, including esophageal and hepatocellular carcinomas.[1].},
}

*Fecal Microbiota Transplantation/methods
Humans
*Immunotherapy/methods
Immune Checkpoint Inhibitors/therapeutic use
Gastrointestinal Microbiome/immunology
Melanoma/therapy/immunology
Neoplasms/therapy/immunology
Esophageal Neoplasms/therapy/immunology/microbiology
Carcinoma, Hepatocellular/therapy/immunology/microbiology
Liver Neoplasms/therapy/immunology
Animals
Feces/microbiology

@article {pmid39141079,
year = {2024},
author = {Suárez-Carantoña, C and Corbacho-Loarte, MD and Del Campo Albendea, L and Kamel-Rey, S and Halperin, AV and Escudero-Sánchez, R and Ponce-Alonso, M and Moreno, S and Cobo, J},
title = {Is advanced age still a risk factor for recurrence of C. difficile infection in the era of new treatments?.},
journal = {Age and ageing},
volume = {53},
number = {8},
pages = {},
doi = {10.1093/ageing/afae182},
pmid = {39141079},
issn = {1468-2834},
mesh = {Humans ; Male ; Aged, 80 and over ; *Clostridium Infections/epidemiology/mortality/microbiology/therapy/diagnosis/drug therapy ; Female ; Retrospective Studies ; Risk Factors ; *Recurrence ; Aged ; Age Factors ; Fecal Microbiota Transplantation ; Anti-Bacterial Agents/therapeutic use ; Clostridioides difficile ; Middle Aged ; Fidaxomicin/therapeutic use ; Broadly Neutralizing Antibodies/therapeutic use ; Antibodies, Monoclonal ; },
abstract = {BACKGROUND: Advanced age has been widely identified as a risk factor for recurrent Clostridioides difficile infection (CDI), but most related studies were performed before the introduction of novel therapies. The aim of this study was to compare CDI characteristics and outcomes in patients over and under 80 years old with CDI and their outcomes in the era of new treatments.

METHODS: This was a retrospective cohort study of patients diagnosed with CDI from January 2021 to December 2022 in an academic hospital. We compared recurrence and mortality at 12 weeks after the end of treatment. An extension of the Fine and Grey model adjusted for competing events was used to assess the effect of age on recurrence.

RESULTS: Four hundred seventy-six patients were considered to have CDI (320 in patients <80 years and 156 in ≥80 years). CDI in older patients was more frequently healthcare-associated and was more severe. Although the Charlson index was almost identical between populations, comorbidities clearly differed. New treatments (bezlotoxumab, fidaxomicin and faecal microbiota transplantation) were more frequently used in older patients without statistical significance (41.3% vs. 33.4%, P = .053). There were 69 (14.5%) recurrences, with no differences by age group after adjusting for competing events. Mortality was greater in the oldest (35.3%) than in the youngest (13.1%); P < .001.

CONCLUSIONS: No differences in CDI recurrence rates were found between age groups. However, there was a high mortality rate in patients ≥80 years old, which emphasises the urgent need to improve the prevention and treatment of CDI in this group.},
}

Humans
Male
Aged, 80 and over
*Clostridium Infections/epidemiology/mortality/microbiology/therapy/diagnosis/drug therapy
Female
Retrospective Studies
Risk Factors
*Recurrence
Aged
Age Factors
Fecal Microbiota Transplantation
Anti-Bacterial Agents/therapeutic use
Clostridioides difficile
Middle Aged
Fidaxomicin/therapeutic use
Broadly Neutralizing Antibodies/therapeutic use
Antibodies, Monoclonal

@article {pmid39141021,
year = {2024},
author = {Mirzababaei, M and Babaei, F and Ghafghazi, S and Rahimi, Z and Asadi, S and Dargahi, L and Nassiri-Asl, M and Haghnazari, L},
title = {Saccharomyces Boulardii alleviates neuroinflammation and oxidative stress in PTZ-kindled seizure rat model.},
journal = {Naunyn-Schmiedeberg's archives of pharmacology},
volume = {},
number = {},
pages = {},
pmid = {39141021},
issn = {1432-1912},
support = {50000886//Kermanshah University of Medical Sciences/ ; },
abstract = {Previous research have reported that modulating the gut microbiome composition by fecal microbiota transplantation and probiotic administration can alleviate seizure occurrence and severity. Saccharomyces boulardii (SB) is a yeast probiotic that has demonstrated ameliorating effects on anxiety, memory and cognitive deficit, and brain amyloidogenesis. In this research, our goal was to examine the anti-seizure effects of SB on the pentylenetetrazole (PTZ)-kindled male Wistar rats. The animals were randomly categorized into four test groups. The rats were orally administered with saline (control and PTZ groups) or S. boulardii (SB + PTZ and SB groups) for 57 days. From the 29th day of the experiment, the animals received intraperitoneally saline (control and SB groups) or PTZ (PTZ and SB + PTZ groups) on alternate days for 30 days. The administration dose of SB and PTZ was 10[10] CFU/ml/day and 35 mg/kg, respectively. We assessed animal seizure behavior, neuroinflammation, oxidative stress, and the levels of matrix metalloproteinase-9 (MMP-9) and brain-derived neurotrophic factor (BDNF) in the hippocampus tissue. S. boulardii hindered the PTZ-induced kindling development. SB treatment elevated glutathione (GSH) and total antioxidant capacity (TAC) and reduced malondialdehyde (MDA) levels. SB also lessened the hippocampal levels of BDNF and MMP-9. Following SB supplementation, proinflammatory cytokines interleukin-1 beta (IL-1β) and IL-6 were lowered, and anti-inflammatory cytokine IL-10 was enhanced. Overall, our data indicated, for the first time, the positive impact of SB on the PTZ-kindled seizure rat model. The anti-seizure activity of SB was mediated by modulating oxidative stress, neuroinflammation, and MMP-9 and BDNF levels.},
}

@article {pmid39140343,
year = {2024},
author = {Wang, R and Huang, G and Li, S and Huang, H and Zhu, G and Wang, L and Yang, J and Yang, S and Jiang, Z and Zhang, W},
title = {Blueberry extract for the treatment of ischaemic stroke through regulating the gut microbiota and kynurenine metabolism.},
journal = {Phytotherapy research : PTR},
volume = {},
number = {},
pages = {},
doi = {10.1002/ptr.8300},
pmid = {39140343},
issn = {1099-1573},
support = {0001/2023/AKP//Science and Technology Development Fund, Macau SAR/ ; 006/2023/SKL//Science and Technology Development Fund, Macau SAR/ ; },
abstract = {Although the gut microbiota and kynurenine (KYN) metabolism have significant protective effects against ischaemic stroke (IS), the exact mechanism has yet to be fully elucidated. Combined serum metabolomics and 16S rRNA gene sequencing were used to reveal the differences between the gut microbiota and metabolites in rats treated with or without blueberry extract. Faecal microbiota transplantation (FMT) was employed to validate the protective role of the gut microbiota in IS. Furthermore, the interaction between Prevotella and IS was also confirmed in patients. Rats with IS experienced neurological impairments accompanied by an impaired intestinal barrier and disturbed intestinal flora, which further contributed to heightened inflammatory responses. Furthermore, Prevotella played a critical role in IS pathophysiology, and a positive correlation between Prevotella and KYN was detected. The role of KYN metabolism in IS was further demonstrated by the finding that IDO was significantly upregulated and that the use of the IDO inhibitor, attenuated KYN metabolic pathway activity and ameliorated neurological damage in rats with IS. Prevotella intervention also significantly improved stroke symptoms and decreasing KYN levels in rats with IS. FMT showed that the beneficial effects of blueberry extract on IS involve gut bacteria, especially Prevotella, which were confirmed by microbiological analyses conducted on IS patients. Moreover, blueberry extract led to significant changes in kynurenic acid levels and tryptophan and IDO levels through interactions with Prevotella. Our study demonstrates for the first time that blueberry extract could modulate "intestinal microecology-KYN metabolism" to improve IS.},
}

@article {pmid39139438,
year = {2024},
author = {Jing, L and Zhang, H and Xiang, Q and Hu, H and Zhai, C and Xu, S and Tian, H},
title = {Role of Trimethylamine N-Oxide in Heart Failure.},
journal = {Reviews in cardiovascular medicine},
volume = {25},
number = {7},
pages = {240},
pmid = {39139438},
issn = {2153-8174},
abstract = {Heart failure (HF) is a clinical syndrome characterizing by typical physical signs and symptomatology resulting from reduced cardiac output and/or intracardiac pressure at rest or under stress due to structural and/or functional abnormalities of the heart. HF is often the final stage of all cardiovascular diseases and a significant risk factor for sudden cardiac arrest, death, and liver or kidney failure. Current pharmacological treatments can only slow the progression and recurrence of HF. With advancing research into the gut microbiome and its metabolites, one such trimethylamine N-oxide (TMAO)-has been implicated in the advancement of HF and is correlated with poor prognosis in patients with HF. However, the precise role of TMAO in HF has not yet been clarified. This review highlights and concludes the available evidence and potential mechanisms associated with HF, with the hope of contributing new insights into the diagnosis and prevention of HF.},
}

@article {pmid39138075,
year = {2024},
author = {Yeom, M and Ahn, S and Hahm, DH and Jang, SY and Jang, SH and Park, SY and Jang, JH and Park, J and Oh, JY and Lee, IS and Kim, K and Kwon, SK and Park, HJ},
title = {Acupuncture ameliorates atopic dermatitis by modulating gut barrier function in a gut microbiota-dependent manner in mice.},
journal = {Journal of integrative medicine},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.joim.2024.07.004},
pmid = {39138075},
issn = {2095-4964},
abstract = {OBJECTIVE: Atopic dermatitis (AD) is a chronic inflammatory skin disease that may be linked to changes in the gut microbiome. Acupuncture has been proven to be effective in reducing AD symptoms without serious adverse events, but its underlying mechanism is not completely understood. The purpose of this study was to investigate whether the potential effect of acupuncture on AD is gut microbiota-dependent.

METHODS: AD-like skin lesions were induced by applying MC903 topically to the cheek of the mouse. Acupuncture was done at the Gok-Ji (LI11) acupoints. AD-like symptoms were assessed by lesion scores, scratching behavior, and histopathological changes; intestinal barrier function was measured by fecal output, serum lipopolysaccharide levels, histopathological changes, and mRNA expression of markers involved in intestinal permeability and inflammation. Gut microbiota was profiled using 16S rRNA gene sequencing from fecal samples.

RESULTS: Acupuncture effectively improved chronic itch as well as the AD-like skin lesions with epidermal thickening, and also significantly altered gut microbiota structure as revealed by β-diversity indices and analysis of similarities. These beneficial effects were eliminated by antibiotic depletion of gut microbiota, but were reproduced in gut microbiota-depleted mice that received a fecal microbiota transplant from acupuncture-treated mice. Interestingly, AD mice had intestinal barrier dysfunction as indicated by increased intestinal permeability, atrophy of the mucosal structure (reduced villus height and crypt depth), decreased expression of tight junctions and mucus synthesis genes, and increased expression of inflammatory mediators in the ileum. Acupuncture attenuated these abnormalities, which was gut microbiota-dependent.

CONCLUSION: Acupuncture ameliorates AD-like phenotypes in a gut microbiota-dependent manner and some of these positive benefits are explained by modulation of the intestinal barrier, providing new perspective for non-pharmacological strategies for modulating gut microbiota to prevent and treat AD. Please cite this article as: Yeom M, Ahn S, Hahm DH, Jang SY, Jang SH, Park SY, Jang JH, Park J, Oh JY, Lee IS, Kim K, Kwon SK, Park HJ. Acupuncture ameliorates atopic dermatitis by modulating gut barrier function in a gut microbiota-dependent manner in mice. J Integr Med. 2024; Epub ahead of print.},
}

@article {pmid39137736,
year = {2024},
author = {Cui, S and Huang, Q and Li, T and Shen, W and Chen, X and Sun, X},
title = {Reduction in renal interstitial fibrosis in aged male mice by intestinal microbiota rejuvenation.},
journal = {Gerontology},
volume = {},
number = {},
pages = {},
doi = {10.1159/000540839},
pmid = {39137736},
issn = {1423-0003},
abstract = {INTRODUCTION: Renal interstitial fibrosis is an important pathological basis for kidney ageing and the progression of ageing nephropathy. In the present research, we established an aged mouse model of faecal microbiota transplantation (FMT), identified the rejuvenation features of the kidney in aged male mice, and preliminarily analysed the possible mechanism by which the rejuvenation of the intestinal microbiota reduces renal interstitial fibrosis and delays senescence in aged male mice.

METHODS: We established an aged male mice model that was treated with FMT (FMT-Old) and a normal aged male mice control group (Old). Differentially expressed cytokines were identified using a cytokine array, and changes in protein expression related to signal transduction pathways in renal tissues were detected using a signalling pathway array. Senescence-associated β-galactosidase and Masson staining were performed to observe the degrees of renal senescence and tubule interstitial fibrosis. Immunohistochemistry was utilized to detect changes in the expression of the ageing markers p53 and p21 and the inflammation-related protein nuclear factor (NF) κB p65 subunit (RelA/p65).

RESULTS: The pathological features of renal senescence in the FMT-Old group were significantly alleviated, and the levels of the ageing indicators p53 and p21 were decreased (P < 0.05). Integrated predictive analysis revealed that six differentially expressed cytokines, macrophage inflammatory protein-3 beta (MIP-3β or CCL-19), E-selectin, Fas ligand, C-X-C motif chemokine 11 (CXCL-11 or I-TAC), CXCL-1 (keratinocyte-derived chemokine), and CCL-3 (MIP-1α) were related to a common upstream regulatory protein, RelA/p65, and the expression of this protein was significantly different between groups according to the signalling pathway array.

CONCLUSION: Our findings suggest that the intestinal microbiota regulates the renal microenvironment by reducing immune inflammatory responses through the inhibition of the NF-κB signalling pathway, thereby delaying renal senescence in aged male mice.},
}

@article {pmid39135690,
year = {2024},
author = {Li, J and Wang, SY and Yan, KX and Wang, P and Jiao, J and Wang, YD and Chen, ML and Dong, Y and Zhong, JC},
title = {Intestinal microbiota by angiotensin receptor blocker therapy exerts protective effects against hypertensive damages.},
journal = {iMeta},
volume = {3},
number = {4},
pages = {e222},
pmid = {39135690},
issn = {2770-596X},
abstract = {Dysbiosis of the gut microbiota has been implicated in hypertension, and drug-host-microbiome interactions have drawn considerable attention. However, the influence of angiotensin receptor blocker (ARB)-shaped gut microbiota on the host is not fully understood. In this work, we assessed the alterations of blood pressure (BP), vasculatures, and intestines following ARB-modified gut microbiome treatment and evaluated the changes in the intestinal transcriptome and serum metabolome in hypertensive rats. Hypertensive patients with well-controlled BP under ARB therapy were recruited as human donors, spontaneously hypertensive rats (SHRs) receiving normal saline or valsartan were considered animal donors, and SHRs were regarded as recipients. Histological and immunofluorescence staining was used to assess the aorta and small intestine, and 16S rRNA amplicon sequencing was performed to examine gut bacteria. Transcriptome and metabonomic analyses were conducted to determine the intestinal transcriptome and serum metabolome, respectively. Notably, ARB-modified fecal microbiota transplantation (FMT), results in marked decreases in systolic BP levels, collagen deposition and reactive oxygen species accumulation in the vasculature, and alleviated intestinal structure impairments in SHRs. These changes were linked with the reconstruction of the gut microbiota in SHR recipients post-FMT, especially with a decreased abundance of Lactobacillus, Aggregatibacter, and Desulfovibrio. Moreover, ARB-treated microbes contributed to increased intestinal Ciart, Per1, Per2, Per3, and Cipc gene levels and decreased Nfil3 and Arntl expression were detected in response to ARB-treated microbes. More importantly, circulating metabolites were dramatically reduced in ARB-FMT rats, including 6beta-Hydroxytestosterone and Thromboxane B2. In conclusion, ARB-modified gut microbiota exerts protective roles in vascular remodeling and injury, metabolic abnormality and intestinal dysfunctions, suggesting a pivotal role in mitigating hypertension and providing insights into the cross-talk between antihypertensive medicines and the gut microbiome.},
}

@article {pmid39135376,
year = {2024},
author = {Wang, J and Jiang, M and Li, X and Ye, Y and Xie, Y and Wu, T and Chen, Y and Yu, H and Wu, H and Yang, Z and Zhou, E},
title = {Inulin Supplementation Alleviates Ochratoxin A-Induced Kidney Injury through Modulating Intestinal Microbiota.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.4c04382},
pmid = {39135376},
issn = {1520-5118},
abstract = {Ochratoxin A (OTA) is a prevalent mycotoxin found in feed that causes significant kidney injury in animals. Further investigation was needed to devise strategies for treating OTA-induced kidney damage through the gut-kidney axis. Evidence indicates the crucial role of intestinal microbiota in kidney damage development. Inulin, a dietary fiber, protects kidneys by modulating intestinal microbiota and promoting short-chain fatty acid (SCFA) production. However, its precise mechanism in OTA-induced kidney damage remained unclear. In this study, chickens were orally administered OTA and inulin for 2 weeks to investigate inulin's effects on OTA-induced kidney damage and underlying mechanisms. The alteration of intestinal microbiota, SCFAs contents, and SCFA receptors was further analyzed. Results demonstrated that inulin supplementation influenced intestinal microbiota, increased SCFAs production, and mitigated OTA-induced kidney damage in chickens. The importance of microbiota in mediating inulin's renal protection was further confirmed by antibiotic and fecal microbiota transplantation experiments. Additionally, inulin exhibited antioxidant and anti-inflammatory properties, alleviating NLRP3 inflammasome activation and pyroptosis. In summary, inulin protected chickens from OTA-induced kidney damage, which might provide a potential strategy to mitigate the harmful effects of mycotoxins through prebiotics and safeguard renal health.},
}

@article {pmid39135306,
year = {2024},
author = {Zuo, S and Huang, Y and Zou, J},
title = {The role of the gut microbiome in modulating immunotherapy efficacy in colorectal cancer.},
journal = {IUBMB life},
volume = {},
number = {},
pages = {},
doi = {10.1002/iub.2908},
pmid = {39135306},
issn = {1521-6551},
support = {2023AH051777//Key Project in Natural Science Research in Higher Education Institutions of Anhui Province/ ; WK2022ZF29//Key Project of Natural Science Foundation of Wannan Medical College/ ; WHWJ2023z007//Key Research Project of Wuhu Municipal Health Commission/ ; DFJH2022018//Climbing Scientific Peak Project for Talents, the Second Affiliated Hospital of Wannan Medical College/ ; },
abstract = {This systematic literature review and meta-analysis provide an overview of the critical role of gut microbiota in modulating the efficacy of immunotherapy for colorectal cancer. Gut microbes influence host immune responses through multiple mechanisms including modulation of immune cell activity, metabolite action, and immune tolerance. The ability of specific gut microbes to improve the efficacy of immune checkpoint inhibitors has been linked to their ability to improve gut barrier function, modulate immune cell activity, and produce key immunomodulatory metabolites such as short-chain fatty acids. In addition, the composition and diversity of the gut microbiota are strongly associated with the efficacy of immunotherapies, demonstrating the potential to improve therapeutic response by modifying the gut microbiota. This paper also discusses the prospect of manipulating the gut microbiota through strategies such as fecal microbial transplantation, probiotic supplementation, and dietary modifications to optimize the efficacy of immunotherapy.},
}

@article {pmid39134825,
year = {2024},
author = {Ni, Y and Tong, Q and Xu, M and Gu, J and Ye, H},
title = {Gut Microbiota-Induced Modulation of the Central Nervous System Function in Parkinson's Disease Through the Gut-Brain Axis and Short-Chain Fatty Acids.},
journal = {Molecular neurobiology},
volume = {},
number = {},
pages = {},
pmid = {39134825},
issn = {1559-1182},
support = {Y20170064//Wenzhou Science and Technology Bureau Project/ ; },
abstract = {Recent insights into Parkinson's disease (PD), a progressive neurodegenerative disorder, suggest a significant influence of the gut microbiome on its pathogenesis and progression through the gut-brain axis. This study integrates 16S rRNA sequencing, high-throughput transcriptomic sequencing, and animal model experiments to explore the molecular mechanisms underpinning the role of gut-brain axis in PD, with a focus on short-chain fatty acids (SCFAs) mediated by the SCFA receptors FFAR2 and FFAR3. Our findings highlighted prominent differences in the gut microbiota composition between PD patients and healthy individuals, particularly in taxa such as Escherichia_Shigella and Bacteroidetes, which potentially impact SCFA levels through secondary metabolite biosynthesis. Notably, fecal microbiota transplantation (FMT) from healthy to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse models significantly improved motor function, enhanced dopamine and serotonin levels in the striatum, and increased the number of dopaminergic neurons in the substantia nigra while reducing glial cell activation. This therapeutic effect was associated with increased levels of SCFAs such as acetate, propionate, and butyrate in the gut of MPTP-lesioned mice. Moreover, transcriptomic analyses revealed upregulated expression of FFAR2 and FFAR3 in MPTP-lesioned mice, indicating their crucial role in mediating the benefits of FMT on the central nervous system. These results provide compelling evidence that gut microbiota and SCFAs play a critical role in modulating the gut-brain axis, offering new insights into PD's etiology and potential targets for therapeutic intervention.},
}

@article {pmid38019088,
year = {2024},
author = {Feuerstadt, P and Crawford, CV and Tan, X and Pokhilko, V and Bancke, L and Ng, S and Guthmueller, B and Bidell, MR and Tillotson, G and Johnson, S and Skinner, AM},
title = {Fecal Microbiota, Live-jslm for the Prevention of Recurrent Clostridioides difficile Infection : Subgroup Analysis of PUNCH CD2 and PUNCH CD3.},
journal = {Journal of clinical gastroenterology},
volume = {58},
number = {8},
pages = {818-824},
pmid = {38019088},
issn = {1539-2031},
support = {IK2 BX005609/BX/BLRD VA/United States ; },
mesh = {Humans ; *Clostridium Infections/prevention & control/microbiology ; Double-Blind Method ; *Fecal Microbiota Transplantation ; Male ; Female ; Middle Aged ; *Anti-Bacterial Agents/administration & dosage/adverse effects ; Adult ; *Clostridioides difficile/isolation & purification ; Aged ; Feces/microbiology ; Recurrence ; Bayes Theorem ; Treatment Outcome ; Gastrointestinal Microbiome ; Vancomycin/administration & dosage/therapeutic use ; Risk Factors ; Secondary Prevention/methods ; },
abstract = {GOALS: To assess fecal microbiota, live-jslm (REBYOTA, abbreviated as RBL, formerly RBX2660) efficacy and safety in participants grouped by recurrent Clostridioides difficile infection (rCDI) risk factors and treatment-related variables.

BACKGROUND: RBL is the first microbiota-based live biotherapeutic approved by the US Food and Drug Administration for the prevention of rCDI in adults after antibiotic treatment for rCDI.

STUDY: Treatment success rates across subgroups for PUNCH CD3 (NCT03244644) were estimated using a Bayesian hierarchical model, borrowing data from PUNCH CD2 (NCT02299570). Treatment-emergent adverse events were summarized for the double-blind treatment period within 8 weeks.

RESULTS: Treatment differences between RBL and placebo at 8 weeks were similar to the total population for most subgroups. Treatment effect sizes were similar between CDI tests, higher for oral vancomycin courses >14 days versus ≤14 days and higher for antibiotic washout periods of 3 days versus ≤2 days. The largest reductions in the rate of rCDI with RBL versus placebo were observed for participants with a 3-day CDI antibiotic washout period and participants with ≥4 previous CDI episodes. Most RBL-treated participants experienced TEAEs that were mild or moderate in severity and related to preexisting conditions.

CONCLUSION: This analysis provides further evidence of RBL efficacy and safety across subgroups, including those at high risk for rCDI.},
}

Humans
*Clostridium Infections/prevention & control/microbiology
Double-Blind Method
*Fecal Microbiota Transplantation
Male
Female
Middle Aged
*Anti-Bacterial Agents/administration & dosage/adverse effects
Adult
*Clostridioides difficile/isolation & purification
Aged
Feces/microbiology
Recurrence
Bayes Theorem
Treatment Outcome
Gastrointestinal Microbiome
Vancomycin/administration & dosage/therapeutic use
Risk Factors
Secondary Prevention/methods

@article {pmid39130120,
year = {2023},
author = {Kahan, T and Chandan, S and Khan, SR and Deliwala, S and Chang, S and Axelrad, J and Shaukat, A},
title = {Safety and Efficacy of Fecal Microbiota Transplant in Chronic Pouchitis-A Systematic Review With Meta-Analysis.},
journal = {Gastro hep advances},
volume = {2},
number = {6},
pages = {843-852},
pmid = {39130120},
issn = {2772-5723},
abstract = {BACKGROUND AND AIMS: Pouchitis is the most common long-term complication after ileal-pouch anal anastomosis in patients with ulcerative colitis. We conducted a systematic review and meta-analysis evaluating the safety and efficacy of fecal microbiota transplant (FMT) in chronic antibiotic dependent and refractory pouchitis.

METHODS: Multiple databases were searched through April 2022 for studies that reported the efficacy and safety of FMT in patients with chronic pouchitis. Meta-analysis using random effects model was performed to calculate pooled rates.

RESULTS: Eight studies with a total of 89 patients were included in our review, with 74 patients having received FMT and 15 patients having received placebo. The mean age ranged from 32.6 to 51.5 years. In patients that received FMT, the pooled rates of overall remission was (Pouchitis Disease Activity Index score < 7) 22% (95% CI, 9%-43%; I[2], 29%), clinical remission was 20% (95% CI, 6%-49%; I[2], 25%), clinical response rate was 42% (95% CI, 30%-54%; I[2], 7%), and the relapse rate 60% (95% CI, 40%-77%, I[2] 16%) over the mean follow up of 4.67 months (range 1-12 months). The pooled proportion of patients with adverse events was 54% (95% CI, 21%-84%; I[2], 73%). There were no serious adverse events or deaths.

CONCLUSION: In patients with chronic pouchitis, FMT is safe though there are mixed results in terms of its long-term efficacy. Future Randomized Controlled Trials with larger sample sizes and greater standardization in terms of preparation, delivery, and length of treatment of FMT are needed to determine efficacy.},
}

@article {pmid39131119,
year = {2022},
author = {Watts, AE and Sninsky, JA and Richey, MM and Donovan, K and Dougherty, MK and McGill, SK},
title = {Family Stool Donation Predicts Failure of Fecal Microbiota Transplant for Clostridioides difficile Infection.},
journal = {Gastro hep advances},
volume = {1},
number = {2},
pages = {141-146},
pmid = {39131119},
issn = {2772-5723},
abstract = {BACKGROUND AND AIMS: Fecal microbiota transplant (FMT) via colonoscopy is highly effective treatment for Clostridioides difficile infection (CDI). We aimed to determine baseline patient characteristics that predict failure to respond to colonoscopy-based FMT.

METHODS: We evaluated adult patients who received FMT for CDI not responding to standard therapies at a single tertiary center between 2014 and 2018 in this retrospective cohort study. We defined clinical success as formed stool or C difficile-negative diarrhea at 2 months after FMT. If patients required a second FMT, follow-up was extended 2 months after repeat infusion. We performed multivariate logistic regression and a random forest model to identify variables predictive of response to FMT.

RESULTS: Clinical success was attained in 87.3% of 103 patients who underwent FMT for CDI. In the multivariate model, the odds of FMT failure for family donation compared with stool bank were odds ratio 4.13 (1.00-7.01 P = .049). Diarrhea while taking anti-CDI antibiotics was common (37.8% of patients) and did not predict failure (odds ratio 0.64, 0.19-2.11 P = .46) in the univariate model. A machine learning model to predict response using clinical factors only achieved a sensitivity of 70%, specificity of 77%, and negative predictive value of 96%.

CONCLUSION: Colonoscopy-based FMT was highly effective for CDI, even in a population where immunosuppression and proton pump inhibitor use were common. Family stool donation was associated with FMT failure, compared with the use of a stool bank. The study suggests that the use of a stool bank may not only improve access to FMT but also its efficacy.},
}