@article {pmid39887250,
year = {2025},
author = {Tang, X and Zeng, T and Deng, W and Zhao, W and Liu, Y and Huang, Q and Deng, Y and Xie, W and Huang, W},
title = {Gut microbe-derived betulinic acid alleviates sepsis-induced acute liver injury by inhibiting macrophage NLRP3 inflammasome in mice.},
journal = {mBio},
volume = {},
number = {},
pages = {e0302024},
doi = {10.1128/mbio.03020-24},
pmid = {39887250},
issn = {2150-7511},
abstract = {UNLABELLED: Sepsis-induced acute liver injury (SALI) is a prevalent and life-threatening complication associated with sepsis. The gut microbiota plays a crucial role in the maintenance of health and the development of diseases. The impact of physical exercise on gut microbiota modulation has been well-documented. However, the potential impact of gut microbiome on exercise training-induced protection against SALI remains uncertain. Here, we discovered exercise training ameliorated SALI and systemic inflammation in septic mice. Notably, gut microbiota pre-depletion abolished the protective effects of exercise training in SALI mice. Fecal microbiota transplantation treatment revealed that exercise training-associated gut microbiota contributed to the beneficial effect of exercise training on SALI. Exercise training modulated the metabolism of Ligilactobacillus and enriched betulinic acid (BA) levels in mice. Functionally, BA treatment conferred protection against SALI by inhibiting the hepatic inflammatory response in mice. BA bound and inactivated hnRNPA2B1, thus suppressing NLRP3 inflammasome activation in macrophages. Collectively, this study reveals gut microbiota is involved in the protective effects of exercise training against SALI, and gut microbiota-derived BA inhibits the hepatic inflammatory response via the hnRNPA2B1-NLRP3 axis, providing a potential therapeutic strategy for SALI.

IMPORTANCE: Sepsis is characterized by a dysregulated immune response to an infection that leads to multiple organ dysfunction. The occurrence of acute liver injury is frequently observed during the initial stage of sepsis and is directly linked to mortality in the intensive care unit. The preventive effect of physical exercise on SALI is well recognized, yet the underlying mechanism remains poorly elucidated. Exercise training alters the gut microbiome in mice, increasing the abundance of Ligilactobacillus and promoting the generation of BA. Additionally, BA supplementation can suppress the NLRP3 inflammasome activation in macrophages by directly binding to hnRNPA2B1, thereby mitigating SALI. These results highlight the beneficial role of gut microbiota-derived BA in inhibiting the hepatic inflammatory response, which represents a crucial stride toward implementing microbiome-based therapeutic strategies for the clinical management of sepsis.},
}

@article {pmid39885417,
year = {2025},
author = {Abdel-Raoof Fouda, M and Abdel-Wahhab, M and Abdelkader, AE and Ibrahim, ME and Elsheikh, TA and Aldeweik, HM and Elfeky, N},
title = {Effect of gut microbiota changes on cytokines IL-10 and IL-17 levels in liver transplantation patients.},
journal = {BMC infectious diseases},
volume = {25},
number = {1},
pages = {140},
pmid = {39885417},
issn = {1471-2334},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Liver Transplantation ; Male ; Female ; *Interleukin-17/blood ; *Interleukin-10/blood ; Middle Aged ; Adult ; Feces/microbiology ; Bacteria/classification/isolation & purification ; Dysbiosis/microbiology ; Aged ; },
abstract = {BACKGROUND: Liver transplantation (LT) is a critical intervention for individuals with end-stage liver disease; yet, post-transplant problems, especially infections, graft rejection, and chronic liver disease, are often linked to systemic inflammation. Cytokines, small signaling molecules, significantly influence immune responses during and post-liver transplantation. Nonetheless, the intricate relationships among cytokines, immune responses, and the gut microbiota, especially gut dysbiosis, are still inadequately comprehended. Thus, this study aims to identify the gut microbiota (GM) and determine their relationship to cytokines (IL-17 and IL-10) in LT patients, due to their importance in enhancing the recovery rate.

RESULT: The research included 31 liver transplant (LT) patients from the Gastroenterology Surgical Center at Mansoura University, resulting in the collection of 174 stool and blood samples from all participants. Fourteen bacterial species have been identified in samples collected at three intervals: one week before, one week post, and two weeks post LT. A change in gut microbiota composition was noted, characterized by a rise in potentially pathogenic bacteria such as Enterococci and Enterobacteriaceae (including Escherichia coli and Klebsiella) and a reduction in beneficial bacteria such as Bacteroidetes and Firmicutes. The examination of patient demographic and clinical data revealed no significant correlations between sex, age, or diagnostic categories and gut microbiota composition. The findings of the Multivariate Analysis of Variance (MANOVA) indicated a substantial effect of gut microbiota composition on cytokine levels (IL-10 and IL-17), with all tests producing p-values of 0.001. The assessment of cytokine levels indicated fluctuating variations at several time points following surgery. IL-10 levels in the GM groups exhibited a statistically significant elevation during the second week post-surgery (p = 0.036), suggesting a potential recovery-related anti-inflammatory response. In contrast, IL-17 levels rose in the NI group over time, indicating a transition to a pro-inflammatory condition.

CONCLUSION: This study emphasizes the pivotal role of the gut microbiota in regulating immune responses following transplantation.},
}

Humans
*Gastrointestinal Microbiome
*Liver Transplantation
Male
Female
*Interleukin-17/blood
*Interleukin-10/blood
Middle Aged
Adult
Feces/microbiology
Bacteria/classification/isolation & purification
Dysbiosis/microbiology
Aged

@article {pmid39881980,
year = {2024},
author = {Renk, H and Schoppmeier, U and Müller, J and Kuger, V and Neunhoeffer, F and Gille, C and Peter, S},
title = {Oxygenation and intestinal perfusion and its association with perturbations of the early life gut microbiota composition of children with congenital heart disease.},
journal = {Frontiers in microbiology},
volume = {15},
number = {},
pages = {1468842},
pmid = {39881980},
issn = {1664-302X},
abstract = {BACKGROUND: Early life gut microbiota is known to shape the immune system and has a crucial role in immune homeostasis. Only little is known about composition and dynamics of the intestinal microbiota in infants with congenital heart disease (CHD) and potential influencing factors.

METHODS: We evaluated the intestinal microbial composition of neonates with CHD (n = 13) compared to healthy controls (HC, n = 30). Fecal samples were analyzed by shotgun metagenomics. Different approaches of statistical modeling were applied to assess the impact of influencing factors on variation in species composition. Unsupervised hierarchical clustering of the microbial composition of neonates with CHD was used to detect associations of distinct clusters with intestinal tissue oxygenation and perfusion parameters, obtained by the "oxygen to see" (O2C) method.

RESULTS: Overall, neonates with CHD showed an intestinal core microbiota dominated by the genera Enterococcus (27%) and Staphylococcus (20%). Furthermore, a lower abundance of the genera Bacteroides (8% vs. 14%), Parabacteroides (1% vs. 3%), Bifidobacterium (4% vs. 12%), and Escherichia (8% vs. 23%) was observed in CHD compared to HCs. CHD patients that were born by vaginal delivery showed a lower fraction of the genera Bacteroides (15% vs. 21%) and Bifidobacterium (7% vs. 22%) compared to HCs and in those born by cesarean section, these genera were not found at all. In infants with CHD, we found a significant impact of oxygen saturation (SpO2) on relative abundances of the intestinal core microbiota by multivariate analysis of variance (F[8,2] = 24.9, p = 0.04). Statistical modeling suggested a large proportional shift from a microbiota dominated by the genus Streptococcus (50%) in conditions with low SpO2 towards the genus Enterococcus (61%) in conditions with high SpO2. We identified three distinct compositional microbial clusters, corresponding neonates differed significantly in intestinal blood flow and global gut perfusion.

CONCLUSION: Early life differences in gut microbiota of CHD neonates versus HCs are possibly linked to oxygen levels. Delivery method may affect microbiota stability. However, further studies are needed to assess the effect of potential interventions including probiotics or fecal transplants on early life microbiota perturbations in neonates with CHD.},
}

@article {pmid39880356,
year = {2025},
author = {Wang, S and Yan, K and Dong, Y and Chen, Y and Song, J and Chen, Y and Liu, X and Qi, R and Zhou, X and Zhong, J and Li, J},
title = {The influence of microplastics on hypertension-associated cardiovascular injury via the modulation of gut microbiota.},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {},
number = {},
pages = {125760},
doi = {10.1016/j.envpol.2025.125760},
pmid = {39880356},
issn = {1873-6424},
abstract = {Microplastics (MPs) have been found to interfere with the gut microbiota and compromise the integrity of the gut barrier. Excessive exposure to MPs markedly elevates the risk of cardiovascular disease, yet their influence on hypertension remains elusive, calling for investigation into their potential impacts on blood pressure (BP) regulation. In the present study, an increase in the concentration of MPs was observed in the fecal samples of individuals suffering from hypertension, as compared to the controls. Oral administration of MPs led to obvious increases in systolic, diastolic and mean BP levels in mice. MPs were associated with promoting myocardial hypertrophy, fibrosis, and cardiac remodeling through alterations in gut microbial composition, such as Prevotella and Coprobacillus, or fecal metabolites Betaine and Glycyrrhetinic acid. The hypertensive damage mediated by MPs was significantly mitigated by the high-fiber diet or antibiotics that targeted the gut microbiota. Notablely, fecal microbiota transplantation from mice treated with MPs led to an increase in systolic BP levels and the development of cardiac dysfunction. Our findings offer valuable insights into the complex interplay between MPs and the gut microbiome in the context of hypertension, and suggest potential strategies for reducing the vascular and cardiac injury caused by MPs.},
}

@article {pmid39879970,
year = {2025},
author = {Stallmach, A},
title = {[The gastrointestinal microbiome - vision and mission].},
journal = {Deutsche medizinische Wochenschrift (1946)},
volume = {150},
number = {4},
pages = {157-162},
doi = {10.1055/a-2303-3368},
pmid = {39879970},
issn = {1439-4413},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Fecal Microbiota Transplantation ; Germany ; Dysbiosis ; Clostridium Infections/therapy ; },
abstract = {The gastrointestinal microbiome influences physiological functions and is altered in a variety of diseases. The causality of "dysbiosis" in the pathogenesis is not always proven; association studies are often involved. Patients with IBD, bacteria, fungi, bacteriophages, and archaea show disease-typical patterns associated with metabolome disturbances. Fecal microbiome transfer (FMT) for treating various diseases is the subject of numerous clinical studies. Currently, recurrent Clostridioides difficile infection (rCDI) is the only confirmed indication recommended in medical guidelines. In Germany, the FMT is subject to the Medicines Act and may only be carried out as part of individual healing attempts or clinical studies. For patient safety, repeated donor screening, ideally with the construction of a chair bench, is necessary. This significantly limits the nationwide availability of the FMT in Germany. Microbiota-based therapeutics prepared from the stool of tested donors have recently been approved by the US Food and Drug Administration (FDA) for the prevention of rCDI. More microbiome-based medicines can be expected in the future.},
}

Humans
*Gastrointestinal Microbiome
*Fecal Microbiota Transplantation
Germany
Dysbiosis
Clostridium Infections/therapy

@article {pmid39879969,
year = {2025},
author = {Weirauch, T and Vehreschild, MJGT},
title = {[Nosocomial gastrointestinal infections and Clostridioides difficile].},
journal = {Deutsche medizinische Wochenschrift (1946)},
volume = {150},
number = {4},
pages = {149-156},
doi = {10.1055/a-2303-3321},
pmid = {39879969},
issn = {1439-4413},
mesh = {Humans ; *Cross Infection/epidemiology ; *Clostridium Infections/therapy/epidemiology ; *Anti-Bacterial Agents/therapeutic use ; *Fecal Microbiota Transplantation ; Clostridioides difficile ; Germany ; Diarrhea/microbiology ; Fidaxomicin/therapeutic use ; Vancomycin/therapeutic use ; },
abstract = {German surveillance data from 2022 reported a prevalence of nosocomial infections among hospitalized patients of 5,2%. Clostridioides-difficile-infections (CDI) are the most frequent cause of nosocomial diarrhea. They are usually caused by antibiotic exposure and the subsequent changes in the gut microbiota. Clinical manifestation ranges from asymptomatic colonization over moderate diarrhea to severe pseudomembranous colitis. According to the current German Gastrointestinal Infection Guidelines, fidaxomicin is the preferred treatment option for CDI, especially in patients at high risk of recurrence or those already suffering from recurrence. Vancomycin can also be used as an alternative for initial CDI treatment. Fecal microbiota transplantation is considered a treatment approach for patients with multiple recurrences.},
}

Humans
*Cross Infection/epidemiology
*Clostridium Infections/therapy/epidemiology
*Anti-Bacterial Agents/therapeutic use
*Fecal Microbiota Transplantation
Clostridioides difficile
Germany
Diarrhea/microbiology
Fidaxomicin/therapeutic use
Vancomycin/therapeutic use

@article {pmid39879083,
year = {2025},
author = {Carroll, A and Bell, MJ and Bleach, ECL and Turner, D and Williams, LK},
title = {Impact of dairy calf management practices on the intestinal tract microbiome pre-weaning.},
journal = {Journal of medical microbiology},
volume = {74},
number = {1},
pages = {},
doi = {10.1099/jmm.0.001957},
pmid = {39879083},
issn = {1473-5644},
mesh = {Animals ; Cattle ; *Gastrointestinal Microbiome/physiology ; *Weaning ; *Animal Husbandry/methods ; Dairying ; },
abstract = {Introduction. Microbiota in the gastrointestinal tract (GIT) consisting of the rumen and hindgut (the small intestine, cecum and colon) in dairy calves play a vital role in their growth and development. This review discusses the development of dairy calf intestinal microbiomes with an emphasis on the impact that husbandry and rearing management have on microbiome development, health and growth of pre-weaned dairy calves.Discussion. The diversity and composition of the microbes that colonize the lower GIT (small and large intestine) can have a significant impact on the growth and development of the calf, through influence on nutrient metabolism, immune modulation, resistance or susceptibility to infection, production outputs and behaviour modification in adult life. The colonization of the calf intestinal microbiome dynamically changes from birth, increasing microbial richness and diversity until weaning, where further dynamic and drastic microbiome change occurs. In dairy calves, neonatal microbiome development prior to weaning is influenced by direct and indirect factors, some of which could be considered stressors, such as maternal interaction, environment, diet, husbandry and weaning practices. The specific impact of these can dictate intestinal microbial colonization, with potential lifelong consequences.Conclusion. Evidence suggests the potential detrimental effect that sudden changes and stress may have on calf health and growth due to management and husbandry practices, and the importance of establishing a stable yet diverse intestinal microbiome population at an early age is essential for calf success. The possibility of improving the health of calves through intestinal microbiome modulation and using alternative strategies including probiotic use, faecal microbiota transplantation and novel approaches of microbiome tracking should be considered to support animal health and sustainability of dairy production systems.},
}

Animals
Cattle
*Gastrointestinal Microbiome/physiology
*Weaning
*Animal Husbandry/methods
Dairying

@article {pmid39878866,
year = {2025},
author = {Zheng, Y and Yu, Y and Chen, M and Zhang, H and Wang, W and Fan, X and Sun, L and Tang, L and Ta, D},
title = {Abdominal LIPUS Stimulation Prevents Cognitive Decline in Hind Limb Unloaded Mice by Regulating Gut Microbiota.},
journal = {Molecular neurobiology},
volume = {},
number = {},
pages = {},
pmid = {39878866},
issn = {1559-1182},
abstract = {Weightlessness usually causes disruption of the gut microbiota and impairs cognitive function. There is a close connection between gut microbiota and neurological diseases. Low-intensity pulsed ultrasound (LIPUS) has a beneficial effect on reducing intestinal inflammation. So we wondered if abdominal LIPUS stimulation can have a positive impact on weightlessness induced cognitive decline by reducing intestinal dysfunction. The findings revealed that the hind limb unloaded mice exhibited evident disruption in intestinal structure and gut microbial homeostasis, along with impairment in their learning and memory capabilities. However, 4-week abdominal LIPUS treatment improved intestinal function in hind limb unloaded mice, characterized by upregulation of tight junction proteins ZO-1 and Occludin expression in the colon, increased diversity and abundance of intestinal microbiota, decreased serum lipopolysaccharide (LPS), and increased short chain fatty acids in colon contents. The hind limb unloaded mice treated with LIPUS exhibited heightened activity levels, improved exploratory tendencies, and significantly enhanced learning and memory faculties, and elevated expression of neuroadaptation-related proteins such as PSD95, GAP43, P-CREB, BDNF, and its receptor TRKB in the hippocampus. Furthermore, the hind limb unloaded mice receiving fecal transplants from the mice whose abdomens were irradiated with LIPUS displayed enhanced cognitive abilities and improved intestinal structure, akin to the outcomes observed in hind limb unloaded mice who received LIPUS abdominal treatment directly. The above results indicate that LIPUS enhances intestinal structure and microbiota, which helps alleviate cognitive impairment caused by weightlessness. LIPUS could be a potential strategy to simultaneously improve gut dysfunction and cognitive decline in astronauts or bedridden patients.},
}

@article {pmid39779879,
year = {2025},
author = {Pribyl, AL and Hugenholtz, P and Cooper, MA},
title = {A decade of advances in human gut microbiome-derived biotherapeutics.},
journal = {Nature microbiology},
volume = {10},
number = {2},
pages = {301-312},
pmid = {39779879},
issn = {2058-5276},
mesh = {Humans ; *Gastrointestinal Microbiome ; Biological Therapy/methods ; Bacteria/genetics/classification ; Fecal Microbiota Transplantation ; Feces/microbiology ; Probiotics/therapeutic use ; },
abstract = {Microbiome science has evolved rapidly in the past decade, with high-profile publications suggesting that the gut microbiome is a causal determinant of human health. This has led to the emergence of microbiome-focused biotechnology companies and pharmaceutical company investment in the research and development of gut-derived therapeutics. Despite the early promise of this field, the first generation of microbiome-derived therapeutics (faecal microbiota products) have only recently been approved for clinical use. Next-generation therapies based on readily culturable and as-yet-unculturable colonic bacterial species (with the latter estimated to comprise 63% of all detected species) have not yet progressed to pivotal phase 3 trials. This reflects the many challenges involved in developing a new class of drugs in an evolving field. Here we discuss the evolution of the live biotherapeutics field over the past decade, from the development of first-generation products to the emergence of rationally designed second- and third-generation live biotherapeutics. Finally, we present our outlook for the future of this field.},
}

Humans
*Gastrointestinal Microbiome
Biological Therapy/methods
Bacteria/genetics/classification
Fecal Microbiota Transplantation
Feces/microbiology
Probiotics/therapeutic use

@article {pmid39877812,
year = {2021},
author = {Zhu, W and Dykstra, K and Zhang, L and Xia, Z},
title = {Gut Microbiome as Potential Therapeutics in Multiple Sclerosis.},
journal = {Current treatment options in neurology},
volume = {23},
number = {11},
pages = {},
pmid = {39877812},
issn = {1092-8480},
support = {R01 NS098023/NS/NINDS NIH HHS/United States ; R01 NS124882/NS/NINDS NIH HHS/United States ; },
abstract = {PURPOSE OF REVIEW: The gut microbiome is an emerging arena to investigate multiple sclerosis (MS) pathogenesis and potential therapeutics. In this review, we summarize the available data and postulate the feasibilities of potential MS therapeutic approaches that modulate the gut microbiome.

RECENT FINDINGS: Growing evidence indicates dysbiosis in the gut bacterial ecosystem in MS. Diet and other interventions produce biologically significant changes in the gut bacterial communities and functions, can potentially regulate the immune system, and benefit people with MS. While well-conducted investigations of the therapeutic mechanisms for targeting gut microbiome in animal models and humans remain limited, promising connections between various mechanisms of gut microbiome regulation and beneficial effects on MS outcomes are emerging.

SUMMARY: To date, studies examining the microbiome-based therapies in MS remain limited in number and follow-up duration. There is a clear need to determine the long-term efficacy and safety of these approaches, and to identify their underlying mechanisms of actions.},
}

@article {pmid39875017,
year = {2025},
author = {Qin, L and Fan, B and Zhou, Y and Zheng, J and Diao, R and Wang, F and Liu, J},
title = {Targeted Gut Microbiome Therapy: Applications and Prospects of Probiotics, Fecal Microbiota Transplantation and Natural Products in the Management of Type 2 Diabetes.},
journal = {Pharmacological research},
volume = {},
number = {},
pages = {107625},
doi = {10.1016/j.phrs.2025.107625},
pmid = {39875017},
issn = {1096-1186},
abstract = {Type 2 diabetes mellitus (T2DM) is considered as one of the most pressing public health challenges worldwide. Studies have shown significant differences in the gut microbiota between healthy individuals and T2DM patients, suggesting that gut microorganisms may play a key role in the onset and progression of T2DM. This review systematically summarizes the relationship between gut microbiota and T2DM, and explores the mechanisms through which gut microorganisms may alleviate T2DM. Additionally, it evaluates the potential of probiotics, fecal microbiota transplantation (FMT)/virome transplantation (FVT), and natural products in modulating gut microbiota to treat T2DM. Although existing studies have suggested that these interventions may delay or even halt the progression of T2DM, most research remained limited to animal models and observational clinical studies, with a lack of high-quality clinical data. This has led to an imbalance between theoretical research and clinical application. Although some studies have explored the regulatory role of the gut virome on the gut microbiota, research in this area remains in its early stages. Based on these current studies, future research should be focused on large-scale, long-term clinical studies and further investigation on the potential role of the gut virome in T2DM. In conclusion, this review aims to summarize the current evidence and explore the applications of gut microbiota in T2DM treatment, as well as providing recommendations for further investigation in this field.},
}

@article {pmid39874238,
year = {2025},
author = {Scher, JU and Nayak, R and Clemente, JC},
title = {Microbiome research in autoimmune and immune-mediated inflammatory diseases: lessons, advances and unmet needs.},
journal = {Annals of the rheumatic diseases},
volume = {84},
number = {1},
pages = {9-13},
doi = {10.1136/ard-2024-225735},
pmid = {39874238},
issn = {1468-2060},
mesh = {Humans ; *Autoimmune Diseases/immunology/microbiology/therapy ; *Gastrointestinal Microbiome/immunology/physiology ; *Dysbiosis/immunology ; Fecal Microbiota Transplantation ; Microbiota/immunology ; Arthritis, Rheumatoid/immunology/microbiology ; Lupus Erythematosus, Systemic/immunology/microbiology ; Immune System Diseases/immunology/microbiology ; },
abstract = {The increasing prevalence of autoimmune and immune-mediated diseases (AIMDs) underscores the need to understand environmental factors that contribute to their pathogenesis, with the microbiome emerging as a key player. Despite significant advancements in understanding how the microbiome influences physiological and inflammatory responses, translating these findings into clinical practice remains challenging. This viewpoint reviews the progress and obstacles in microbiome research related to AIMDs, examining molecular techniques that enhance our understanding of microbial contributions to disease. We discuss significant discoveries linking specific taxa and metabolites to diseases such as rheumatoid arthritis, systemic lupus erythematosus and spondyloarthritis, highlighting the role of gut dysbiosis and host-microbiome interactions. Furthermore, we explore the potential of microbiome-based therapeutics, including faecal microbiota transplantation and pharmacomicrobiomics, while addressing the challenges of identifying robust microbial targets. We advocate for integrative, transdisease studies and emphasise the need for diverse cohort research to generalise findings across populations. Understanding the microbiome's role in AIMDs will pave the way for personalised medicine and innovative therapeutic strategies.},
}

Humans
*Autoimmune Diseases/immunology/microbiology/therapy
*Gastrointestinal Microbiome/immunology/physiology
*Dysbiosis/immunology
Fecal Microbiota Transplantation
Microbiota/immunology
Arthritis, Rheumatoid/immunology/microbiology
Lupus Erythematosus, Systemic/immunology/microbiology
Immune System Diseases/immunology/microbiology

@article {pmid39873952,
year = {2025},
author = {Pezeshki, B and Abdulabbas, HT and Alturki, AD and Mansouri, P and Zarenezhad, E and Nasiri-Ghiri, M and Ghasemian, A},
title = {Synergistic Interactions Between Probiotics and Anticancer Drugs: Mechanisms, Benefits, and Challenges.},
journal = {Probiotics and antimicrobial proteins},
volume = {},
number = {},
pages = {},
pmid = {39873952},
issn = {1867-1314},
abstract = {Research into the role of probiotics-often referred to as "living supplements"-in cancer therapy is still in its early stages, and uncertainties regarding their effectiveness remain. Relevantly, chemopreventive and therapeutic effects of probiotics have been determined. There is also substantial evidence supporting their potential in cancer treatment such as immunotherapy. Probiotics employ various mechanisms to inhibit cancer initiation and progression. These include colonizing and protecting the gastrointestinal tract (GIT), producing metabolites, inducing apoptosis and autophagy, exerting anti-inflammatory properties, preventing metastasis, enhancing the effectiveness of immune checkpoint inhibitors (ICIs), promoting cancer-specific T cell infiltration, arresting the cell cycle, and exhibiting direct or indirect synergistic effects with anticancer drugs. Additionally, probiotics have been shown to activate tumor suppressor genes and inhibit pro-inflammatory transcription factors. They also increase reactive oxygen species production within cancer cells. Synergistic interactions between probiotics and various anticancer drugs, such as cisplatin, cyclophosphamide, 5-fluorouracil, trastuzumab, nivolumab, ipilimumab, apatinib, gemcitabine, tamoxifen, sorafenib, celecoxib and irinotecan have been observed. The combination of probiotics with anticancer drugs holds promise in overcoming drug resistance, reducing recurrence, minimizing side effects, and lowering treatment costs. In addition, fecal microbiota transplantation (FMT) and prebiotics supplementation has increased cytotoxic T cells within tumors. However, probiotics may leave some adverse effects such as risk of infection and gastrointestinal effects, antagonistic effects with drugs, and different responses among patients. These findings highlight insights for considering specific strains and engineered probiotic applications, preferred doses and timing of treatment, and personalized therapies to enhance the efficacy of cancer therapy. Accordingly, targeted interventions and guidelines establishment needs extensive randomized controlled trials as probiotic-based cancer therapy has not been approved by Food and Drug Administration (FDA).},
}

@article {pmid39873191,
year = {2025},
author = {An, L and Li, S and Chang, Z and Lei, M and He, Z and Xu, P and Zhang, S and Jiang, Z and Iqbal, MS and Sun, X and Liu, H and Duan, X and Wu, W},
title = {Gut microbiota modulation via fecal microbiota transplantation mitigates hyperoxaluria and calcium oxalate crystal depositions induced by high oxalate diet.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2457490},
pmid = {39873191},
issn = {1949-0984},
mesh = {Animals ; *Gastrointestinal Microbiome ; *Hyperoxaluria/therapy/metabolism ; *Fecal Microbiota Transplantation ; *Calcium Oxalate/metabolism/chemistry ; Rats ; Male ; *Oxalates/metabolism/urine ; Diet ; Rats, Sprague-Dawley ; Kidney/metabolism/microbiology/pathology ; Bacteria/classification/metabolism/genetics/isolation & purification ; Disease Models, Animal ; Kidney Calculi/therapy/prevention & control/microbiology/metabolism/diet therapy ; Feces/microbiology/chemistry ; },
abstract = {Hyperoxaluria, including primary and secondary hyperoxaluria, is a disorder characterized by increased urinary oxalate excretion and could lead to recurrent calcium oxalate kidney stones, nephrocalcinosis and eventually end stage renal disease. For secondary hyperoxaluria, high dietary oxalate (HDOx) or its precursors intake is a key reason. Recently, accumulated studies highlight the important role of gut microbiota in the regulation of oxalate homeostasis. However, the underlying mechanisms involving gut microbiota and metabolite disruptions in secondary hyperoxaluria remain poorly understood. Here, we investigated the therapeutic efficacy of fecal microbiota transplantation (FMT) sourced from healthy rats fed with standard pellet diet against urinary oxalate excretion, renal damage and calcium oxalate (CaOx) crystal depositions via using hyperoxaluria rat models. We observed dose-dependent increases in urinary oxalate excretion and CaOx crystal depositions due to hyperoxaluria, accompanied by significant reductions in gut microbiota diversity characterized by shifts in Ruminococcaceae_UCG-014 and Parasutterella composition. Metabolomic analysis validated these findings, revealing substantial decreases in key metabolites associated with these microbial groups. Transplanting microbes from healthy rats effectively reduced HDOx-induced urinary oxalate excretion and CaOx crystal depositions meanwhile restoring Ruminococcaceae_UCG-014 and Parasutterella populations and their associated metabolites. Furthermore, FMT treatment could significantly decrease the urinary oxalate excretion and CaOx crystal depositions in rat kidneys via, at least in part, upregulating the expressions of intestinal barrier proteins and oxalate transporters in the intestine. In conclusion, our study emphasizes the effectiveness of FMT in countering HDOx-induced hyperoxaluria by restoring gut microbiota and related metabolites. These findings provide insights on the complex connection between secondary hyperoxaluria caused by high dietary oxalate and disruptions in gut microbiota, offering promising avenues for targeted therapeutic strategies.},
}

Animals
*Gastrointestinal Microbiome
*Hyperoxaluria/therapy/metabolism
*Fecal Microbiota Transplantation
*Calcium Oxalate/metabolism/chemistry
Rats
Male
*Oxalates/metabolism/urine
Diet
Rats, Sprague-Dawley
Kidney/metabolism/microbiology/pathology
Bacteria/classification/metabolism/genetics/isolation & purification
Disease Models, Animal
Kidney Calculi/therapy/prevention & control/microbiology/metabolism/diet therapy
Feces/microbiology/chemistry

@article {pmid39870907,
year = {2025},
author = {Misselwitz, B and Haller, D},
title = {[The intestinal microbiota in inflammatory bowel diseases].},
journal = {Innere Medizin (Heidelberg, Germany)},
volume = {},
number = {},
pages = {},
pmid = {39870907},
issn = {2731-7099},
abstract = {BACKGROUND: The intestinal microbiota comprises all living microorganisms in the gastrointestinal tract and is crucial for its function. Clinical observations and laboratory findings confirm a central role of the microbiota in chronic inflammatory bowel diseases (IBD). However, many mechanistic details remain unclear.

OBJECTIVES: Changes in the microbiota and the causal relationship with the pathogenesis of IBD are described and current and future diagnostic and therapeutic options are discussed.

MATERIALS AND METHODS: Narrative review.

RESULTS: The intestinal microbiota is altered in composition, diversity, and function in IBD patients, but specific (universal) IBD-defining bacteria have not been identified. The healthy microbiota has numerous anti-inflammatory functions such as the production of short-chain fatty acids or competition with pathogens. In contrast, the IBD microbiota promotes inflammation through the destruction of the intestinal barrier and direct interaction with the immune system. The balance between pro- and anti-inflammatory effects of the microbiota appears to be crucial for the development of intestinal inflammation. Microbiota-based IBD diagnostics show promise but are not yet ready for clinical use. Probiotics and fecal microbiota transplantation have clinical effects, especially in ulcerative colitis, but the potential of microbiota-based therapies is far from being fully realized.

CONCLUSION: IBD dysbiosis remains undefined so far. It is unclear how the many parallel pro- and anti-inflammatory mechanisms contribute to IBD pathogenesis. An inadequate mechanistic understanding hinders the development of microbiota-based diagnostics and therapies.},
}

@article {pmid39870349,
year = {2025},
author = {Vázquez-Cuesta, S and Olmedo, M and Kestler, M and Álvarez-Uría, A and De la Villa, S and Alcalá, L and Marín, M and Rodríguez-Fernández, S and Sánchez-Martínez, C and Muñoz, P and Bouza, E and Reigadas, E},
title = {Prospective analysis of biomarkers associated with successful faecal microbiota transplantation in recurrent Clostridioides difficile Infection.},
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.2025.01.026},
pmid = {39870349},
issn = {1469-0691},
abstract = {OBJECTIVES: Faecal microbiota transplantation (FMT) is an established treatment for recurrent Clostridioides difficile infection (R-CDI). This study aimed to identify calprotectin and microbiome characteristics as potential biomarkers of FMT success.

METHODS: We conducted a prospective study of patients who underwent oral FMT (single dose of 4-5 capsules) for R-CDI (January 2018 to December 2022). Samples were collected at three time points: at CDI diagnosis, within 24 hours prior to FMT administration, and 30 days post-FMT. Calprotectin levels were assessed and the V4 region of the 16S rRNA gene was sequenced to analyse the microbiota composition. Sequencing data analysis and statistical analysis were performed using MOTHUR and R.

RESULTS: Ninety-seven patients underwent FMT (totalling 105 procedures). A total of 221 samples were processed, including 21 donor samples, 24 capsule contents, and 176 patient faecal samples (39 at diagnosis, 63 pre-FMT, and 74 post-FMT). FMT achieved an overall success rate of 85.1% (86/101 cases). The abundance of Bacteroides, Ruminococcus, Megamonas, and certain Prevotella operational taxonomic units (OTUs) was significantly higher in capsules associated with 100% success compared to less effective capsules. FMT engraftment was observed in 95% of patients with favourable outcomes versus 62% of those with recurrences (p = 0.006). Additionally, a negative correlation was found between calprotectin levels and specific microbial genera, suggesting an association with successful outcomes.

CONCLUSIONS: This study highlights differences in the evolution of faecal microbiota, bacterial engraftment, and inflammation markers (e.g., calprotectin) between patients with varying FMT outcomes. Potential biomarkers for successful FMT were identified, providing valuable insights for optimizing FMT strategies.},
}

@article {pmid39870263,
year = {2025},
author = {Ren, P and Liu, M and Wei, B and Tang, Q and Wang, Y and Xue, C},
title = {Fucoidan exerts antitumor effects by regulating gut microbiota and tryptophan metabolism.},
journal = {International journal of biological macromolecules},
volume = {300},
number = {},
pages = {140334},
doi = {10.1016/j.ijbiomac.2025.140334},
pmid = {39870263},
issn = {1879-0003},
abstract = {Fucoidan, a water-soluble polysaccharide derived from marine organisms, has garnered significant attention for its ability to regulate gut microbiota and its anti-tumor properties. However, the existence of a correlation between the anti-tumor effect of fucoidan and its regulation of the gut microbiota remains unknown. In pursuit of this objective, we culled the gut microbiota of mice with broad-spectrum antibiotics to generate pseudo-sterile tumor-bearing mice. Subsequently, fecal microbial transplants were introduced into the pseudo-sterile tumor-bearing mice. The antitumor effects of fucoidan were found to be dependent on the gut microbiota. Fucoidan promoted the proliferation of Akkermansia, Bifidobacterium and Lactobacillus, which have immunomodulatory effects. Furthermore, through regulation of gut microbiota, fucoidan influenced the metabolic process of tryptophan and facilitated its conversion to indole-3-acetic acid. In addition, fucoidan decreased the kynurenine/tryptophan ratio in serum, increased the proportion of CD8+ T cells, and suppressed the expression level of IDO1 in tumor tissues. Our results confirm that fucoidan enhances anti-tumor immune responses and subsequently exhibits anti-tumor effects by modulating the gut microbiota. Our research contributes to the comprehension of the mechanism of anti-tumor effects of fucoidan and facilitates the development of fucoidan as a dietary supplement for cancer patients.},
}

@article {pmid39230037,
year = {2025},
author = {Vaughn, BP and Khoruts, A and Fischer, M},
title = {Diagnosis and Management of Clostridioides difficile in Inflammatory Bowel Disease.},
journal = {The American journal of gastroenterology},
volume = {120},
number = {2},
pages = {313-319},
doi = {10.14309/ajg.0000000000003076},
pmid = {39230037},
issn = {1572-0241},
mesh = {Humans ; *Clostridium Infections/diagnosis/therapy ; *Inflammatory Bowel Diseases/complications/diagnosis/microbiology/therapy ; *Anti-Bacterial Agents/therapeutic use ; *Clostridioides difficile ; Risk Factors ; Gastrointestinal Microbiome ; Fecal Microbiota Transplantation ; Recurrence ; Broadly Neutralizing Antibodies ; Antibodies, Monoclonal ; },
abstract = {Patients with inflammatory bowel disease (IBD) have an increased risk of Clostridioides difficile infection (CDI), which can lead to worse IBD outcomes. The diagnosis of CDI in patients with IBD is complicated by higher C. difficile colonization rates and shared clinical symptoms of intestinal inflammation. Traditional risk factors for CDI, such as antibiotic exposure, may be lacking in patients with IBD because of underlying intestinal microbiota dysbiosis. Although CDI disproportionately affects people with IBD, patients with IBD are typically excluded from CDI clinical trials creating a knowledge gap in the diagnosis and management of these 2 diseases. This narrative review aims to provide a comprehensive overview of the diagnosis, treatment, and prevention of CDI in patients with IBD. Distinguishing CDI from C. difficile colonization in the setting of an IBD exacerbation is important to avoid treatment delays. When CDI is diagnosed, extended courses of anti- C. difficile antibiotics may lead to better CDI outcomes. Regardless of a diagnosis of CDI, the presence of C. difficile in a patient with IBD should prompt a disease assessment of the underlying IBD. Microbiota-based therapies and bezlotoxumab seem to be effective in preventing CDI recurrence in patients with IBD. Patients with IBD should be considered at high risk of CDI recurrence and evaluated for a preventative strategy when diagnosed with CDI. Ultimately, the comanagement of CDI in a patient with IBD requires a nuanced, patient-specific approach to distinguish CDI from C. difficile colonization, prevent CDI recurrence, and manage the underlying IBD.},
}

Humans
*Clostridium Infections/diagnosis/therapy
*Inflammatory Bowel Diseases/complications/diagnosis/microbiology/therapy
*Anti-Bacterial Agents/therapeutic use
*Clostridioides difficile
Risk Factors
Gastrointestinal Microbiome
Fecal Microbiota Transplantation
Recurrence
Broadly Neutralizing Antibodies
Antibodies, Monoclonal

@article {pmid39869428,
year = {2025},
author = {Kayal, M and Boland, B},
title = {Approach to Therapy for Chronic Pouchitis.},
journal = {Annual review of medicine},
volume = {76},
number = {1},
pages = {167-173},
doi = {10.1146/annurev-med-032224-120544},
pmid = {39869428},
issn = {1545-326X},
mesh = {*Pouchitis/etiology/therapy ; Humans ; Chronic Disease ; *Proctocolectomy, Restorative/adverse effects/methods ; *Anti-Bacterial Agents/therapeutic use ; *Colitis, Ulcerative/surgery ; Colonic Pouches/adverse effects ; Probiotics/therapeutic use ; Fecal Microbiota Transplantation/methods ; },
abstract = {Chronic pouchitis (CP) occurs in approximately 20% of patients with ulcerative colitis after total proctocolectomy with ileal pouch anal anastomosis and is categorized as antibiotic dependent, antibiotic refractory, or Crohn's disease-like. The management of CP is challenging because of limited evidence and few randomized controlled trials. In this review, we discuss the medical management of CP and its supporting data delineated by type of therapy.},
}

*Pouchitis/etiology/therapy
Humans
Chronic Disease
*Proctocolectomy, Restorative/adverse effects/methods
*Anti-Bacterial Agents/therapeutic use
*Colitis, Ulcerative/surgery
Colonic Pouches/adverse effects
Probiotics/therapeutic use
Fecal Microbiota Transplantation/methods

@article {pmid39869016,
year = {2025},
author = {Martin Fuentes, A},
title = {The role of the microbiome in skin cancer development and treatment.},
journal = {Current opinion in oncology},
volume = {},
number = {},
pages = {},
doi = {10.1097/CCO.0000000000001120},
pmid = {39869016},
issn = {1531-703X},
abstract = {PURPOSE OF REVIEW: Recent research underscores the significant influence of the skin and gut microbiota on melanoma and nonmelanoma skin cancer (NMSC) development and treatment outcomes. This review aims to synthesize current findings on how microbiota modulates immune responses, particularly enhancing the efficacy of immunotherapies such as immune checkpoint inhibitors (ICIs).

RECENT FINDINGS: The microbiota's impact on skin cancer is multifaceted, involving immune modulation, inflammation, and metabolic interactions. Beneficial strains like Bifidobacterium and Lactobacillus have shown potential in supporting anti-PD-1 and anti-CTLA-4 therapies by promoting T-cell activation and immune surveillance. Evidence from preclinical and clinical studies, including fecal microbiota transplantation (FMT), highlights improved response rates in patients with microbiota-rich profiles. Notably, certain bacterial metabolites, such as inosine, contribute to enhanced antitumor activity by stimulating IFN-γ in CD8+ T cells.

SUMMARY: Understanding the interplay between microbiota and skin cancer treatment opens promising avenues for adjunctive therapies. Probiotic and prebiotic interventions, FMT, and microbiota modulation are emerging as complementary strategies to improve immunotherapy outcomes and address treatment resistance in melanoma and NMSC.},
}

@article {pmid39868555,
year = {2025},
author = {Chatterjee, J and Qi, X and Mu, R and Li, X and Eligator, T and Ouyang, M and Bozeman, SL and Rodgers, R and Aggarwal, S and Campbell, DE and Schriefer, LA and Baldridge, MT and Gutmann, DH},
title = {Intestinal Bacteroides drives glioma progression by regulating CD8+ T cell tumor infiltration.},
journal = {Neuro-oncology},
volume = {},
number = {},
pages = {},
doi = {10.1093/neuonc/noaf024},
pmid = {39868555},
issn = {1523-5866},
abstract = {BACKGROUND: The intestinal microbiota regulates normal brain physiology and the pathogenesis of several neurological disorders. While prior studies suggested that this regulation operates through immune cells, the underlying mechanisms remain unclear. Leveraging two well characterized murine models of low-grade glioma (LGG) occurring in the setting of the neurofibromatosis type 1 (NF1) cancer predisposition syndrome, we sought to determine the impact of the gut microbiome on optic glioma progression.

METHODS: Nf1-mutant mice genetically engineered to develop optic pathway gliomas (Nf1OPG mice) by 3 months of age were reared under germ-free (GF) conditions, treated with specific cocktails of antibiotics, or given fecal matter transplants (FMTs). Intestinal microbial species were identified by 16S genotyping. Neutralizing TGFβ antibodies were delivered systemically, while in vitro experiments used isolated murine microglia and T cells. Single cell RNA sequencing analysis was performed using established methods.

RESULTS: Nf1 OPG mice raised in a GF environment or postnatally treated with vancomycin did not harbor optic gliomas or exhibit OPG-induced retinal nerve fiber layer thinning, which was reversed following conventionally raised mouse FMT or colonization with Bacteroides species. Moreover, this intestinal microbiota-regulated gliomagenesis was mediated by circulating TGFβ, such that systemic TGFβ neutralization reduced Nf1-OPG growth. TGFβ was shown to act on tumor-associated monocytes to induce Ccl3 expression and recruit CD8+ T cells necessary for glioma growth.

CONCLUSIONS: Taken together, these findings establish, for the first time, a mechanistic relationship between Bacteroides in the intestinal microbiome and NF1-LGG pathobiology, suggesting both future predictive risk assessment strategies and therapeutic opportunities.},
}

@article {pmid39868290,
year = {2025},
author = {Weagley, J and Makimaa, H and Cárdenas, LAC and Romani, A and Sullender, M and Aggarwal, S and Hogarty, M and Rodgers, R and Kennedy, E and Foster, L and Schriefer, LA and Baldridge, MT},
title = {Dynamics of Bacterial and Viral Transmission in Experimental Microbiota Transplantation.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.01.15.633206},
pmid = {39868290},
issn = {2692-8205},
abstract = {Mouse models are vital tools for discerning the relative contributions of host and microbial genetics to disease, often requiring the transplantation of microbiota between different mouse strains. Transfer methods include antibiotic treatment of recipients and colonization using either co-housing with donors or the transplantation of fecal or cecal donor material. However, the efficiency and dynamics of these methods in reconstituting recipients with donor microbes is not well understood. We thus directly compared co-housing, fecal transplantation, and cecal transplantation methods. Donor mice from Taconic Biosciences, possessing distinct microbial communities, served as the microbial source for recipient mice from Jackson Laboratories, which were treated with antibiotics to disrupt their native microbiota. We monitored microbial populations longitudinally over the course of antibiotics treatment and reconstitution using 16S rRNA gene sequencing, quantitative PCR, and shotgun sequencing of viral-like particles. As expected, antibiotic treatment rapidly depleted microbial biomass and diversity, with slow and incomplete natural recovery of the microbiota in non-transplanted control mice. While all transfer methods reconstituted recipient mice with donor microbiota, co-housing achieved this more rapidly for both bacterial and viral communities. This study provides valuable insights into microbial transfer methods, enhancing reproducibility and informing best practices for microbiota transplantation in mouse models.},
}

@article {pmid39864578,
year = {2025},
author = {Attiq, A},
title = {Early-Life Antibiotic Exposures: Paving the Pathway for Dysbiosis-Induced Disorders.},
journal = {European journal of pharmacology},
volume = {},
number = {},
pages = {177298},
doi = {10.1016/j.ejphar.2025.177298},
pmid = {39864578},
issn = {1879-0712},
abstract = {Microbiota encompasses a diverse array of microorganisms inhabiting specific ecological niches. Gut microbiota significantly influences physiological processes, including gastrointestinal motor function, neuroendocrine signalling, and immune regulation. They play a crucial role in modulating the central nervous system and bolstering body defence mechanisms by influencing the proliferation and differentiation of innate and adaptive immune cells. Given the potential consequences of antibiotic therapy on gut microbiota equilibrium, there is a need for prudent antibiotic use to mitigate associated risks. Observational studies have linked increased antibiotic usage to various pathogenic conditions, including obesity, inflammatory bowel disease, anxiety-like effects, asthma, and pulmonary carcinogenesis. Addressing dysbiosis incidence requires proactive measures, including prophylactic use of β-lactamase drugs (SYN-004, SYN-006, and SYN-007), hydrolysing the β-lactam in the proximal GIT for maintaining intestinal flora homeostasis. Prebiotic and probiotic supplementations are crucial in restoring intestinal flora equilibrium by competing with pathogenic bacteria for nutritional resources and adhesion sites, reducing luminal pH, neutralising toxins, and producing antimicrobial agents. Faecal microbiota transplantation (FMT) shows promise in restoring gut microbiota composition. Rational antibiotic use is essential to preserve microflora and improve patient compliance with antibiotic regimens by mitigating associated side effects. Given the significant implications on gut microbiota composition, concerted intervention strategies must be pursued to rectify and reverse the occurrence of antibiotic-induced dysbiosis. Here, antibiotics-induced microbiota dysbiosis mechanisms and their systemic implications are reviewed. Moreover, proposed interventions to mitigate the impact on gut microflora are also discussed herein.},
}

@article {pmid39863610,
year = {2025},
author = {Reddi, S and Senyshyn, L and Ebadi, M and Podlesny, D and Minot, SS and Gooley, T and Kabage, AJ and Hill, GR and Lee, SJ and Khoruts, A and Rashidi, A},
title = {Fecal microbiota transplantation to prevent acute graft-versus-host disease: pre-planned interim analysis of donor effect.},
journal = {Nature communications},
volume = {16},
number = {1},
pages = {1034},
pmid = {39863610},
issn = {2041-1723},
support = {P30 CA015704/CA/NCI NIH HHS/United States ; ACT9016-24//Leukemia and Lymphoma Society (Leukemia & Lymphoma Society)/ ; },
mesh = {Humans ; *Graft vs Host Disease/prevention & control/microbiology ; *Fecal Microbiota Transplantation/methods ; Male ; Female ; Middle Aged ; Adult ; *Gastrointestinal Microbiome ; *Hematopoietic Stem Cell Transplantation/adverse effects ; Double-Blind Method ; *Tissue Donors ; *Transplantation, Homologous/adverse effects ; Feces/microbiology ; Acute Disease ; Aged ; Young Adult ; },
abstract = {Gut microbiota disruptions after allogeneic hematopoietic cell transplantation (alloHCT) are associated with increased risk of acute graft-versus-host disease (aGVHD). We designed a randomized, double-blind placebo-controlled trial to test whether healthy-donor fecal microbiota transplantation (FMT) early after alloHCT reduces the incidence of severe aGVHD. Here, we report the results from the single-arm run-in phase which identified the best of 3 stool donors for the randomized phase. The primary and key secondary endpoints were microbiota engraftment and severe aGVHD, respectively. Three cohorts of patients (20 total) received FMT, each from a different donor. FMT was safe and effective in restoring microbiota diversity and commensal species. Microbiota engraftment, determined from shotgun sequencing data, correlated with larger microbiota compositional shifts toward donor and better clinical outcomes. Donor 3 yielded a median engraftment rate of 66%, higher than donors 1 (P = 0.02) and 2 (P = 0.03) in multivariable analysis. Three patients developed severe aGVHD; all 3 had received FMT from donor 1. Donor 3 was selected as the sole donor for the randomized phase. Our findings suggest a clinically relevant donor effect and demonstrate feasibility of evidence-based donor selection. FMT is a holistic microbiota restoration approach that can be performed as a precision therapeutic. ClinicalTrials.gov identifier NCT06026371.},
}

Humans
*Graft vs Host Disease/prevention & control/microbiology
*Fecal Microbiota Transplantation/methods
Male
Female
Middle Aged
Adult
*Gastrointestinal Microbiome
*Hematopoietic Stem Cell Transplantation/adverse effects
Double-Blind Method
*Tissue Donors
*Transplantation, Homologous/adverse effects
Feces/microbiology
Acute Disease
Aged
Young Adult

@article {pmid39863438,
year = {2025},
author = {Jin, J and Cai, X and Rao, P and Xu, J and Li, J},
title = {Microbiota and immune dynamics in rheumatoid arthritis: Mechanisms and therapeutic potential.},
journal = {Best practice & research. Clinical rheumatology},
volume = {},
number = {},
pages = {102035},
doi = {10.1016/j.berh.2025.102035},
pmid = {39863438},
issn = {1532-1770},
abstract = {Rheumatoid arthritis (RA) is a complex autoimmune disease with growing evidence implicating the microbiota as a critical contributor to its pathogenesis. This review explores the multifaceted roles of microbial dysbiosis in RA, emphasizing its impact on immune cell modulation, autoantibody production, gut barrier integrity, and joint inflammation. Animal models reveal how genetic predisposition and environmental factors interact with specific microbial taxa to influence disease susceptibility. Dysbiosis-driven metabolic disruptions, including alterations in short-chain fatty acids and bile acids, further exacerbate immune dysregulation and systemic inflammation. Emerging therapeutic strategies-probiotics, microbial metabolites, fecal microbiota transplantation, and antibiotics-offer innovative avenues for restoring microbial balance and mitigating disease progression. By integrating microbiota-targeted approaches with existing treatments, this review highlights the potential to revolutionize RA management through precision medicine and underscores the need for further research to harness the microbiota's therapeutic potential.},
}

@article {pmid39863236,
year = {2025},
author = {Qin, N and Liu, H and Wang, X and Liu, Y and Chang, H and Xia, X},
title = {Sargassum fusiforme polysaccharides protect mice against Citrobacter rodentium infection via intestinal microbiota-driven microRNA-92a-3p-induced Muc2 production.},
journal = {International journal of biological macromolecules},
volume = {},
number = {},
pages = {140271},
doi = {10.1016/j.ijbiomac.2025.140271},
pmid = {39863236},
issn = {1879-0003},
abstract = {Sargassum fusiforme, widely consumed in Asian countries, has been proven to have various biological activities. However, the impacts and mechanisms of Sargassum fusiforme polysaccharides (SFPs) on intestinal bacterial infection are not yet fully understood. Our findings indicate that SFPs pretreatment ameliorates intestinal inflammation by reducing C. rodentium colonization, increasing colon length and levels of IL-10 and IL-22, decreasing IL-1β, IL-6, TNF-α, and IL-17 levels, inhibiting colonic crypt elongation and hyperplasia, and enhancing the intestinal mucosal barrier. The protective effects against intestinal bacterial infection are linked to enhanced clearance of C. rodentium and improvements in the intestinal mucosal barrier and C. rodentium-induced intestinal microbiota dysbiosis. Fecal microbiota transplantation experiments were conducted to evaluate the functional impact of microbiota induced by SFPs. The results suggest that intestinal microbiota modified by SFPs effectively countered C. rodentium infection. In addition, our study identified that miRNA-92a-3p is partially complementary to the 3'-UTR of the Notch1 gene, thereby repressing the Notch1-Hes1 signaling pathway and enhancing Muc2 secretion. Taken together, these findings reveal that SFPs protect mice from C. rodentium infection by activating the miR-92a-3p/Notch1-Hes1 regulatory axis driven by the intestinal microbiota, which stimulates Muc2 production to maintain intestinal barrier homeostasis.},
}

@article {pmid39862968,
year = {2025},
author = {Huang, P and Di, L and Cui, S and Wang, X and Cao, T and Jiang, S and Huang, L},
title = {Postoperative delirium after cardiac surgery associated with perioperative gut microbiota dysbiosis: Evidence from human and antibiotic-treated mouse model.},
journal = {Anaesthesia, critical care & pain medicine},
volume = {},
number = {},
pages = {101484},
doi = {10.1016/j.accpm.2025.101484},
pmid = {39862968},
issn = {2352-5568},
abstract = {BACKGROUND: Research links gut microbiota to postoperative delirium (POD) through the gut-brain axis. However, changes in gut microbiota and fecal short-chain fatty acids (SCFAs) in POD patients during the perioperative period and their association with POD are unclear.

METHODS: We conducted a nested case-control study among patients undergoing off-pump coronary artery bypass grafting, focusing on POD as the main outcome. POD patients were matched 1:1 with non-POD patients based on sociodemographic characteristics, health, and diet. Fecal samples were collected pre- and post-surgery to assess gut microbiota and SCFA changes. Postoperative fecal samples were transplanted into antibiotic-treated mice to evaluate delirium-like behavior and neuroinflammation.

RESULTS: Out of 120 patients, 60 were matched. Before surgery, gut microbiota in both groups was similar. After surgery, POD patients had lower alpha diversity and distinct microbiota compared to non-POD patients. LEfSe analysis showed POD was linked to increased opportunistic pathogens (Enterococcus) and decreased SCFA producers (Bacteroides, Ruminococcus, etc.). SCFAs were significantly reduced in POD patients and negatively correlated with delirium severity and plasma inflammation. Mice receiving fecal transplants from POD patients exhibited delirium-like behavior and neuroinflammation.

CONCLUSIONS: Postoperative delirium is associated with gut microbiota dysbiosis, marked by an increase in opportunistic pathogens and a decrease in SCFA-producing genera.

REGISTRATION: Chinese Clinical Trial Registry ChiCTR2300070477.},
}

@article {pmid39862808,
year = {2025},
author = {Xiao, Y and He, X and Zhang, H and Wu, X and Ai, R and Xu, J and Wen, Q and Zhang, F and Cui, B},
title = {Washed microbiota transplantation effectively improves nutritional status in gastrointestinal disease-related malnourished children.},
journal = {Nutrition (Burbank, Los Angeles County, Calif.)},
volume = {132},
number = {},
pages = {112679},
doi = {10.1016/j.nut.2024.112679},
pmid = {39862808},
issn = {1873-1244},
abstract = {BACKGROUND AND AIM: Gut microbiota dysbiosis plays a critical role in malnutrition caused by food intolerance and intestinal inflammation in children, which needs to be addressed. We assessed the efficacy and safety of washed microbiota transplantation (WMT) for gastrointestinal disease-related malnourished children.

METHODS: This was a prospective observational study involving gastrointestinal disease-related malnourished pediatric patients who underwent WMT. The primary outcome was the clinical response rate at 3 mo post-WMT. Clinical response was defined as an improvement in the children's nutritional status of one level or more. The secondary outcomes were changes in gastrointestinal symptoms, laboratory nutritional indicators, and adverse events during the WMT procedure.

RESULTS: 29 patients undergoing 74 WMTs were included for analysis. In total, 48.3% (14/29) of patients achieved clinical response post-WMT. Gastrointestinal symptoms, including diarrhea, mucous stool, abdominal pain, abdominal distention, and hematochezia, were significantly relieved post-WMT (all P < 0.05). Serum albumin and prealbumin levels were increased significantly post-WMT (P = 0.028 and 0.028, respectively). Eight self-limiting and transient adverse events, including diarrhea, abdominal pain, and abdominal distension, occurred after WMT.

CONCLUSION: This study indicated that WMT might be effective and safe for improving nutritional status and gastrointestinal symptoms in gastrointestinal disease-related malnourished children at 3-mo follow-up. WMT was expected to be a new therapeutic option for these patients.},
}

@article {pmid39861773,
year = {2025},
author = {Ortiz-Islas, E and Montes, P and Rodríguez-Pérez, CE and Ruiz-Sánchez, E and Sánchez-Barbosa, T and Pichardo-Rojas, D and Zavala-Tecuapetla, C and Carvajal-Aguilera, K and Campos-Peña, V},
title = {Evolution of Alzheimer's Disease Therapeutics: From Conventional Drugs to Medicinal Plants, Immunotherapy, Microbiotherapy and Nanotherapy.},
journal = {Pharmaceutics},
volume = {17},
number = {1},
pages = {},
pmid = {39861773},
issn = {1999-4923},
support = {CF-2023-G-971 and CBF-2023-2024-1982//Ciencia de Frontera/ ; },
abstract = {Alzheimer's disease (AD) represents an escalating global health crisis, constituting the leading cause of dementia among the elderly and profoundly impairing their quality of life. Current FDA-approved drugs, such as rivastigmine, donepezil, galantamine, and memantine, offer only modest symptomatic relief and are frequently associated with significant adverse effects. Faced with this challenge and in line with advances in the understanding of the pathophysiology of this neurodegenerative condition, various innovative therapeutic strategies have been explored. Here, we review novel approaches inspired by advanced knowledge of the underlying pathophysiological mechanisms of the disease. Among the therapeutic alternatives, immunotherapy stands out, employing monoclonal antibodies to specifically target and eliminate toxic proteins implicated in AD. Additionally, the use of medicinal plants is examined, as their synergistic effects among components may confer neuroprotective properties. The modulation of the gut microbiota is also addressed as a peripheral strategy that could influence neuroinflammatory and degenerative processes in the brain. Furthermore, the therapeutic potential of emerging approaches, such as the use of microRNAs to regulate key cellular processes and nanotherapy, which enables precise drug delivery to the central nervous system, is analyzed. Despite promising advances in these strategies, the incidence of Alzheimer's disease continues to rise. Therefore, it is proposed that achieving effective treatment in the future may require the integration of combined approaches, maximizing the synergistic effects of different therapeutic interventions.},
}

@article {pmid39859091,
year = {2025},
author = {Almonajjed, MB and Wardeh, M and Atlagh, A and Ismaiel, A and Popa, SL and Rusu, F and Dumitrascu, DL},
title = {Impact of Microbiota on Irritable Bowel Syndrome Pathogenesis and Management: A Narrative Review.},
journal = {Medicina (Kaunas, Lithuania)},
volume = {61},
number = {1},
pages = {},
pmid = {39859091},
issn = {1648-9144},
mesh = {Humans ; *Irritable Bowel Syndrome/therapy/microbiology/physiopathology ; *Gastrointestinal Microbiome/physiology ; *Fecal Microbiota Transplantation/methods ; *Probiotics/therapeutic use ; Brain-Gut Axis/physiology ; Dysbiosis/therapy/complications ; Quality of Life ; Synbiotics/administration & dosage ; Prebiotics/administration & dosage ; },
abstract = {Irritable bowel syndrome (IBS) is a prevalent gastrointestinal disorder, affecting 3-5% of the global population and significantly impacting patients' quality of life and healthcare resources. Alongside physical symptoms such as abdominal pain and altered bowel habits, many individuals experience psychological comorbidities, including anxiety and depression. Recent research has highlighted the critical role of the gut microbiota in IBS, with dysbiosis, characterized by an imbalance in microbial diversity, frequently observed in patients. The gut-brain axis, a bidirectional communication network between the gut and central nervous system, plays a central role in the development of IBS symptoms. Although interventions such as probiotics, prebiotics, synbiotics, and fecal microbiota transplantation (FMT) have demonstrated potential in modulating the gut microbiota and alleviating symptoms, their efficacy remains an area of ongoing investigation. This review examines the interactions between the gut microbiota, immune system, and brain, emphasizing the need for personalized therapeutic strategies. Future research should aim to identify reliable microbiota-based biomarkers for IBS and refine microbiome-targeted therapies to enhance patient outcomes.},
}

Humans
*Irritable Bowel Syndrome/therapy/microbiology/physiopathology
*Gastrointestinal Microbiome/physiology
*Fecal Microbiota Transplantation/methods
*Probiotics/therapeutic use
Brain-Gut Axis/physiology
Dysbiosis/therapy/complications
Quality of Life
Synbiotics/administration & dosage
Prebiotics/administration & dosage

@article {pmid39858858,
year = {2025},
author = {Onisiforou, A and Charalambous, EG and Zanos, P},
title = {Shattering the Amyloid Illusion: The Microbial Enigma of Alzheimer's Disease Pathogenesis-From Gut Microbiota and Viruses to Brain Biofilms.},
journal = {Microorganisms},
volume = {13},
number = {1},
pages = {},
pmid = {39858858},
issn = {2076-2607},
support = {#101031962//European Commission Marie Skłodowska-Curie fellowship/ ; EXCELLENCE/0421/0543//Research & Innovation Foundation of Cyprus - Excellence Hubs 2021/ ; NA//IDSA Foundation/ ; },
abstract = {For decades, Alzheimer's Disease (AD) research has focused on the amyloid cascade hypothesis, which identifies amyloid-beta (Aβ) as the primary driver of the disease. However, the consistent failure of Aβ-targeted therapies to demonstrate efficacy, coupled with significant safety concerns, underscores the need to rethink our approach to AD treatment. Emerging evidence points to microbial infections as environmental factors in AD pathoetiology. Although a definitive causal link remains unestablished, the collective evidence is compelling. This review explores unconventional perspectives and emerging paradigms regarding microbial involvement in AD pathogenesis, emphasizing the gut-brain axis, brain biofilms, the oral microbiome, and viral infections. Transgenic mouse models show that gut microbiota dysregulation precedes brain Aβ accumulation, emphasizing gut-brain signaling pathways. Viral infections like Herpes Simplex Virus Type 1 (HSV-1) and Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) may lead to AD by modulating host processes like the immune system. Aβ peptide's antimicrobial function as a response to microbial infection might inadvertently promote AD. We discuss potential microbiome-based therapies as promising strategies for managing and potentially preventing AD progression. Fecal microbiota transplantation (FMT) restores gut microbial balance, reduces Aβ accumulation, and improves cognition in preclinical models. Probiotics and prebiotics reduce neuroinflammation and Aβ plaques, while antiviral therapies targeting HSV-1 and vaccines like the shingles vaccine show potential to mitigate AD pathology. Developing effective treatments requires standardized methods to identify and measure microbial infections in AD patients, enabling personalized therapies that address individual microbial contributions to AD pathogenesis. Further research is needed to clarify the interactions between microbes and Aβ, explore bacterial and viral interplay, and understand their broader effects on host processes to translate these insights into clinical interventions.},
}

@article {pmid39858421,
year = {2024},
author = {Gabrielli, M and Zileri Dal Verme, L and Zocco, MA and Nista, EC and Ojetti, V and Gasbarrini, A},
title = {The Role of the Gastrointestinal Microbiota in Parkinson's Disease.},
journal = {Biomolecules},
volume = {15},
number = {1},
pages = {},
pmid = {39858421},
issn = {2218-273X},
mesh = {*Parkinson Disease/microbiology/metabolism ; Humans ; *Gastrointestinal Microbiome ; *Dysbiosis/microbiology ; *Probiotics/therapeutic use ; Animals ; Fecal Microbiota Transplantation ; Helicobacter Infections/microbiology ; Prebiotics ; Brain-Gut Axis/physiology ; Helicobacter pylori ; },
abstract = {BACKGROUND/OBJECTIVES: Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons leading to debilitating motor and non-motor symptoms. Beyond its well-known neurological features, emerging evidence underscores the pivotal role of the gut-brain axis and gastrointestinal microbiota in PD pathogenesis. Dysbiosis has been strongly linked to PD and is associated with increased intestinal permeability, chronic inflammation, and the production of neurotoxic metabolites that may exacerbate neuronal damage.

METHODS: This review delves into the complex interplay between PD and dysbiosis, shedding light on two peculiar subsets of dysbiosis, Helicobacter pylori infection and small-intestinal bacterial overgrowth. These conditions may not only contribute to PD progression but also influence therapeutic responses such as L-dopa efficacy.

CONCLUSIONS: The potential to modulate gut microbiota through probiotics, prebiotics, and synbiotics; fecal microbiota transplantation; and antibiotics represents a promising frontier for innovative PD treatments. Despite this potential, the current evidence is limited by small sample sizes and methodological variability across studies. Rigorous, large-scale, randomized placebo-controlled trials with standardized treatments in terms of composition, dosage, and duration are urgently needed to validate these findings and pave the way for microbiota-based therapeutic strategies in PD management.},
}

*Parkinson Disease/microbiology/metabolism
Humans
*Gastrointestinal Microbiome
*Dysbiosis/microbiology
*Probiotics/therapeutic use
Animals
Fecal Microbiota Transplantation
Helicobacter Infections/microbiology
Prebiotics
Brain-Gut Axis/physiology
Helicobacter pylori

@article {pmid39858303,
year = {2024},
author = {Morado, F and Nanda, N},
title = {A Review of Therapies for Clostridioides difficile Infection.},
journal = {Antibiotics (Basel, Switzerland)},
volume = {14},
number = {1},
pages = {},
pmid = {39858303},
issn = {2079-6382},
abstract = {Clostridioides difficile is an urgent public health threat that affects approximately half a million patients annually in the United States. Despite concerted efforts aimed at the prevention of Clostridioides difficile infection (CDI), it remains a leading cause of healthcare-associated infections. CDI is associated with significant clinical, social, and economic burdens. Therefore, it is imperative to provide optimal and timely therapy for CDI. We conducted a systematic literature review and offer treatment recommendations based on available evidence for the treatment and prevention of CDI.},
}

@article {pmid39857680,
year = {2025},
author = {Radoš, L and Golčić, M and Mikolašević, I},
title = {The Relationship Between the Modulation of Intestinal Microbiota and the Response to Immunotherapy in Patients with Cancer.},
journal = {Biomedicines},
volume = {13},
number = {1},
pages = {},
pmid = {39857680},
issn = {2227-9059},
abstract = {The intestinal microbiota is an important part of the human body, and its composition can affect the effectiveness of immunotherapy. In the last few years, the modulation of intestinal microbiota in order to improve the effectiveness of immunotherapy has become a current topic in the scientific community, but there is a lack of research in this area. In this review, the goal was to analyze the current relevant literature related to the modulation of intestinal microbiota and the effectiveness of immunotherapy in the treatment of cancer. The effects of antibiotics, probiotics, diet, and fecal microbial transplantation were analyzed separately. It was concluded that the use of antibiotics, especially broad-spectrum types or larger quantities, causes dysbiosis of the intestinal microbiota, which can reduce the effectiveness of immunotherapy. While dysbiosis could be repaired by probiotics and thus improve the effectiveness of immunotherapy, the use of commercial probiotics without evidence of intestinal dysbiosis has not yet been sufficiently tested to confirm its safety for cancer for immunotherapy-treated cancer patients. A diet consisting of sufficient amounts of fiber, as well as a diet with higher salt content positively correlates with the success of immunotherapy. Fecal transplantation is a safe and realistic adjuvant option for the treatment of cancer patients with immunotherapy, but more clinical trials are necessary. Modulating the microbiota composition indeed changes the effectiveness of immunotherapy, but in the future, more human studies should be organized to precisely determine the types and procedures of microbiota modulation.},
}

@article {pmid39857657,
year = {2024},
author = {Li, W and Gao, W and Yan, S and Yang, L and Zhu, Q and Chu, H},
title = {Gut Microbiota as Emerging Players in the Development of Alcohol-Related Liver Disease.},
journal = {Biomedicines},
volume = {13},
number = {1},
pages = {},
pmid = {39857657},
issn = {2227-9059},
support = {National Nature Science Foundation of China (No.81974078, No.81570530, and No.81370550)//Ling Yang/ ; National Key R&D Program of China (No.2022YFA1305600)//Huikuan Chu/ ; Ministry of Science and Technology of China (No.2023YFC2413804)//Ling Yang/ ; Natural Science Foundation of Hubei Province (No.2019ACA1333)//Ling Yang/ ; },
abstract = {The global incidence and mortality rates of alcohol-related liver disease are on the rise, reflecting a growing health concern worldwide. Alcohol-related liver disease develops due to a complex interplay of multiple reasons, including oxidative stress generated during the metabolism of ethanol, immune response activated by immunogenic substances, and subsequent inflammatory processes. Recent research highlights the gut microbiota's significant role in the progression of alcohol-related liver disease. In patients with alcohol-related liver disease, the relative abundance of pathogenic bacteria, including Enterococcus faecalis, increases and is positively correlated with the level of severity exhibited by alcohol-related liver disease. Supplement probiotics like Lactobacillus, as well as Bifidobacterium, have been found to alleviate alcohol-related liver disease. The gut microbiota is speculated to trigger specific signaling pathways, influence metabolite profiles, and modulate immune responses in the gut and liver. This research aimed to investigate the role of gut microorganisms in the onset and advancement of alcohol-related liver disease, as well as to uncover the underlying mechanisms by which the gut microbiota may contribute to its development. This review outlines current treatments for reversing gut dysbiosis, including probiotics, fecal microbiota transplantation, and targeted phage therapy. Particularly, targeted therapy will be a vital aspect of future alcohol-related liver disease treatment. It is to be hoped that this article will prove beneficial for the treatment of alcohol-related liver disease.},
}

@article {pmid39855927,
year = {2025},
author = {Wang, X and Zhao, D and Bi, D and Li, L and Tian, H and Yin, F and Zuo, T and Ianiro, G and Han, YW and Li, N and Chen, Q and Qin, H},
title = {Fecal microbiota transplantation: transitioning from chaos and controversial realm to scientific precision era.},
journal = {Science bulletin},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.scib.2025.01.029},
pmid = {39855927},
issn = {2095-9281},
abstract = {With the popularization of modern lifestyles, the spectrum of intestinal diseases has become increasingly diverse, presenting significant challenges in its management. Traditional pharmaceutical interventions have struggled to keep pace with these changes, leaving many patients refractory to conventional pharmaceutical treatments. Fecal microbiota transplantation (FMT) has emerged as a promising therapeutic approach for enterogenic diseases. Still, controversies persist regarding its active constituents, mechanism of action, scheme of treatment evaluation, indications, and contraindications. In this review, we investigated the efficacy of FMT in addressing gastrointestinal and extraintestinal conditions, drawing from follow-up data on over 8000 patients. We systematically addressed the controversies surrounding FMT's clinical application. We delved into key issues such as its technical nature, evaluation methods, microbial restoration mechanisms, and impact on the host-microbiota interactions. Additionally, we explored the potential colonization patterns of FMT-engrafted new microbiota throughout the entire intestine and elucidated the specific pathways through which the new microbiota modulates host immunity, metabolism, and genome.},
}

@article {pmid39855612,
year = {2025},
author = {Sutanto, H and Elisa, E and Rachma, B and Fetarayani, D},
title = {Gut Microbiome Modulation in Allergy Treatment: The Role of Fecal Microbiota Transplantation.},
journal = {The American journal of medicine},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.amjmed.2025.01.005},
pmid = {39855612},
issn = {1555-7162},
abstract = {The prevalence of allergic diseases has been rising, paralleling lifestyle changes and environmental exposures that have altered human microbiome composition. This review article examines the intricate relationship between the gut microbiome and allergic diseases, emphasizing the potential of fecal microbiota transplantation as a promising novel treatment approach. It explains how reduced microbial exposure in modern societies contributes to immune dysregulation and the increasing incidence of allergies. The discussion also addresses immune homeostasis and its modulation by the gut microbiome, highlighting the shift from eubiosis to dysbiosis in allergic conditions. Furthermore, this article reviews existing studies and emerging research on the role of fecal microbiota transplantation in restoring microbial balance, providing insights into its mechanisms, efficacy, and safety.},
}

@article {pmid39854760,
year = {2025},
author = {Chen, S and Zhang, D and Li, D and Zeng, F and Chen, C and Bai, F},
title = {Microbiome characterization of patients with Crohn disease and the use of fecal microbiota transplantation: A review.},
journal = {Medicine},
volume = {104},
number = {4},
pages = {e41262},
doi = {10.1097/MD.0000000000041262},
pmid = {39854760},
issn = {1536-5964},
support = {2021818//Hainan Province Clinical Medical Center/ ; YSPTZX202313//The specific research fund of The Innovation Platform for Academicians of Hainan Province/ ; 22A200078//Hainan Provincial Health Industry Research Project/ ; Qhyb2022-133//Hainan Provincial Postgraduate Innovation Research Project/ ; },
mesh = {Humans ; *Crohn Disease/therapy/microbiology ; *Fecal Microbiota Transplantation/methods ; *Gastrointestinal Microbiome ; },
abstract = {Inflammatory bowel disease is a chronic inflammatory condition predominantly affecting the intestines, encompassing both ulcerative colitis and Crohn disease (CD). As one of the most common gastrointestinal disorders, CD's pathogenesis is closely linked with the intestinal microbiota. Recently, fecal microbiota transplantation (FMT) has gained attention as a potential treatment for CD, with the effective reestablishment of intestinal microecology considered a crucial mechanism of FMT therapy. This article synthesizes the findings of population-based cohort studies to enhance our understanding of gut microbial characteristics in patients with CD. It delves into the roles of "beneficial" and "pathogenic" bacteria in CD's development. This article systematically reviews and compares data on clinical response rates, remission rates, adverse events, and shifts in bacterial microbiota. Among these studies, gut microbiome analysis was conducted in only 7, and a single study examined the metabolome. Overall, FMT has demonstrated a partial restoration of typical CD-associated microbiological alterations, leading to increased α-diversity in responders and a moderate shift in patient microbiota toward the donor profile. Several factors, including donor selection, delivery route, microbial state (fresh or frozen), and recipient condition, are identified as pivotal in influencing FMT's effectiveness. Future prospective clinical studies with larger patient cohorts and improved methodologies are imperative. In addition, standardization of FMT procedures, coupled with advanced genomic techniques such as macroproteomics and culture genomics, is necessary. These advancements will further clarify the bacterial microbiota alterations that significantly contribute to FMT's therapeutic effects in CD treatment, as well as elucidate the underlying mechanisms of action.},
}

Humans
*Crohn Disease/therapy/microbiology
*Fecal Microbiota Transplantation/methods
*Gastrointestinal Microbiome

@article {pmid39854205,
year = {2025},
author = {Yang, CJ and Peng, YS and Sung, PC and Hsieh, SY},
title = {Protocol for oral fecal gavage to reshape the gut microbiota in mice.},
journal = {STAR protocols},
volume = {6},
number = {1},
pages = {103585},
doi = {10.1016/j.xpro.2024.103585},
pmid = {39854205},
issn = {2666-1667},
abstract = {Fecal microbiota transplantation (FMT) is clinically applied, while oral FMT (oral fecal gavage [OFG]) is preferred for experimental mice. Here, we present a protocol for OFG in antibiotic-pretreated mice, demonstrating the progressive, time-dependent evolution of the gut microbiota in the recipients. We describe steps for fecal sample collection and preparation procedures, oral gavage, and monitoring gut microbiota changes. This protocol serves as a general guide for reshaping the gut microbiota in recipient mice for various experimental applications. For complete details on the use and execution of this protocol, please refer to Yang et al.[1].},
}

@article {pmid39854158,
year = {2025},
author = {Lau, RI and Su, Q and Ng, SC},
title = {Long COVID and gut microbiome: insights into pathogenesis and therapeutics.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2457495},
doi = {10.1080/19490976.2025.2457495},
pmid = {39854158},
issn = {1949-0984},
mesh = {*Gastrointestinal Microbiome ; Humans ; *Fecal Microbiota Transplantation ; *COVID-19/therapy/microbiology ; *Probiotics/therapeutic use ; *Dysbiosis/therapy/microbiology ; *SARS-CoV-2 ; *Post-Acute COVID-19 Syndrome ; Prebiotics/administration & dosage ; },
abstract = {Post-acute coronavirus disease 2019 syndrome (PACS), following severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection or coronavirus disease 2019 (COVID-19), is typically characterized by long-term debilitating symptoms affecting multiple organs and systems. Unfortunately, there is currently a lack of effective treatment strategies. Altered gut microbiome has been proposed as one of the plausible mechanisms involved in the pathogenesis of PACS; extensive studies have emerged to bridge the gap between the persistent symptoms and the dysbiosis of gut microbiome. Recent clinical trials have indicated that gut microbiome modulation using probiotics, prebiotics, and fecal microbiota transplantation (FMT) led to improvements in multiple symptoms related to PACS, including fatigue, memory loss, difficulty in concentration, gastrointestinal upset, and disturbances in sleep and mood. In this review, we highlight the latest evidence on the key microbial alterations observed in PACS, as well as the use of microbiome-based therapeutics in managing PACS symptoms. These novel findings altogether shed light on the treatment of PACS and other chronic conditions.},
}

*Gastrointestinal Microbiome
Humans
*Fecal Microbiota Transplantation
*COVID-19/therapy/microbiology
*Probiotics/therapeutic use
*Dysbiosis/therapy/microbiology
*SARS-CoV-2
*Post-Acute COVID-19 Syndrome
Prebiotics/administration & dosage

@article {pmid39851261,
year = {2025},
author = {Zhao, X and Qiu, Y and Liang, L and Fu, X},
title = {Interkingdom signaling between gastrointestinal hormones and the gut microbiome.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2456592},
doi = {10.1080/19490976.2025.2456592},
pmid = {39851261},
issn = {1949-0984},
mesh = {*Gastrointestinal Microbiome/physiology ; Humans ; Animals ; *Dysbiosis/microbiology ; *Gastrointestinal Hormones/metabolism ; *Bacteria/metabolism/classification/genetics ; Fecal Microbiota Transplantation ; Signal Transduction ; Homeostasis ; Inflammatory Bowel Diseases/microbiology/metabolism ; Gastrointestinal Tract/microbiology/metabolism ; },
abstract = {The interplay between the gut microbiota and gastrointestinal hormones plays a pivotal role in the health of the host and the development of diseases. As a vital component of the intestinal microecosystem, the gut microbiota influences the synthesis and release of many gastrointestinal hormones through mechanisms such as modulating the intestinal environment, producing metabolites, impacting mucosal barriers, generating immune and inflammatory responses, and releasing neurotransmitters. Conversely, gastrointestinal hormones exert feedback regulation on the gut microbiota by modulating the intestinal environment, nutrient absorption and utilization, and the bacterial biological behavior and composition. The distributions of the gut microbiota and gastrointestinal hormones are anatomically intertwined, and close interactions between the gut microbiota and gastrointestinal hormones are crucial for maintaining gastrointestinal homeostasis. Interventions leveraging the interplay between the gut microbiota and gastrointestinal hormones have been employed in the clinical management of metabolic diseases and inflammatory bowel diseases, such as bariatric surgery and fecal microbiota transplantation, offering promising targets for the treatment of dysbiosis-related diseases.},
}

*Gastrointestinal Microbiome/physiology
Humans
Animals
*Dysbiosis/microbiology
*Gastrointestinal Hormones/metabolism
*Bacteria/metabolism/classification/genetics
Fecal Microbiota Transplantation
Signal Transduction
Homeostasis
Inflammatory Bowel Diseases/microbiology/metabolism
Gastrointestinal Tract/microbiology/metabolism

@article {pmid39850178,
year = {2024},
author = {Gandhi, DN and Pande, DN and Harikrishna, A and Advilkar, A and Basavan, I and Ansari, R},
title = {Beyond the Brain: Attention Deficit/Hyperactivity Disorder and the Gut-Brain Axis.},
journal = {Cureus},
volume = {16},
number = {12},
pages = {e76291},
pmid = {39850178},
issn = {2168-8184},
abstract = {Attention-deficit/hyperactivity disorder (ADHD) is a complex neurodevelopmental condition, predominantly affecting children, characterized by inattention, hyperactivity, and impulsivity. A growing body of evidence has highlighted the potential influence of the gut microbiota on the onset and presentation of ADHD symptoms. The gut microbiota, a diverse microbial ecosystem residing within the gastrointestinal tract, exerts multiple effects on systemic physiology, including immune modulation, metabolic regulation, and neuronal signalling. The bidirectional gut-brain axis serves as a conduit for communication between gut microbes and the central nervous system, implicating its disruption in neurodevelopmental disorders such as ADHD. This comprehensive literature review aims to shed light on how alterations in the gut microbiota influence the development and manifestation of ADHD symptoms. Examining potential mechanisms involving gut microbial metabolites and their impact on neurotransmitter modulation, neuro-endocrine signalling and neuroinflammation, we dissect the intricate interplay shaping ADHD pathology. Insights into these complex interactions hold promise for personalized therapeutic interventions aimed at modulating the gut microbiota to ameliorate ADHD symptoms. Discussions encompass dietary interventions, faecal microbiota-targeted therapies, and emerging probiotic approaches, underscoring their potential as adjunctive or alternative strategies in managing ADHD. Further research elucidating the precise mechanisms driving these interactions may pave the way for targeted and personalized interventions for individuals grappling with ADHD.},
}

@article {pmid39848238,
year = {2025},
author = {Szajewska, H},
title = {An Overview of Early-Life Gut Microbiota Modulation Strategies.},
journal = {Annals of nutrition & metabolism},
volume = {},
number = {},
pages = {1-6},
doi = {10.1159/000541492},
pmid = {39848238},
issn = {1421-9697},
abstract = {BACKGROUND: The gut microbiota, or microbiome, is essential for human health. Early-life factors such as delivery mode, diet, and antibiotic use shape its composition, impacting both short- and long-term health outcomes. Dysbiosis, or alterations in the gut microbiota, is linked to conditions such as allergies, asthma, obesity, diabetes, inflammatory bowel disease, and necrotizing enterocolitis in preterm infants.

SUMMARY: This article reviews current strategies to influence the early-life gut microbiome and their potential health impacts. It also briefly summarizes guidelines on using biotics for gastrointestinal and allergic diseases in children. Key strategies include vaginal or fecal microbiota transplantation for cesarean-born infants, breastfeeding, and biotic-supplemented formulas. While vaginal microbial transfer and maternal fecal microbiota transplantation show short-term benefits, further research is needed to determine long-term safety and efficacy. Breast milk, rich in human milk oligosaccharides, promotes a healthy microbiota and offers protection against infections. Biotic-supplemented formulas can improve the gut microbiota in formula-fed infants and show clinical effects, though each biotic must be evaluated separately. Probiotics given as dietary supplements outside of infant formulas show promise for treating gastrointestinal disorders but require further investigation.},
}

@article {pmid39845805,
year = {2024},
author = {Shen, Y and Gao, Y and Yang, G and Zhao, Z and Zhao, Y and Gao, L and Li, S},
title = {Anti-colorectal cancer effect of total minor ginsenosides produced by lactobacilli transformation of major ginsenosides by inducing apoptosis and regulating gut microbiota.},
journal = {Frontiers in pharmacology},
volume = {15},
number = {},
pages = {1496346},
pmid = {39845805},
issn = {1663-9812},
abstract = {OBJECTIVE: Minor ginsenosides have demonstrated promising anticancer effects in previous reports. Total minor ginsenosides (TMG) were obtained through the fermentation of major ginsenosides with Lactiplantibacillus plantarum, and potential anticancer effects of TMGs on the mouse colon cancer cell line CT26.WT, in vitro and in vivo, were investigated.

MATERIALS AND METHODS: We employed the Cell Counting Kit-8 (CCK-8), TdT-mediated dUTP nick end labeling (TUNEL), and Western blot analysis in vitro to explore the anti-proliferative and pro-apoptotic functions of TMG in CT26.WT cells. In vivo, a xenograft model was established by subcutaneously injecting mice with CT26.WT cells and administering a dose of 100 mg/kg/day TMG to the tumor-bearing mice. The level of apoptosis and expression of various proteins in the tumor tissues were detected by immunohistochemistry and Western blot. High-throughput 16S rRNA sequencing was used to determine the alterations in the gut microbiota.

RESULTS: In vitro studies demonstrated that TMG significantly inhibited proliferation and promoted apoptosis in CT26.WT cells. Interestingly, TMG induced apoptosis in CT26.WT cells by affecting the Bax/Bcl-2/caspase-3 pathway. Furthermore, the result of the transplanted tumor model indicated that TMG substantially enhanced the activities of Bax and caspase-3, reduced the activity of Bcl-2, and suppressed the expression of Raf/MEK/ERK protein levels. Fecal analysis revealed that TMG reconstructed the gut microbiota in colorectal cancer-affected mice by augmenting the abundance of the advantageous bacterium Lactobacillus and decreasing the abundance of the harmful bacterium Proteus.

CONCLUSION: TMG can exhibit potent anti-colorectal cancer effects through diverse apoptotic mechanisms, with their mode of action closely related to the regulation of gut microbiota.},
}

@article {pmid39845049,
year = {2024},
author = {Wu, R and Mai, Z and Song, X and Zhao, W},
title = {Hotspots and research trends of gut microbiome in polycystic ovary syndrome: a bibliometric analysis (2012-2023).},
journal = {Frontiers in microbiology},
volume = {15},
number = {},
pages = {1524521},
pmid = {39845049},
issn = {1664-302X},
abstract = {INTRODUCTION: Polycystic ovary syndrome (PCOS) is a common gynecological condition affecting individuals of reproductive age and is linked to the gut microbiome. This study aimed to identify the hotspots and research trends within the domain of the gut microbiome in PCOS through bibliometric analysis.

METHODS: Utilizing bibliometric techniques, we examined the literature on the gut microbiome in PCOS from the Web of Science Core Collection spanning the period from 2012 to 2023. Analytical tools such as CiteSpace, VOSviewer, and Bibliometric R packages were employed to evaluate various metrics, including countries/regions, institutions, authors, co-cited authors, authors' H-index, journals, co-references, and keywords.

RESULTS: A total of 191 publications were identified in the field of gut microbiome in PCOS, with an increase in annual publications from 2018 to 2023. People's Republic of China was the most productive country, followed by the United States of America (USA), India. Shanghai Jiao Tong University, Fudan University, and Beijing University of Chinese Medicine were the top three most publications institutions. Thackray VG was identified as the most prolific author, holding the highest H-index, while Liu R received the highest total number of citations. The journal "Frontiers in Endocrinology" published the most articles in this domain. The most frequently co-cited reference was authored by Qi XY. The analysis of keyword burst detection identified "bile acids" (2021-2023) as the leading frontier keyword. Additionally, "gut dysbiosis," "phenotypes," "adolescents," "metabolomics," "metabolites," "fecal microbiota transplantation," and "IL-22" have emerged as the primary keywords reflecting recent research trends.

CONCLUSION: This bibliometric analysis explores how the gut microbiome influences endocrine and metabolic disorders related to PCOS, emphasizing its role in the development of PCOS and treatments targeting the gut microbiome. The findings serve as a valuable resource for researchers, enabling them to identify critical hotspots and emerging areas of investigation in this field.},
}

@article {pmid39844078,
year = {2025},
author = {Fan, X and Li, J and Gao, Y and Li, L and Zhang, H and Bi, Z},
title = {The mechanism of enterogenous toxin methylmalonic acid aggravating calcium-phosphorus metabolic disorder in uremic rats by regulating the Wnt/β-catenin pathway.},
journal = {Molecular medicine (Cambridge, Mass.)},
volume = {31},
number = {1},
pages = {19},
pmid = {39844078},
issn = {1528-3658},
mesh = {Animals ; Rats ; *Wnt Signaling Pathway ; *Calcium/metabolism ; Male ; *Phosphorus/metabolism ; *Uremia/metabolism/etiology ; *Methylmalonic Acid/metabolism ; Podocytes/metabolism/pathology ; Gastrointestinal Microbiome/drug effects ; Disease Models, Animal ; Rats, Sprague-Dawley ; Apoptosis/drug effects ; beta Catenin/metabolism ; Kidney/pathology/metabolism ; },
abstract = {BACKGROUND: Uremia (UR) is caused by increased UR-related toxins in the bloodstream. We explored the mechanism of enterogenous toxin methylmalonic acid (MMA) in calcium-phosphorus metabolic disorder in UR rats via the Wnt/β-catenin pathway.

METHODS: The UR rat model was established by 5/6 nephrectomy. The fecal bacteria of UR rats were transplanted into Sham rats. Sham rats were injected with exogenous MMA or Salinomycin (SAL). Pathological changes in renal/colon tissues were analyzed. MMA concentration, levels of renal function indicators, serum inflammatory factors, Ca[2+]/P[3+], and parathyroid hormone, intestinal flora structure, fecal metabolic profile, intestinal permeability, and glomerular filtration rate (GFR) were assessed. Additionally, rat glomerular podocytes were cultured, with cell viability and apoptosis measured.

RESULTS: Intestinal flora richness and diversity in UR rats were decreased, along with unbalanced flora structure. Among the screened 133 secondary differential metabolites, the MMA concentration rose, showing the most significant difference. UR rat fecal transplantation caused elevated MMA concentration in the serum and renal tissues of Sham rats. The intestinal flora metabolite MMA or exogenous MMA promoted intestinal barrier impairment, increased intestinal permeability, induced glomerular podocyte loss, and reduced GFR, causing calcium-phosphorus metabolic disorder. The intestinal flora metabolite MMA or exogenous MMA induced inflammatory responses and facilitated glomerular podocyte apoptosis by activating the Wnt/β-catenin pathway, which could be counteracted by repressing the Wnt/β-catenin pathway.

CONCLUSIONS: Enterogenous toxin MMA impelled intestinal barrier impairment in UR rats, enhanced intestinal permeability, and activated the Wnt/β-catenin pathway to induce glomerular podocyte loss and reduce GFR, thus aggravating calcium-phosphorus metabolic disorder.},
}

Animals
Rats
*Wnt Signaling Pathway
*Calcium/metabolism
Male
*Phosphorus/metabolism
*Uremia/metabolism/etiology
*Methylmalonic Acid/metabolism
Podocytes/metabolism/pathology
Gastrointestinal Microbiome/drug effects
Disease Models, Animal
Rats, Sprague-Dawley
Apoptosis/drug effects
beta Catenin/metabolism
Kidney/pathology/metabolism

@article {pmid39840995,
year = {2025},
author = {Hua, D and Yang, Q and Li, X and Zhou, X and Kang, Y and Zhao, Y and Wu, D and Zhang, Z and Li, B and Wang, X and Qi, X and Chen, Z and Cui, G and Hong, W},
title = {The combination of Clostridium butyricum and Akkermansia muciniphila mitigates DSS-induced colitis and attenuates colitis-associated tumorigenesis by modulating gut microbiota and reducing CD8[+] T cells in mice.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0156724},
doi = {10.1128/msystems.01567-24},
pmid = {39840995},
issn = {2379-5077},
abstract = {UNLABELLED: The gut microbiota is closely associated with inflammatory bowel disease (IBD) and colorectal cancer (CRC). Probiotics such as Clostridium butyricum (CB) or Akkermansia muciniphila (AKK) have the potential to treat inflammatory bowel disease (IBD) or colorectal cancer (CRC). However, research on the combined therapeutic effects and immunomodulatory mechanisms of CB and AKK in treating IBD or CRC has never been studied. This study evaluates the potential of co-administration of CB and AKK in treating DSS/AOM-induced IBD and colitis-associated CRC. Our results indicate that compared to mono-administration, the co-administration of CB and AKK not only significantly alleviates symptoms such as weight loss, colon shortening, and increased Disease Activity Index in IBD mice but also regulates the gut microbiota composition and effectively suppresses colonic inflammatory responses. In the colitis-associated CRC mice model, a combination of CB and AKK significantly alleviates weight loss and markedly reduces inflammatory infiltration of macrophages and cytotoxic T lymphocytes (CTLs) in the colon, thereby regulating anti-tumor immunity and inhibiting the occurrence of inflammation-induced CRC. In addition, we found that the combined probiotic therapy of CB and AKK can enhance the sensitivity of colitis-associated CRC mice to the immune checkpoint inhibitor anti-mouse PD-L1 (aPD-L1), significantly improving the anti-tumor efficacy of immunotherapy and the survival rate of colitis-associated CRC mice. Furthermore, fecal microbiota transplantation therapy showed that transplanting feces from CRC mice treated with the co-administration of CB and AKK into other CRC mice alleviated the tumor loads in the colon and significantly extended their survival rate. Our study suggests that the combined use of two probiotics, CB and AKK, can not only alleviate chronic intestinal inflammation but also inhibit the progression to CRC. This may be a natural and relatively safe method to support the gut microbiota and enhance the host's immunity against cancer.

IMPORTANCE: Our study suggests that the combined administration of CB and AKK probiotics, as opposed to a single probiotic strain, holds considerable promise in preventing the advancement of IBD to CRC. This synergistic effect is attributed to the ability of this probiotic combination to more effectively modulate the gut microbiota, curb inflammatory reactions, bolster the efficacy of immunotherapeutic approaches, and optimize treatment results via fecal microbiota transplantation.},
}

@article {pmid39840614,
year = {2025},
author = {Liu, W and Wang, J and Yang, H and Li, C and Lan, W and Chen, T and Tang, Y},
title = {The Metabolite Indole-3-Acetic Acid of Bacteroides Ovatus Improves Atherosclerosis by Restoring the Polarisation Balance of M1/M2 Macrophages and Inhibiting Inflammation.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e2413010},
doi = {10.1002/advs.202413010},
pmid = {39840614},
issn = {2198-3844},
support = {82360105//Innovative Research Group Project of the National Natural Science Foundation of China/ ; 20232ACB206001//Natural Science Foundation of Jiangxi Province/ ; 20223BBG71010//Key Research and Development Program of Jiangxi Province/ ; 2024SSY07061//Jiangxi Province Key Laboratory of bioengineering drugs/ ; },
abstract = {Emerging research has highlighted the significant role of the gut microbiota in atherosclerosis (AS), with microbiota-targeted interventions offering promising therapeutic potential. A central component of this process is gut-derived metabolites, which play a crucial role in mediating the distal functioning of the microbiota. In this study, a comprehensive microbiome-metabolite analysis using fecal and serum samples from patients with atherosclerotic cardiovascular disease and volunteers with risk factors for coronary heart disease and culture histology is performed, and identified the core strain Bacteroides ovatus (B. ovatus). Fecal microbiota transplantation experiments further demonstrated that the gut microbiota significantly influences AS progression, with B. ovatus alone exerting effects comparable to volunteer feces from volunteers. Notably, B. ovatus alleviated AS primarily by restoring the intestinal barrier and enhancing bile acid metabolism, particularly through the production of indole-3-acetic acid (IAA), a tryptophan-derived metabolite. IAA inhibited the TLR4/MyD88/NF-κB pathway in M1 macrophages, promoted M2 macrophage polarisation, and restored the M1/M2 polarisation balance, ultimately reducing aortic inflammation. These findings clarify the mechanistic interplay between the gut microbiota and AS, providing the first evidence that B. ovatus, a second-generation probiotic, can improve bile acid metabolism and reduce inflammation, offering a theoretical foundation for future AS therapeutic applications involving this strain.},
}

@article {pmid39840031,
year = {2024},
author = {Lim, MY and Hong, S and Nam, YD},
title = {Understanding the role of the gut microbiome in solid tumor responses to immune checkpoint inhibitors for personalized therapeutic strategies: a review.},
journal = {Frontiers in immunology},
volume = {15},
number = {},
pages = {1512683},
pmid = {39840031},
issn = {1664-3224},
mesh = {Humans ; *Gastrointestinal Microbiome/drug effects/immunology ; *Immune Checkpoint Inhibitors/therapeutic use ; *Neoplasms/immunology/therapy/drug therapy/microbiology ; *Precision Medicine ; Animals ; Immunotherapy/methods ; Treatment Outcome ; },
abstract = {Immunotherapy, especially immune checkpoint inhibitor (ICI) therapy, has yielded remarkable outcomes for some patients with solid cancers, but others do not respond to these treatments. Recent research has identified the gut microbiota as a key modulator of immune responses, suggesting that its composition is closely linked to responses to ICI therapy in cancer treatment. As a result, the gut microbiome is gaining attention as a potential biomarker for predicting individual responses to ICI therapy and as a target for enhancing treatment efficacy. In this review, we discuss key findings from human observational studies assessing the effect of antibiotic use prior to ICI therapy on outcomes and identifying specific gut bacteria associated with favorable and unfavorable responses. Moreover, we review studies investigating the possibility of patient outcome prediction using machine learning models based on gut microbiome data before starting ICI therapy and clinical trials exploring whether gut microbiota modulation, for example via fecal microbiota transplantation or live biotherapeutic products, can improve results of ICI therapy in patients with cancer. We also briefly discuss the mechanisms through which the gut microbial-derived products influence immunotherapy effectiveness. Further research is necessary to fully understand the complex interactions between the host, gut microbiota, and immunotherapy and to develop personalized strategies that optimize responses to ICI therapy.},
}

Humans
*Gastrointestinal Microbiome/drug effects/immunology
*Immune Checkpoint Inhibitors/therapeutic use
*Neoplasms/immunology/therapy/drug therapy/microbiology
*Precision Medicine
Animals
Immunotherapy/methods
Treatment Outcome

@article {pmid39839105,
year = {2024},
author = {Correa Lopes, B and Turck, J and Tolbert, MK and Giaretta, PR and Suchodolski, JS and Pilla, R},
title = {Prolonged storage reduces viability of Peptacetobacter (Clostridium) hiranonis and core intestinal bacteria in fecal microbiota transplantation preparations for dogs.},
journal = {Frontiers in microbiology},
volume = {15},
number = {},
pages = {1502452},
pmid = {39839105},
issn = {1664-302X},
abstract = {INTRODUCTION: Fecal microbiota transplantation (FMT) has been described useful as an adjunct treatment for chronic enteropathy in dogs. Different protocols can be used to prepare and store FMT preparations, however, the effect of these methods on microbial viability is unknown. We aimed (1) to assess the viability of several core intestinal bacterial species by qPCR and (2) to assess Peptacetobacter (Clostridium) hiranonis viability through culture to further characterize bacterial viability in different protocols for FMT preparations.

METHODS: Bacterial abundances were assessed in feces from six healthy dogs by qPCR after propidium monoazide (PMA-qPCR) treatment for selective quantitation of viable bacteria. Conservation methods tested included lyophilization (stored at 4°C and at -20°C) and freezing with glycerol-saline solution (12.5%) and without any cryoprotectant (stored at -20°C). Additionally, the abundance of P. hiranonis was quantified using bacterial culture.

RESULTS: Using PMA-qPCR, the viability of Faecalibacterium, Escherichia coli, Streptococcus, Blautia, Fusobacterium, and P. hiranonis was reduced in lyophilized fecal samples kept at 4°C and -20°C up to 6 months (p < 0.05). In frozen feces without cryoprotectant, only Streptococcus and E. coli were not significantly reduced for up to 3 months (p > 0.05). Lastly, no differences were observed in the viability of those species in glycerol-preserved samples up to 6 months (p > 0.05). When using culture to evaluate the viability of P. hiranonis, we observed that P. hiranonis abundance was lower in lyophilized samples kept at 4°C than -20°C; and P. hiranonis abundance was higher in glycerol-preserved samples for up to 6 months than in samples preserved without glycerol for up to 3 months. Moreover, the highest abundance of P. hiranonis was observed in glycerol-preserved feces. After 3 months, P. hiranonis was undetectable by culture in 83% (5/6) of the frozen samples without glycerol.

DISCUSSION: While the lyophilization procedure initially reduced P. hiranonis abundance, P. hiranonis viability was stable thereafter for up to 6 months at -20°C. The higher bacterial viability detected in fecal samples preserved with glycerol confirms the use of this cryoprotectant as a reliable method to keep bacteria alive in the presence of fecal matrix for FMT purposes.},
}

@article {pmid39838262,
year = {2025},
author = {Ye, J and Shi, R and Wu, X and Fan, H and Zhao, Y and Hu, X and Wang, L and Bo, X and Li, D and Ge, Y and Wang, D and Xia, B and Zhao, Z and Xiao, C and Zhao, B and Wang, Y and Liu, X},
title = {Stevioside mitigates metabolic dysregulation in offspring induced by maternal high-fat diet: the role of gut microbiota-driven thermogenesis.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2452241},
doi = {10.1080/19490976.2025.2452241},
pmid = {39838262},
issn = {1949-0984},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; Female ; *Diet, High-Fat/adverse effects ; Pregnancy ; Mice ; *Diterpenes, Kaurane/pharmacology/metabolism ; *Glucosides/pharmacology/metabolism ; *Thermogenesis/drug effects ; *Mice, Inbred C57BL ; Pregnancy in Obesity/metabolism ; Male ; Prenatal Exposure Delayed Effects/microbiology ; Bacteria/classification/metabolism/isolation & purification/genetics/drug effects ; Lactobacillus/metabolism ; Lipid Metabolism/drug effects ; Obesity/metabolism/microbiology ; Dietary Supplements ; },
abstract = {Maternal obesity poses a significant threat to the metabolic profiles of offspring. Microorganisms acquired from the mother early in life critically affect the host's metabolic functions. Natural non-nutritive sweeteners, particularly stevioside (STV), play a crucial role in reducing obesity and affecting gut microbiota composition. Based on this, we hypothesized that maternal STV supplementation could improve the health of mothers and offspring by altering their gut microbiota. Our study found that maternal STV supplementation reduced obesity during pregnancy, decreased abnormal lipid accumulation in offspring mice caused by maternal obesity, and modified the gut microbiota of both dams and offspring, notably increasing the abundance of Lactobacillus apodemi (L. apodemi). Co-housing and fecal microbiota transplant experiments confirmed that gut microbiota mediated the effects of STV on metabolic disorders. Furthermore, treatment with L. apodemi alone replicated the beneficial effects of STV, which were associated with increased thermogenesis. In summary, maternal STV supplementation could alleviate lipid metabolic disorders in offspring by enhancing L. apodemi levels and promoting thermogenic activity, potentially involving changes in bile acid metabolism pathways.},
}

Animals
*Gastrointestinal Microbiome/drug effects
Female
*Diet, High-Fat/adverse effects
Pregnancy
Mice
*Diterpenes, Kaurane/pharmacology/metabolism
*Glucosides/pharmacology/metabolism
*Thermogenesis/drug effects
*Mice, Inbred C57BL
Pregnancy in Obesity/metabolism
Male
Prenatal Exposure Delayed Effects/microbiology
Bacteria/classification/metabolism/isolation & purification/genetics/drug effects
Lactobacillus/metabolism
Lipid Metabolism/drug effects
Obesity/metabolism/microbiology
Dietary Supplements

@article {pmid39837364,
year = {2025},
author = {Liu, H and Yang, S and Zhang, Q and Wang, S and Zhang, B and Xu, Y and Fu, X and Zhou, S and Zhang, P and Wang, H and Di, L and Xu, X and Xu, X and Liu, C and Yang, C and Wang, Y and Jiang, R},
title = {S-ketamine alleviates morphine-induced hyperalgesia via decreasing the gut Enterobacteriaceae levels: Comparison with R-ketamine.},
journal = {Neuroscience},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.neuroscience.2025.01.022},
pmid = {39837364},
issn = {1873-7544},
abstract = {BACKGROUND: Opioid-induced hyperalgesia (OIH) is a serious complication during the pain treatment. Ketamine has been commonly reported to treat OIH, but the mechanisms remain unclear. Gut microbiota is recently recognized as one of the important mechanisms underlying the occurrence and treatment of OIH. However, whether ketamine enantiomers could alleviate OIH through gut microbiota that still needs to be clarified.

METHODS: The OIH model was established by morphine injection for 3 consecutive days, followed by hierarchical clustering analysis of behavioral results into susceptible or resilient group. Broad-spectrum antibiotic cocktail (ABx) was used to eradicated the gut microbiota of mice. Subsequently, fecal microbiota transplantation (FMT) was performed. S- or R-ketamine was administered as pretreatment 30 min before morphine injection. Fecal samples were collected for 16S rRNA gene sequencing after completion of all behavioral tests.

RESULTS: Approximately 60% of the mice developed OIH after morphine exposure with abnormal locomotion and anxiety-like behaviors. Pseudo germ-free mice treated with ABx did not develop hyperalgesia, whereas pseudo germ-free mice that received fecal microbiota transplantation from OIH mice developed hyperalgesia. Interestingly, S-ketamine but not R-ketamine rescued mice from OIH. The principal co-ordinates analysis (PCoA) suggested that the distribution of gut microbiota differed among the groups. Importantly, levels of Enterobacteriaceae were increased in OIH susceptible group, while decreased after S-ketamine treatment.

CONCLUSION: S-ketamine but not R-ketamine was able to alleviate morphine-induced OIH, and this mechanism is probably related to decreasing the levels of gut Enterobacteriaceae.},
}

@article {pmid39836853,
year = {2024},
author = {Aristizábal, AM and Montaña, LP and Gutiérrez, J and Medina, D and Franco, AA and Manzi, E and Zapata, ÁD and Mosquera, W},
title = {Intra-mesenteric steroids for steroid-refractory graft-versus-host disease in pediatric patients: A safe option.},
journal = {Biomedica : revista del Instituto Nacional de Salud},
volume = {44},
number = {Sp. 2},
pages = {63-71},
doi = {10.7705/biomedica.7394},
pmid = {39836853},
issn = {2590-7379},
mesh = {Humans ; *Graft vs Host Disease/drug therapy/etiology ; Child ; *Hematopoietic Stem Cell Transplantation/adverse effects ; Adolescent ; Male ; Female ; Child, Preschool ; *Methylprednisolone/therapeutic use/administration & dosage ; Retrospective Studies ; Drug Resistance ; Infant ; Glucocorticoids/therapeutic use ; },
abstract = {INTRODUCTION: Graft-versus-host disease is a serious complication after hematopoietic stem cell transplantation and is a major cause of death post-transplantation. Approximately 50% of acute graft-versus-host disease patients do not respond to systemic steroids and their prognosis is poor regardless of the treatment. This study describes our experience with pediatric patients diagnosed with steroid-refractory graft-versus-host disease who received intra-mesenteric steroid treatment.

OBJECTIVE: To determine the outcomes of intra-mesenteric steroid use in the management of pediatric patients diagnosed with refractory graft-versus-host disease.

MATERIALS AND METHODS: The study included patients under 18 years old with allogeneic hematopoietic stem cell transplantation who underwent intra-mesenteric steroid injection for resistant gastrointestinal graft-versus-host disease between January, 2016, and December, 2021. Methylprednisolone was administered via intra-arterial injection through the celiac trunk and the superior and inferior mesenteric arteries.

RESULTS: We collected data on 21 patients: nine (90%) responded with a subjective decrease in fecal output and a reduction in bilirubin and transaminases. Seven patients required a second intra-mesenteric injection and presented a complete response in 85% of the cases. Only one patient experienced local complications after the procedure. Twelve patients (57%) died with one death due to acute graft-versus-host disease.

CONCLUSION: Reports in the adult population have shown an approximately 50% response rate with few complications, making it a second-line management standard. As far as we know, this is the largest pediatric cohort reported in Latin America. Our findings suggest that intra-mesenteric steroid administration for managing hepatic and gastrointestinal graftversus-host disease may be considered an early adjuvant treatment in patients with steroidrefractory graft-versus-host disease.},
}

Humans
*Graft vs Host Disease/drug therapy/etiology
Child
*Hematopoietic Stem Cell Transplantation/adverse effects
Adolescent
Male
Female
Child, Preschool
*Methylprednisolone/therapeutic use/administration & dosage
Retrospective Studies
Drug Resistance
Infant
Glucocorticoids/therapeutic use

@article {pmid39836604,
year = {2025},
author = {Wu, X and Wei, J and Ran, W and Liu, D and Yi, Y and Gong, M and Liu, X and Gong, Q and Li, H and Gao, J},
title = {The Gut Microbiota-Xanthurenic Acid-Aromatic Hydrocarbon Receptor Axis Mediates the Anticolitic Effects of Trilobatin.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e2412234},
doi = {10.1002/advs.202412234},
pmid = {39836604},
issn = {2198-3844},
support = {GCC[2023]042//Guizhou Province/ ; HZ(2024)302//Science and technology project of Zunyi/ ; ZYSE-2022-02//Zunyi Medical University/ ; [2021]1350-037//Talent project of Guizhou platform/ ; 2022(2022JH2/101300058)//Liaoning Province/ ; },
abstract = {Current treatments for ulcerative colitis (UC) remain limited, highlighting the need for novel therapeutic strategies. Trilobatin (TLB), a naturally derived food additive, exhibits potential anti-inflammatory properties. In this study, a dextran sulfate sodium (DSS)-induced animal model is used to investigate the effects of TLB on UC. It is found TLB significantly alleviates DSS-induced UC in mice, as evidenced by a reduction in the disease activity index, an increase in colon length, improvement in histopathological lesions. Furthermore, TLB treatment results in a decrease in proinflammatory cytokines and an increase in anti-inflammatory cytokines. TLB mitigates UC by modulating the intestinal microbiota, particularly Akkermansia, which enhances tryptophan metabolism and upregulates the production of xanthurenic acid (XANA). To confirm the role of TLB-induced microbiota changes, experiments are performed with pseudogerm-free mice and fecal transplantation. It is also identified XANA as a key metabolite that mediates TLB's protective effects. Both TLB and XANA markedly activate the aromatic hydrocarbon receptor (AhR). Administration of an AhR antagonist abrogates their protective effects, thereby confirming the involvement of AhR in the underlying mechanism. In conclusion, the study reveals a novel mechanism through which TLB alleviates UC by correcting microbiota imbalances, regulating tryptophan metabolism, enhancing XANA production, and activating AhR.},
}

@article {pmid39834471,
year = {2024},
author = {Song, Y and Liu, S and Zhang, L and Zhao, W and Qin, Y and Liu, M},
title = {The effect of gut microbiome-targeted therapies in nonalcoholic fatty liver disease: a systematic review and network meta-analysis.},
journal = {Frontiers in nutrition},
volume = {11},
number = {},
pages = {1470185},
pmid = {39834471},
issn = {2296-861X},
abstract = {BACKGROUND: The incidence of NAFLD is increasing. Preclinical evidences indicate that modulation of the gut microbiome could be a promising target in nonalcoholic fatty liver disease.

METHOD: A systematic review and network meta-analysis was conducted to compare the effect of probiotics, synbiotics, prebiotics, fecal microbiota transplant, and antibiotics on the liver-enzyme, metabolic effects and liver-specific in patients with NAFLD. The randomized controlled trails (RCTs), limited to English language were searched from database such as Pubmed, Embase, Web of science and Cochrane Library from inception to November 2024. Review Manager 5.3 was used to to draw a Cochrane bias risk. Inconsistency test and publication-bias were assessed by Stata 14.0. Random effect model was used to assemble direct and indirect evidences. The effects of the intervention were presented as mean differences with 95% confidence interval.

RESULTS: A total of 1921 patients from 37 RCTs were eventually included in our study. 23 RCTs evaluated probiotics, 10 RCTs evaluated synbiotics, 4 RCTs evaluated prebiotics, 3 RCTs evaluated FMT and one RCT evaluated antibiotics. Probiotics and synbiotics were associated with a significantly reduction in alanine aminotransferase [ALT, (MD: -5.09; 95%CI: -9.79, -0.39), (MD: -7.38, 95CI%: -11.94, -2.82)] and liver stiffness measurement by elastograph [LSM, (MD: -0.37;95%CI: -0.49, -0.25), (MD: -1.00;95%CI: -1.59, -0.41)]. In addition to, synbiotics was superior to probiotics in reducing LSM. Synbiotics was associated with a significant reduction of Controlled Attenuation Parameter [CAP, (MD: -39.34; 95%CI: -74.73, -3.95)]. Both probiotics and synbiotics were associated with a significant reduction of aspartate transaminase [AST, (MD: -7.81; 95%CI: -15.49, -0.12), (MD: -13.32; 95%CI: -23, -3.64)]. Probiotics and Allogenic FMT was associated with a significant reduction of Homeostatic Model Assessment for Insulin Resistance [HOMA-IR, (MD: -0.7, 95%CI: -1.26, -0.15), (MD: -1.8, 95%CI: -3.53, - 0.07)]. Probiotics was associated with a significant reduction of body mass index [BMI, MD: -1.84, 95%CI: -3.35, -0.33].

CONCLUSION: The supplement of synbiotics and probiotics maybe a promising way to improve liver-enzyme, LSM, and steatosis in patients with NAFLD. More randomized controlled trials are needed to determine the efficacy of FMT and antibiotics on NAFLD. And the incidence of adverse events of MTTs should be further explored.

https://www.crd.york.ac.uk/prospero/, CRD42023450093.},
}

@article {pmid39829898,
year = {2025},
author = {Ni, M and Fan, Y and Liu, Y and Li, Y and Qiao, W and Davey, LE and Zhang, XS and Ksiezarek, M and Mead, E and Touracheau, A and Jiang, W and Blaser, MJ and Valdivia, RH and Fang, G},
title = {Epigenetic phase variation in the gut microbiome enhances bacterial adaptation.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
pmid = {39829898},
issn = {2692-8205},
abstract = {The human gut microbiome within the gastrointestinal tract continuously adapts to variations in diet, medications, and host physiology. A central strategy for genetic adaptation is epigenetic phase variation (ePV) mediated by bacterial DNA methylation, which can regulate gene expression, enhance clonal heterogeneity, and enable a single bacterial strain to exhibit variable phenotypic states. Genome-wide and site-specific ePV have been well characterized in human pathogens' antigenic variation and virulence factor production. However, the role of ePV in facilitating adaptation within the human microbiome remains poorly understood. Here, we comprehensively cataloged genome-wide and site-specific ePV in human infant and adult gut microbiomes. First, using long-read metagenomic sequencing, we detected genome-wide ePV mediated by complex structural variations of DNA methyltransferases, highlighting the ones associated with antibiotics or fecal microbiota transplantation. Second, we analyzed an extensive collection of public short-read metagenomic sequencing datasets, uncovering a greater prevalence of genome-wide ePV in the human gut microbiome. Third, we quantitatively detected site-specific ePVs using single-molecule methylation analysis to identify dynamic variations associated with antibiotic treatment or probiotic engraftment. Finally, we performed an in-depth assessment of an Akkermansia muciniphila isolate from an infant, highlighting that ePV can regulate gene expression and enhance the bacterial adaptive capacity by employing a bet-hedging strategy to increase tolerance to differing antibiotics. Our findings indicate that epigenetic modifications are a common and broad strategy used by bacteria in the human gut to adapt to their environment.},
}

@article {pmid39829204,
year = {2025},
author = {Liu, C and Wong, PY and Barua, N and Li, B and Wong, HY and Zhang, N and Chow, SKH and Wong, SH and Yu, J and Ip, M and Cheung, WH and Duque, G and Brochhausen, C and Sung, JJY and Wong, RMY},
title = {From Clinical to Benchside: Lacticaseibacillus and Faecalibacterium Are Positively Associated With Muscle Health and Alleviate Age-Related Muscle Disorder.},
journal = {Aging cell},
volume = {},
number = {},
pages = {e14485},
doi = {10.1111/acel.14485},
pmid = {39829204},
issn = {1474-9726},
support = {C4032-21GF//Collaborative Research Fund, HKSAR Research Grants Council/ ; 14116223//General Research Fund, HKSAR Research Grants Council/ ; },
abstract = {Sarcopenia is an age-related muscle disorder that increases risks of adverse clinical outcomes, but its treatments are still limited. Gut microbiota is potentially associated with sarcopenia, and its role is still unclear. To investigate the role of gut microbiota in sarcopenia, we first compared gut microbiota and metabolites composition in old participants with or without sarcopenia. Fecal microbiota transplantation (FMT) from human donors to antibiotic-treated recipient mice was then performed. Specific probiotics and their mechanisms to treat aged mice were identified. Old people with sarcopenia had different microbial composition and metabolites, including Paraprevotella, Lachnospira, short-chain fatty acids, and purine. After FMT, mice receiving microbes from people with sarcopenia displayed lower muscle mass and strength compared with those receiving microbes from non-sarcopenic donors. Lacticaseibacillus rhamnosus (LR) and Faecalibacterium prausnitzii (FP) were positively related to muscle health of old people, and enhanced muscle mass and function of aged mice. Transcriptomics showed that genes related to tricarboxylic acid cycle (TCA) were enriched after treatments. Metabolic analysis showed increased substrates of TCA cycle in both LR and FP supernatants. Muscle mitochondria density, ATP content, NAD[+]/NADH, mitochondrial dynamics and biogenesis proteins, as well as colon tight junction proteins of aged mice were improved by both probiotics. LR and the combination of two probiotics also benefit intestinal immune health by reducing CD8[+] IFNγ[+] T cells. Gut microbiota dysbiosis is a pathogenesis of sarcopenia, and muscle-related probiotics could alleviate age-related muscle disorders mainly through mitochondria improvement. Further clinical translation is warranted.},
}

@article {pmid39827989,
year = {2025},
author = {Cheng, CK and Ye, L and Wang, Y and Wang, YL and Xia, Y and Wong, SH and Chen, S and Huang, Y},
title = {Exercised gut microbiota improves vascular and metabolic abnormalities in sedentary diabetic mice through gut‒vascular connection.},
journal = {Journal of sport and health science},
volume = {},
number = {},
pages = {101026},
doi = {10.1016/j.jshs.2025.101026},
pmid = {39827989},
issn = {2213-2961},
abstract = {BACKGROUND: Exercise elicits cardiometabolic benefits, reducing the risks of cardiovascular diseases and type 2 diabetes. This study aimed to investigate the vascular and metabolic effects of gut microbiota from exercise-trained donors on sedentary mice with type 2 diabetes and the potential mechanism.

METHODS: Leptin receptor-deficient diabetic (db/db) and nondiabetic (db/m[+]) mice underwent running treadmill exercise for 8 weeks, during which fecal microbiota transplantation (FMT) was parallelly performed from exercise-trained to sedentary diabetic (db/db) mice. Endothelial function, glucose homeostasis, physical performance, and vascular signaling of recipient mice were assessed. Vascular and intestinal stresses, including inflammation, oxidative stress, and endoplasmic reticulum (ER) stress, were investigated. RNA sequencing analysis on mouse aortic and intestinal tissues was performed. Gut microbiota profiles of recipient mice were evaluated by metagenomic sequencing.

RESULTS: Chronic exercise improved vascular and metabolic abnormalities in donor mice. Likewise, FMT from exercised donors retarded body weight gain and slightly improved grip strength and rotarod performance in recipient mice. Exercise-associated FMT enhanced endothelial function in different arteries, suppressed vascular and intestinal stresses, and improved glucose homeostasis in recipient mice, with noted microRNA-181b upregulation in aortas and intestines. Altered gut microbiota profiles and gut-derived factors (e.g., short-chain fatty acids and glucagon-like peptide-1) as well as improved intestinal integrity shall contribute to the cardiometabolic benefits, implying a gut‒vascular connection.

CONCLUSION: This proof-of-concept study indicates that exercised microbiota confers cardiometabolic benefits on sedentary db/db mice, extending the beneficial mechanism of exercise through gut‒vascular communication. The findings open up new therapeutic opportunities for cardiometabolic diseases and shed light on the development of exercise mimetics by targeting the gut microbiota.},
}

@article {pmid39827465,
year = {2025},
author = {Zhang, Y and Hao, R and Chen, J and Huang, K and Li, S and Cao, H and Guan, X},
title = {Gut-Derived Ursodeoxycholic Acid from Saponins of Quinoa Regulated Colitis via Inhibiting the TLR4/NF-κB Pathway.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.4c09151},
pmid = {39827465},
issn = {1520-5118},
abstract = {Alteration of the gut microbiota and its metabolites plays a key role in the development of inflammatory bowel disease (IBD). Here, we investigated the mechanism of saponins, a byproduct from quinoa (SQ) processing, in regulating IBD. SQ ameliorated gut microbiota dysbiosis revealed by 16S rRNA sequencing and improved colonic antioxidant activities and barrier integrity in dextran sulfate sodium (DSS)-treated mice. Broad-spectrum antibiotics further proved that the gut-protective effects of SQ were mediated by gut microbiota. Next, fecal microbiota transplantation (FMT) of SQ-induced gut microbiota/metabolites to inoculate DSS-treated mice alleviated colitis significantly. Untargeted metabolomics and lipidomics revealed that ursodeoxycholic acid (UDCA) was enriched as a microbial metabolite after SQ supplementation. UDCA was then found to attenuate DSS-induced colitis in vivo by targeting the TLR4/NF-κB pathway, which was also verified in a Caco-2 cell model treated with a TLR4 agonist/antagonist. Overall, our findings established that gut microbiota-UDCA-TLR4/NF-κB signaling plays a key role in mediating the protective effects of SQ.},
}

@article {pmid39826789,
year = {2025},
author = {Du, X and Liu, L and Yang, L and Zhang, Y and Dong, K and Li, Y and Chen, Y and Yang, Q and Zhu, X and Li, Q},
title = {Cumulative experience meets modern science: Remarkable effects of TongXieYaoFang formula on facilitating intestinal mucosal healing and secretory function.},
journal = {Journal of ethnopharmacology},
volume = {341},
number = {},
pages = {119370},
doi = {10.1016/j.jep.2025.119370},
pmid = {39826789},
issn = {1872-7573},
abstract = {TongXieYaoFang (TXYF), a classical formula used in Traditional Chinese Medicine, is renowned for its efficacy in treating chronic abdominal pain and diarrhoea. Modern research suggests that fundamental relief from these symptoms depends on complete intestinal mucosal healing, which normalises gut secretory functions. Consensus between traditional and modern medical theories indicates that TXYF is particularly suitable for treating the remission phase of ulcerative colitis (UC). Unfortunately, its potential in the remission phase has not received sufficient attention, and its use has been largely limited to a supportive role during the acute phase.

AIM OF THE STUDY: This study aimed to elucidate the efficacy of TXYF in promoting intestinal mucosal healing and enhancing gut secretory function during the non-acute damage phase, as well as to identify the underlying mechanisms contributing to its effects.

METHODS: A mouse model of dextran sulphate sodium salt (DSS)-induced colitis was optimised to specifically evaluate the effects of TXYF on mucosal healing during the repair phase. The effects of TXYF on murine colon function were assessed by measuring faecal pellet count and water content, and further evaluated through immunohistochemical analyses. The underlying mechanisms of action of TXYF were elucidated using mouse intestinal organoid cultures, intestinal stem cell (ISCs) transplantation, immunofluorescence, and western blotting. Active components of TXYF were identified via LC-MS/MS analysis and integrated with network pharmacology for bioinformatics assessment.

RESULTS: TXYF significantly promoted mucosal healing, as reflected by reduced disease activity scores, increased colon length, enhanced epithelial proliferation, and decreased histological damage. Furthermore, TXYF enhanced the recovery of critical intestinal functions, including barrier integrity, absorption, secretion, and motility. Notably, the improvement in the secretory function was particularly pronounced. Mechanistically, these therapeutic effects were mediated by the upregulation of the Atonal homolog 1/SAM pointed domain containing ETS transcription factor/Mucin 2 pathway, which facilitates the differentiation and maturation of ISCs into goblet cells, thereby contributing to both mucosal repair and enhanced secretory function.

CONCLUSIONS: Our study demonstrated that TXYF significantly promotes intestinal mucosal healing and enhances secretory function. These findings offer a solid basis for exploring the potential applications of TXYF in UC management during the remission phase.},
}

@article {pmid39809266,
year = {2025},
author = {Wang, D and Jiang, Y and Jiang, J and Pan, Y and Yang, Y and Fang, X and Liang, L and Li, H and Dong, Z and Fan, S and Ma, D and Zhang, XS and Li, H and He, Y and Li, N},
title = {Gut microbial GABA imbalance emerges as a metabolic signature in mild autism spectrum disorder linked to overrepresented Escherichia.},
journal = {Cell reports. Medicine},
volume = {6},
number = {1},
pages = {101919},
doi = {10.1016/j.xcrm.2024.101919},
pmid = {39809266},
issn = {2666-3791},
mesh = {*Gastrointestinal Microbiome/genetics ; *Autism Spectrum Disorder/metabolism/microbiology/genetics ; *gamma-Aminobutyric Acid/metabolism ; Humans ; Animals ; Female ; Male ; Mice ; Child ; Child, Preschool ; Metabolomics/methods ; RNA, Ribosomal, 16S/genetics ; Escherichia/metabolism/genetics ; Feces/microbiology ; Glutamic Acid/metabolism ; Mice, Inbred C57BL ; Escherichia coli/genetics/metabolism ; Metabolome ; },
abstract = {Gut microbiota (GM) alterations have been implicated in autism spectrum disorder (ASD), yet the specific functional architecture remains elusive. Here, employing multi-omics approaches, we investigate stool samples from two distinct cohorts comprising 203 children with mild ASD or typical development. In our screening cohort, regression-based analysis for metabolomic profiling identifies an elevated γ-aminobutyric acid (GABA) to glutamate (Glu) ratio as a metabolic signature of ASD, independent of age and gender. In the validating cohort, we affirm the GABA/Glu ratio as an ASD diagnostic indicator after adjusting for geography, age, gender, and specific food-consuming frequency. Integrated analysis of metabolomics, 16S rRNA sequencing, and metagenomics reveals a correlation between overrepresented Escherichia and disrupted GABA metabolism. Furthermore, we observe social behavioral impairments in weaning mice transplanted with E. coli, suggesting a potential link to ASD symptomatology. Collectively, these findings provide insights into potential diagnostic and therapeutic strategies aimed at evaluating and restoring gut microbial neurotransmitter homeostasis.},
}

*Gastrointestinal Microbiome/genetics
*Autism Spectrum Disorder/metabolism/microbiology/genetics
*gamma-Aminobutyric Acid/metabolism
Humans
Animals
Female
Male
Mice
Child
Child, Preschool
Metabolomics/methods
RNA, Ribosomal, 16S/genetics
Escherichia/metabolism/genetics
Feces/microbiology
Glutamic Acid/metabolism
Mice, Inbred C57BL
Escherichia coli/genetics/metabolism
Metabolome

@article {pmid39826698,
year = {2025},
author = {Song, Y and Cui, Y and Zhong, Y and Wang, Y and Zheng, X},
title = {Fecal microbiota transplantation combined with inulin promotes the development and function of early immune organs in chicks.},
journal = {Journal of biotechnology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jbiotec.2025.01.012},
pmid = {39826698},
issn = {1873-4863},
abstract = {Modern management of chicks hinders the vertical transmission of intestinal microbiota, which is closely related to immunity. Inulin is a substrate that can be utilized by the microbiota. This study aimed to determine whether fecal microbiota transplantation (FMT) combined with inulin played a "1+1>2" role in enhancing the development and function of immune organs. Chicks were treated with 1% inulin and/or fecal microbiota suspension on days 1-6. The growth performance, immune organ development, and immune indicators were evaluated on days 7, 14, and 21. Results showed that the combination of FMT and inulin significantly increased the immune organ index on day 7 and promoted the morphological structure and the expression of proliferating cell nuclear antigen (PCNA) in immune organs on days 7, 14, and 21. Each treatment increased the gene expression of interferon-gamma (IFN-γ), interleukin-4 (IL-4), interleukin-2 (IL-2), B cell-activating factor receptor (BAFFR), B cell linker (BLNK), C-X-C Motif Chemokine Ligand 12 (CXCL12), C-X-C Motif Chemokine Receptor 4 (CXCR4), and Biotin (Bu-1) to varying degrees. FMT combined with inulin significantly increased the expression of IgA-positive cells on days 7 and 14. In conclusion, the synergistic effect of FMT and inulin had beneficial impacts on the development and function of immune organs.},
}

@article {pmid39826450,
year = {2025},
author = {Zhu, Z and Zuo, S and Zhu, Z and Wang, C and Du, Y and Chen, F},
title = {THSWD upregulates the LTF/AMPK/mTOR/Becn1 axis and promotes lysosomal autophagy in hepatocellular carcinoma cells by regulating gut flora and metabolic reprogramming.},
journal = {International immunopharmacology},
volume = {148},
number = {},
pages = {114091},
doi = {10.1016/j.intimp.2025.114091},
pmid = {39826450},
issn = {1878-1705},
abstract = {THSWD has the effect of reducing inflammation, improving microcirculation, and regulating immune status in patients with hepatocellular carcinoma. Regardless of its clear therapeutic effect, the underlying mechanism of action against hepatocellular carcinoma is not clear. To identify critical gut microbiota and its associated metabolites related to THSWD inhibition against hepatocellular carcinoma progression, we assessed the microbe-dependent anti-hepatocellular carcinoma effects of THSWD through 16 s rRNA gene sequencing, fecal microbial transplantation and antibiotic treatment. Metabolic analyses, transcriptomic analyses, and molecular experiments were performed to explore how THSWD modulates the gut microbiota against hepatocellular carcinoma progression. As confirmed by in vivo and in vitro assays, THSWD reduced tumour growth rate and promoted apoptosis in hepatocellular carcinoma cells in hepatocellular carcinoma model mice, and liver and kidney indexes were detected and confirmed the safety of THSWD. Transcriptomic analysis revealed that the targets of THSWD were significantly enriched in multiple lysosomal autophagy signalling pathways, suggesting that lysosomal autophagy is probably associated with THSWD's therapeutic effect. Based on the integrated data analysis, THSWD delays hepatocellular carcinoma progression by increasing the intestinal microbiota Duncaniella and augmenting the metabolite glabrol, and the joint analysis of metabolic and genomic data suggests that this metabolite is associated with lysosomal autophagy, and cellular experiments confirmed that the The differential metabolite glabrol induces apoptosis in hepatocellular carcinoma cells by triggering the lysosomal autophagy-mediated apoptosis signalling pathway. Supplementation with glabrol metabolites up regulates the LTF/AMPK/mTOR/Beclin1 axis and promotes hepatocellular carcinoma cells with lysosomal autophagy and induced apoptosis in hepatocellular carcinoma cells.},
}

@article {pmid39826104,
year = {2025},
author = {Lin, A and Jiang, A and Huang, L and Li, Y and Zhang, C and Zhu, L and Mou, W and Liu, Z and Zhang, J and Cheng, Q and Wei, T and Luo, P},
title = {From chaos to order: optimizing fecal microbiota transplantation for enhanced immune checkpoint inhibitors efficacy.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2452277},
doi = {10.1080/19490976.2025.2452277},
pmid = {39826104},
issn = {1949-0984},
mesh = {Humans ; *Fecal Microbiota Transplantation ; *Immune Checkpoint Inhibitors/therapeutic use ; *Gastrointestinal Microbiome ; *Neoplasms/therapy/microbiology ; Animals ; Immunotherapy/methods ; Tumor Microenvironment/drug effects ; Treatment Outcome ; Combined Modality Therapy ; },
abstract = {The integration of fecal microbiota transplantation (FMT) with immune checkpoint inhibitors (ICIs) presents a promising approach for enhancing cancer treatment efficacy and overcoming therapeutic resistance. This review critically examines the controversial effects of FMT on ICIs outcomes and elucidates the underlying mechanisms. We investigate how FMT modulates gut microbiota composition, microbial metabolite profiles, and the tumor microenvironment, thereby influencing ICIs effectiveness. Key factors influencing FMT efficacy, including donor selection criteria, recipient characteristics, and administration protocols, are comprehensively discussed. The review delineates strategies for optimizing FMT formulations and systematically monitoring post-transplant microbiome dynamics. Through a comprehensive synthesis of evidence from clinical trials and preclinical studies, we elucidate the potential benefits and challenges of combining FMT with ICIs across diverse cancer types. While some studies report improved outcomes, others indicate no benefit or potential adverse effects, emphasizing the complexity of host-microbiome interactions in cancer immunotherapy. We outline critical research directions, encompassing the need for large-scale, multi-center randomized controlled trials, in-depth microbial ecology studies, and the integration of multi-omics approaches with artificial intelligence. Regulatory and ethical challenges are critically addressed, underscoring the imperative for standardized protocols and rigorous long-term safety assessments. This comprehensive review seeks to guide future research endeavors and clinical applications of FMT-ICIs combination therapy, with the potential to improve cancer patient outcomes while ensuring both safety and efficacy. As this rapidly evolving field advances, maintaining a judicious balance between openness to innovation and cautious scrutiny is crucial for realizing the full potential of microbiome modulation in cancer immunotherapy.},
}

Humans
*Fecal Microbiota Transplantation
*Immune Checkpoint Inhibitors/therapeutic use
*Gastrointestinal Microbiome
*Neoplasms/therapy/microbiology
Animals
Immunotherapy/methods
Tumor Microenvironment/drug effects
Treatment Outcome
Combined Modality Therapy

@article {pmid39825784,
year = {2025},
author = {Zhang, R and Sun, X and Lu, H and Zhang, X and Zhang, M and Ji, X and Yu, X and Tang, C and Wu, Z and Mao, Y and Zhu, J and Ji, M and Yang, Z},
title = {Akkermansia muciniphila Mediated the Preventive Effect of Disulfiram on Acute Liver Injury via PI3K/Akt Pathway.},
journal = {Microbial biotechnology},
volume = {18},
number = {1},
pages = {e70083},
pmid = {39825784},
issn = {1751-7915},
support = {2024YQFH05//"YiQi''funding project/ ; },
mesh = {*Akkermansia ; *Phosphatidylinositol 3-Kinases/metabolism ; *Gastrointestinal Microbiome/drug effects ; *Proto-Oncogene Proteins c-akt/metabolism ; Animals ; *Disulfiram/pharmacology ; *RNA, Ribosomal, 16S/genetics ; *Chemical and Drug Induced Liver Injury/prevention & control ; Male ; Apoptosis/drug effects ; Signal Transduction/drug effects ; Disease Models, Animal ; Hepatocytes/drug effects ; Mice ; DNA, Ribosomal/genetics/chemistry ; },
abstract = {Acetaminophen induced acute liver injury (ALI) has a high incidence and is a serious medical problem, but there is a lack of effective treatment. The enterohepatic axis is one of the targets of recent attention due to its important role in liver diseases. Disulfiram (DSF) is a multitarget drug that has been proven to play a role in a variety of liver diseases and can affect intestinal flora, but whether it can alleviate ALI is not clear. We utilised bacterial 16S rRNA gene profiling, antimicrobial treatments, and faecal microbiota transplantation tests to explore whether DSF therapy for ALI is dependent on gut microbiota. Our findings indicate that DSF primarily restores intestinal microbiome balance by modulating the abundance of Akkermansia muciniphila (A. muciniphila), leading to significant alleviation of ALI symptoms in a gut microbiota dependent manner. We also found that A. muciniphila can promote the activation of PI3K/Akt pathway, correct the Bcl-2/Bax ratio, and further inhibit hepatocyte apoptosis. In conclusion, DSF ameliorates ALI by modulating the intestinal microbiome and activating the PI3K/AKT pathway through A. muciniphila.},
}

*Akkermansia
*Phosphatidylinositol 3-Kinases/metabolism
*Gastrointestinal Microbiome/drug effects
*Proto-Oncogene Proteins c-akt/metabolism
Animals
*Disulfiram/pharmacology
*RNA, Ribosomal, 16S/genetics
*Chemical and Drug Induced Liver Injury/prevention & control
Male
Apoptosis/drug effects
Signal Transduction/drug effects
Disease Models, Animal
Hepatocytes/drug effects
Mice
DNA, Ribosomal/genetics/chemistry

@article {pmid39824679,
year = {2025},
author = {Elyas, S and Barata, P and Vaishampayan, U},
title = {Clinical Applications of Microbiome in Renal Cell Carcinoma.},
journal = {European urology focus},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.euf.2024.12.006},
pmid = {39824679},
issn = {2405-4569},
abstract = {Advancements in microbiome research reveal its impact on cancer treatment outcomes, particularly in renal cell carcinoma (RCC). While immune checkpoint inhibitors (ICIs) have improved survival in metastatic RCC, composition of the gut microbiome has the potential to influence their efficacy. Antibiotic-induced microbiome disruptions correlate with diminished outcomes, while strains such as Akkermansia muciniphila, Clostridium butyricum, and others enhance immune responses and progression-free survival. Some prebiotics such as inulin gel can alter the gut flora to overcome the resistant strains occurring in response to immune therapy. This mini-review explores microbiome-targeted interventions, such as pre/probiotics and fecal microbiota transplantation, for overcoming ICI resistance. Although promising, prospective randomized trials are needed to standardize clinical applications and optimize microbiome-targeted treatments. The standard use of gut-modulating therapy cannot be recommended at present outside of clinical trials. A double-blind placebo-controlled randomized trial of ICI ± gut modulating therapy is being planned in frontline therapy of advanced RCC (BIOFRONT trial by the Southwest Oncology Group).},
}

@article {pmid39821840,
year = {2025},
author = {Vinterberg, JE and Oddsdottir, J and Nye, M and Pinton, P},
title = {Management of Recurrent Clostridioides difficile Infection (rCDI): A Systematic Literature Review to Assess the Feasibility of Indirect Treatment Comparison (ITC).},
journal = {Infectious diseases and therapy},
volume = {},
number = {},
pages = {},
pmid = {39821840},
issn = {2193-8229},
abstract = {Recurrent Clostridioides difficile infection (rCDI) is a major cause of increased morbidity, mortality, and healthcare costs. Fecal-microbiota-based therapies are recommended for rCDI on completion of standard-of-care (SoC) antibiotics to prevent further recurrence: these therapies include conventional fecal-microbiota transplantation and the US Food and Drug Administration-approved therapies REBYOTA® (RBL) and VOWST Oral Spores™ (VOS). As an alternative to microbiota-based therapies, bezlotoxumab, a monoclonal antibody, is used as adjuvant to SoC antibiotics to prevent rCDI. There are no head-to-head clinical trials comparing different microbiota-based therapies or bezlotoxumab for rCDI. To address this gap, we conducted a systematic literature review to identify clinical trials on rCDI treatments and assess the feasibility of using them to conduct an indirect treatment comparison (ITC). The feasibility analysis determined that trial heterogeneity, particularly relating to inclusion criteria, may significantly compromise ITC and prevent cross-trial comparisons. Our analysis underlines the need to adopt standardized protocols to ensure comparability across trials.},
}

@article {pmid39821715,
year = {2025},
author = {Berry, P and Khanna, S},
title = {The evolving landscape of live biotherapeutics in the treatment of Clostridioides difficile infection.},
journal = {Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology},
volume = {},
number = {},
pages = {},
pmid = {39821715},
issn = {0975-0711},
abstract = {Clostridioides difficile (C. difficile) infection (CDI) is common after antibiotic exposure and presents significant morbidity, mortality and healthcare costs worldwide. The rising incidence of recurrent CDI, driven by hypervirulent strains, widespread antibiotic use and increased community transmission, has led to an urgent need for novel therapeutic strategies. Conventional antibiotic treatments, although effective, face limitations due to rising antibiotic resistance and high recurrence rates, which can reach up to 60% after multiple infections. This has prompted exploration of alternative therapies such as fecal microbiota-based therapies, including fecal microbiota transplantation (FMT) and live biotherapeutics (LBPs), which demonstrate superior efficacy in preventing recurrence. They are aimed at restoring the gut microbiota. Fecal microbiota, live-jslm and fecal microbiota spores, live-brpk have been approved by the U.S. Food and Drug Administration in individuals aged 18 years or older for recurrent CDI after standard antimicrobial treatment. They have demonstrated high efficacy and a favorable safety profile in clinical trials. Another LBP under study includes VE-303, which is not derived from human donor stool. This review provides a comprehensive overview of the current therapeutic landscape for CDI, including its epidemiology, pathophysiology, risk factors, diagnostic modalities and treatment strategies. The review delves into the emerging role of live biotherapeutics, with a particular focus on fecal microbiota-based therapies. We explore their development, mechanisms of action, clinical applications and potential to revolutionize CDI management.},
}

@article {pmid39821305,
year = {2025},
author = {Shi, L and Duan, Y and Fang, N and Zhang, N and Yan, S and Wang, K and Hou, T and Wang, Z and Jiang, X and Gao, Q and Zhang, S and Li, Y and Zhang, Y and Gong, Y},
title = {Lactobacillus gasseri prevents ibrutinib-associated atrial fibrillation through butyrate.},
journal = {Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology},
volume = {},
number = {},
pages = {},
doi = {10.1093/europace/euaf018},
pmid = {39821305},
issn = {1532-2092},
abstract = {Ibrutinib, a widely used anti-cancer drug, is known to significantly increase the susceptibility to atrial fibrillation (AF). While it is recognized that drugs can reshape the gut microbiota, influencing both therapeutic effectiveness and adverse events, the role of gut microbiota in ibrutinib-induced AF remains largely unexplored. Utilizing 16S rRNA gene sequencing, fecal microbiota transplantation, metabonomics, electrophysiological examination, and molecular biology methodologies, we sought to validate the hypothesis that gut microbiota dysbiosis promotes ibrutinib-associated AF and to elucidate the underlying mechanisms. We found that ibrutinib administration predisposes rats to AF. Interestingly, ibrutinib-associated microbial transplantation conferred increased susceptibility to AF in rats. Notably, ibrutinib induced a significantly decrease in the abundance of Lactobacillus gasseri (L. gasseri), and oral supplementation of L. gasseri or its metabolite, butyrate, effectively prevented rats from ibrutinib-induced AF. Mechanistically, butyrate inhibits the generation of reactive oxygen species (ROS), thereby ameliorating atrial structural remodeling. Furthermore, we demonstrated that ibrutinib inhibited the growth of L. gasseri by disrupting the intestinal barrier integrity. Collectively, our findings provide compelling experimental evidence supporting the potential efficacy of targeting gut microbes in preventing ibrutinib-associated AF, opening new avenues for therapeutic interventions.},
}

@article {pmid39747680,
year = {2025},
author = {Menon, R and Bhattarai, SK and Crossette, E and Prince, AL and Olle, B and Silber, JL and Bucci, V and Faith, J and Norman, JM},
title = {Multi-omic profiling a defined bacterial consortium for treatment of recurrent Clostridioides difficile infection.},
journal = {Nature medicine},
volume = {31},
number = {1},
pages = {223-234},
pmid = {39747680},
issn = {1546-170X},
mesh = {*Clostridium Infections/therapy/microbiology ; Humans ; *Clostridioides difficile ; *Recurrence ; *Gastrointestinal Microbiome ; *Anti-Bacterial Agents/therapeutic use ; Feces/microbiology ; Male ; Female ; Fecal Microbiota Transplantation ; Middle Aged ; Bile Acids and Salts/metabolism ; Adult ; Aged ; Multiomics ; },
abstract = {Donor-derived fecal microbiota treatments are efficacious in preventing recurrent Clostridioides difficile infection (rCDI), but they have inherently variable quality attributes, are difficult to scale and harbor the risk of pathogen transfer. In contrast, VE303 is a defined consortium of eight purified, clonal bacterial strains developed for prevention of rCDI. In the phase 2 CONSORTIUM study, high-dose VE303 was well tolerated and reduced the odds of rCDI by more than 80% compared to placebo. VE303 organisms robustly colonized the gut in the high-dose group and were among the top taxa associated with non-recurrence. Multi-omic modeling identified antibiotic history, baseline stool metabolites and serum cytokines as predictors of both on-study CDI recurrence and VE303 colonization. VE303 potentiated early recovery of the host microbiome and metabolites with increases in short-chain fatty acids, secondary bile acids and bile salt hydrolase genes after antibiotic treatment for CDI, which is considered important to prevent CDI recurrences. These results support the idea that VE303 promotes efficacy in rCDI through multiple mechanisms.},
}

*Clostridium Infections/therapy/microbiology
Humans
*Clostridioides difficile
*Recurrence
*Gastrointestinal Microbiome
*Anti-Bacterial Agents/therapeutic use
Feces/microbiology
Male
Female
Fecal Microbiota Transplantation
Middle Aged
Bile Acids and Salts/metabolism
Adult
Aged
Multiomics

@article {pmid39816955,
year = {2025},
author = {Wang, Q and Ji, J and Xiao, S and Wang, J and Yan, X and Fang, L},
title = {Explore Alteration of Lung and Gut Microbiota in a Murine Model of OVA-Induced Asthma Treated by CpG Oligodeoxynucleotides.},
journal = {Journal of inflammation research},
volume = {18},
number = {},
pages = {445-461},
pmid = {39816955},
issn = {1178-7031},
abstract = {AIM: We sought to investigate the impact of CpG oligodeoxynucleotides (CpG-ODN) administration on the lung and gut microbiota in asthmatic mice, specifically focusing on changes in composition, diversity, and abundance, and to elucidate the microbial mechanisms underlying the therapeutic effects of CpG-ODN and identify potential beneficial bacteria indicative of its efficacy.

METHODS: HE staining were used to analyze inflammation in lung, colon and small intestine tissues. High-throughput sequencing technology targeting 16S rRNA was employed to analyze the composition, diversity, and correlation of microbiome in the lung, colon and small intestine of control, model and CpG-ODN administration groups.

RESULTS: (1) Histopathologically, both lung and intestinal tissue in asthmatic mice exhibited significant structural damage and inflammatory response, whereas the structure of both lung and intestinal tissue approached normal levels, accompanied by a notable improvement in the inflammatory response after CpG-ODN treatment. (2) In the specific microbiota composition analysis, bacterial dysbiosis observed in the asthmatic mice, accompanied by enrichment of Proteobacteria found to cause lung and intestinal epithelial damage and inflammatory reaction. After CpG-ODN administration, bacterial dysbiosis was improved, and a notable enrichment of beneficial bacteria, indicating a novel microecology. Meanwhile Oscillospira and Clostridium were identified as two biomarkers of the CpG-ODN treatment. (3) Heatmap analysis revealed significant correlations among lung, small intestine, and colon microbiota.

CONCLUSION: CpG-ODN treatment can ameliorate OVA-induced asthma in mice. One side, preserving the structural integrity of the lung and intestine, safeguarding the mucosal physical barrier, the other side, improving the dysbiosis of lung and gut microbiota in asthmatic mice. Beneficial bacteria and metabolites take up microecological advantages, regulate immune cells and participate in the mucosal immune response to protect the immune barrier. Meanwhile, Oscillospira and Clostridium as biomarkers for CpG-ODN treatment, has reference significance for exploring precise Fecal microbiota transplantation treatment for asthma.},
}

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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