@article {pmid40487274,
year = {2025},
author = {Roy, K and Moncada, E and Reddivari, L},
title = {Ulcerative Colitis but Not Dextran Sodium Sulfate-Induced Colitis-Associated Microbiota Promotes Early Biomarkers of Colitis in Interleukin-10 -/- Mice.},
journal = {Gastro hep advances},
volume = {4},
number = {6},
pages = {100636},
pmid = {40487274},
issn = {2772-5723},
abstract = {BACKGROUND AND AIMS: Inflammatory bowel diseases, including Crohn's disease and ulcerative colitis (UC), are inflammatory gastrointestinal conditions in which the pathogenesis is influenced by immune dysfunction, genetics, and environmental factors. Of the 2 conditions, UC is more prevalent, and there is a positive correlation between bacterial dysbiosis and colitis severity and incidence. Therefore, we hypothesize that mice that are genetically predisposed to colitis when colonized with colitic associated bacteria will exhibit an early onset of colitis biomarkers.

METHODS: Four sets of germ-free interleukin-10 -/- mice were gavaged orally with pooled fecal samples from 2 healthy individuals or an individual with severe colitis or healthy mice or dextran sodium sulfate (DSS)-induced colitis mice. The disease activity index was used to rank colitis severity weekly in transplanted mice for eight weeks.

RESULTS: There were significant differences in alpha (Shannon Index) and beta diversity (Bray-Curtis) between healthy and colitic-associated microbiota recipients, indicating dysbiosis (human fecal microbial transplantation P = 8.09∗10[-6], P = .001); (Mice fecal microbiota transplant P = .0197, P = .025). Despite the lack of colitis development, UC-associated microbiota recipients had reduced mucus thickness and increased expression of proinflammatory cytokines in the distal colon compared to healthy-associated microbiota recipients. However, DSS-induced colitis associated microbiota recipients did not show an increase in colitis biomarkers compared to healthy associated microbiota recipients.

CONCLUSION: This study demonstrates that UC-associated bacterial dysbiosis induces colonic inflammation and mucus thinning, biomarkers of early colitis onset, in interleukin-10 -/- mice compared to mice with healthy human associated bacteria.Colitis induction depends on bacterial community stability as DSS-induced colitis associated microbiota recipients did not show an increase in colitis or colitis biomarkers in the absence of DSS.},
}

@article {pmid40486846,
year = {2025},
author = {Shang, M and Ning, J and Zang, C and Ma, J and Yang, Y and Wan, Z and Zhao, J and Jiang, Y and Chen, Q and Dong, Y and Wang, J and Li, F and Bao, X and Zhang, D},
title = {Microbial metabolite 3-indolepropionic acid alleviated PD pathologies by decreasing enteric glia cell gliosis via suppressing IL-13Rα1 related signaling pathways.},
journal = {Acta pharmaceutica Sinica. B},
volume = {15},
number = {4},
pages = {2024-2038},
pmid = {40486846},
issn = {2211-3835},
abstract = {Although enteric glial cell (EGC) abnormal activation is reported to be involved in the pathogenesis of Parkinson's disease (PD), and inhibition of EGC gliosis alleviated gut and dopaminergic neuronal dysfunction was verified in our previous study, the potential role of gut microbiota on EGC function in PD still need to be addressed. In the present study, fecal microbiota transplantation revealed that EGC function was regulated by gut microbiota. By employing 16S rRNA and metabolomic analysis, we identified that 3-indolepropionic acid (IPA) was the most affected differential microbial metabolite that regulated EGC gliosis. The protective effects of IPA on PD were validated in rotenone-stimulated EGCs and rotenone (30 mg/kg i.g. for 4 weeks)-induced PD mice, as indicated by decreased inflammation, improved intestinal and brain barrier as well as dopaminergic neuronal function. Mechanistic study showed that IPA targeted pregnane X receptor (PXR) in EGCs, and inhibition of IL-13Rα1 involved cytokine-cytokine receptor interaction pathway, leading to inactivation of downstream JAK1-STAT6 pathway. Our data not only provided evidence that EGC gliosis was critical in spreading intestinal damage to brain, but also highlighted the potential role of microbial metabolite IPA in alleviating PD pathological damages through gut-brain axis.},
}

@article {pmid40486731,
year = {2025},
author = {Zhou, C and Feng, X and Liu, H and Cai, T and Li, Y and Fan, H},
title = {Bidirectional modulation of Alzheimer's disease via gut microbiota: rescue by fecal transplantation from healthy donors and aggravation by colitis-associated dysbiosis.},
journal = {Frontiers in neuroscience},
volume = {19},
number = {},
pages = {1593854},
pmid = {40486731},
issn = {1662-4548},
abstract = {INTRODUCTION: Emerging evidence implicates gut microbiota dysbiosis as a key modulator for the pathogenesis of Alzheimer's disease (AD) via the gut-brain axis. To investigate the causal role of microbial communities in AD progression, we performed fecal microbiota transplantation (FMT) in APP/PS1 transgenic mice using donor microbiota from healthy wild-type mice or dextran sulfate sodium (DSS)-induced colitis mice.

METHODS: Cognitive function, amyloid-beta (Aβ) pathology, and pro-inflammatory cytokine levels were assessed in mice. 16S ribosomal RNA sequencing of gut microbiota and bioinformatic functional analyses were applied to identify the specific microbial communities potentially involved in AD progression.

RESULTS: FMT-WT mice (fecal microbiota transplantation from healthy wild-type mice) exhibited significant improvements in spatial memory (Morris Water Maze), exploratory behavior (Y-maze), and locomotor activity (Open Field Test), alongside reduced Aβ plaque burden and normalized expression of pro-inflammatory cytokines (IL-6, IL-1β, TNF-α) in both gut and brain tissues. Conversely, FMT-DSS mice (fecal microbiota transplantation from DSS-treated donors) displayed exacerbated cognitive deficits, heightened Aβ deposition, and elevated pro-inflammatory cytokine levels. Microbial profiling revealed stark contrasts: FMT-WT mice harbored beneficial taxa (Bacteroides, Lachnospiraceae) linked to anti-inflammatory products like short-chain fatty acid, while FMT-DSS mice showed blooms of pathogenic genera (Erysipelatoclostridium, Enterobacteriaceae) associated with neurotoxic metabolites. Functional analyses predicted enrichment of neuroprotective pathways (e.g., lysine metabolism) in FMT-WT and pro-inflammatory pathways (e.g., carbon metabolism) in FMT-DSS. Crucially, neuroinflammation occurred independently of gut barrier disruption, implicating circulating microbial metabolites as key mediators.

DISCUSSION: Our findings demonstrate that gut microbiota composition bidirectionally influences AD progression, with FMT from healthy donors attenuating neuroinflammation and pathology, while colitis-associated dysbiosis exacerbates disease hallmarks. Our study positions microbiota-targeted therapies as a promising strategy to modulate AD progression through the gut-brain axis.},
}

@article {pmid40485937,
year = {2025},
author = {Liu, Y and Zhang, P and Sun, H},
title = {A narrative review of research advances in gut microbiota and microecological agents in children with attention deficit hyperactivity disorder (ADHD).},
journal = {Frontiers in psychiatry},
volume = {16},
number = {},
pages = {1588135},
pmid = {40485937},
issn = {1664-0640},
abstract = {The role of gut microecology in attention deficit hyperactivity disorder (ADHD) has garnered growing attention. Studies have suggested a potential link between ADHD development and an imbalance in gut microbiota composition. This review aims to analyze the characteristics of the gut microbiota in children with ADHD, explore how changes in the gut microbiota affect ADHD through nervous, neuroendocrine, and immune pathways, and discuss the potential application of microecological agents and fecal microbiota transplantation in the prevention and treatment of ADHD in children. Pubmed, Google Scholar, EBSCO, Scopus and Medline were utilized to conduct searches using the following key terms:Attention Deficit Hyperactivity Disorder OR ADHD AND gut microbiota OR probiotics OR prebiotics OR synbiotics OR fecal microbiota transplantation OR FMT. Studies published in English from all years were included. A thorough review of numerous papers and their references was conducted to identify relevant articles. Sorting and analysis revealed that the gut microbiota of children with ADHD has changed to some extent, and targeting the gut microbiota, using microecological agents or fecal microbiota transplantation, especially in combination with central nervous system stimulants, may provide additional benefits for children with ADHD.},
}

@article {pmid40485663,
year = {2025},
author = {Radford-Smith, DE and Oke, K and Costa, CFFA and Anthony, DC},
title = {Systematic review and meta-analysis of microbiota-gut-astrocyte axis perturbation in neurodegeneration, brain injury, and mood disorders.},
journal = {Brain, behavior, & immunity - health},
volume = {46},
number = {},
pages = {101013},
pmid = {40485663},
issn = {2666-3546},
abstract = {BACKGROUND: Astrocytes are essential for preserving homeostasis, maintaining the blood-brain barrier, and they are a key element of the tripartite neuronal synapse. Despite such multifaceted roles, their importance as contributors to the microbiota-gut-brain axis studies, which typically focus on microglia and neurons, has been largely overlooked. This meta-analysis provides the first systematic review of the microbiota-gut-astrocyte (MGA) axis in vivo, integrating findings across distinct neurological diseases.

METHODS: A systematic narrative review was conducted per PRISMA guidelines. The search term employed for PubMed was "Microbiota"[MeSH] AND (astrocyte OR glial) NOT (Review[Publication Type]) and for Web of Science, Embase, and Scopus, "Microbio∗ AND (astrocyte OR glial)" with filters applied to exclude review articles. Searches were completed by May 9th[,] 2024. Data extracted included study models, interventions, and outcomes related to astrocyte biology and rodent behaviour. SYRCLE's risk of bias tool was used to assess individual study designs.

RESULTS: 53 studies met the inclusion criteria, covering rodent models of stroke and traumatic (acute) brain injury, chronic neurodegenerative diseases including Alzheimer's and Parkinson's disease and other heterogeneous models of cognitive impairment and affective disorders. Significant heterogeneity in methodology was observed between studies. Five studies had a high risk of bias, and 15 were low risk. Astrocyte biology, typically measured by GFAP expression, was increased in neurodegeneration and acute brain injury models but varied significantly in mood disorder models, depending on the source of stress. Common findings across diseases included altered gut microbiota, particularly an increased Bacteroidetes/Firmicutes ratio and compromised gut barrier integrity, linked to increased GFAP expression. Faecal microbiota transplants and microbial metabolite analyses suggested a direct impact of the gut microbiota on astrocyte biology and markers of neuroinflammation.

CONCLUSIONS: This review and meta-analysis describes the impact of the gut microbiota on astrocyte biology, and argues that the MGA axis is a promising therapeutic target for neurological disorders. However, it is clear that our understanding of the relationship between the gut microbiota and astrocyte behaviour is incomplete, including how different subtypes of astrocytes may be affected. Future studies must adopt new, multi-dimensional studies of astrocyte function and dysfunction, to elucidate their role in disease and explore the therapeutic potential of gut microbiota modulation.},
}

@article {pmid40484955,
year = {2025},
author = {Lin, A and Huang, L and Jiang, A and Zhu, L and Mou, W and Li, Y and Zhang, C and Liu, Z and Zhang, J and Cheng, Q and Wei, T and Luo, P},
title = {Microbiota boost immunotherapy? A meta-analysis dives into fecal microbiota transplantation and immune checkpoint inhibitors.},
journal = {BMC medicine},
volume = {23},
number = {1},
pages = {341},
pmid = {40484955},
issn = {1741-7015},
support = {2021A1515012593//Natural Science Foundation of Guangdong Province/ ; 82373129//National Natural Science Foundation of China/ ; 82172750//National Natural Science Foundation of China/ ; 2022A1515111212//Basic and Applied Basic Research Foundation of Guangdong Province/ ; 2023A04J1257//Science and Technology Program of Guangzhou/ ; NO.2023RC3074//Hunan Youth Science and Technology Talent Project/ ; },
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; *Immune Checkpoint Inhibitors/therapeutic use ; *Neoplasms/therapy ; *Gastrointestinal Microbiome ; *Immunotherapy/methods ; Treatment Outcome ; },
abstract = {BACKGROUND: Immune checkpoint inhibitors (ICIs) are a cornerstone of modern cancer treatment, but their effectiveness is limited. Fecal microbiota transplantation (FMT), which alters the gut microbiome, has shown promise in enhancing ICIs' therapeutic effects.

METHODS: We conducted a comprehensive search of relevant studies available up to September 30, 2024, to analyze the clinical efficacy and safety of combining FMT with ICIs in cancer treatment. The primary endpoint was the objective response rate (ORR), with secondary evaluations of survival outcomes and safety.

RESULTS: A total of 10 studies involving 164 patients with solid tumors were included. The pooled ORR was 43% (95% CI: 0.35-0.51). Subgroup analysis revealed that the combination of anti-PD-1 and anti-CTLA-4 therapies was associated with a significantly higher ORR (60%) compared to anti-PD-1 monotherapy (37%; P = 0.01). The incidence of grade 1-2 adverse events (AEs) was 42% (95% CI: 0.32-0.52), while grade 3-4 AEs occurred in 37% of patients (95% CI: 0.28-0.46).

CONCLUSIONS: This meta-analysis provides preliminary evidence supporting the use of FMT as a strategy to enhance the efficacy of ICIs in patients with advanced or refractory solid tumors. However, larger-scale randomized controlled trials with long-term follow-up are required to confirm and optimize treatment protocols.},
}

Humans
*Fecal Microbiota Transplantation/methods
*Immune Checkpoint Inhibitors/therapeutic use
*Neoplasms/therapy
*Gastrointestinal Microbiome
*Immunotherapy/methods
Treatment Outcome

@article {pmid40484558,
year = {2025},
author = {Liu, W and Yu, L and Chen, Q and Zhang, C and Wang, L and Yu, N and Peng, D and Ou, J and Chen, W and Zhang, Y and Wang, Y},
title = {Poria cocos polysaccharides alleviate obesity-related adipose tissue insulin resistance via gut microbiota-derived short-chain fatty acids activation of FGF21/PI3K/AKT signaling.},
journal = {Food research international (Ottawa, Ont.)},
volume = {215},
number = {},
pages = {116671},
doi = {10.1016/j.foodres.2025.116671},
pmid = {40484558},
issn = {1873-7145},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Insulin Resistance ; *Obesity/metabolism ; *Polysaccharides/pharmacology ; Mice ; Proto-Oncogene Proteins c-akt/metabolism ; Male ; *Fatty Acids, Volatile/metabolism ; Fibroblast Growth Factors/metabolism ; Signal Transduction/drug effects ; Diet, High-Fat/adverse effects ; *Adipose Tissue/metabolism/drug effects ; Mice, Inbred C57BL ; Phosphatidylinositol 3-Kinases/metabolism ; *Wolfiporia/chemistry ; },
abstract = {Obesity is a chronic condition that increases the risk of metabolic disorders, with intestinal dysbiosis and adipose tissue insulin resistance (Adipose-IR) playing key roles in its pathogenesis. Poria cocos polysaccharides (PCP), derived from traditional Chinese medicine, have shown potential in improving glucose metabolism and modulating gut microbiota. However, whether PCP can alleviate obesity-induced Adipose-IR and its dependence on gut microbiota remain unclear. This study investigated the effects of PCP on Adipose-IR in high-fat diet (HFD)-induced obese mice. PCP supplementation reduced body weight, adipose tissue mass, and improved glucose tolerance and lipid metabolism. Histological analysis showed alleviation of adipocyte hypertrophy and colonic barrier damage. PCP also modulated gut microbiota, enhancing the abundance of Lactobacillus, Allobaculum, and Phascolarctobacterium, and increased fecal short-chain fatty acids (SCFAs). These changes activated fibroblast growth factor 21 (FGF21), phosphoinositide 3-kinase (PI3K), protein kinase B (AKT), and glucose transporter 4 (GLUT4) expression, improving insulin sensitivity. Antibiotic treatment and fecal microbiota transplantation (FMT) further confirmed that PCP's effects on glucose and lipid metabolism are gut microbiota-dependent. Our findings suggest that PCP may serve as a prebiotic agent to alleviate obesity-induced Adipose-IR and metabolic disorders, supporting its potential for functional food development.},
}

Animals
*Gastrointestinal Microbiome/drug effects
*Insulin Resistance
*Obesity/metabolism
*Polysaccharides/pharmacology
Mice
Proto-Oncogene Proteins c-akt/metabolism
Male
*Fatty Acids, Volatile/metabolism
Fibroblast Growth Factors/metabolism
Signal Transduction/drug effects
Diet, High-Fat/adverse effects
*Adipose Tissue/metabolism/drug effects
Mice, Inbred C57BL
Phosphatidylinositol 3-Kinases/metabolism
*Wolfiporia/chemistry

@article {pmid40482880,
year = {2025},
author = {Conrad, MA and Kaplan, AL and Weinbrom, S and Nastasio, S and Jo, D and Conover, K and Lo, K and Liu, E and Crawford, M and Michail, S and Nicholson, M and Hourigan, SK and Kelsen, JR and Kahn, SA},
title = {Fidaxomicin Treatment of Clostridioides difficile Infections and Recurrences in Children and Adolescents: A Retrospective Multicenter Study.},
journal = {The Journal of pediatrics},
volume = {},
number = {},
pages = {114681},
doi = {10.1016/j.jpeds.2025.114681},
pmid = {40482880},
issn = {1097-6833},
abstract = {OBJECTIVE: To report the effectiveness and tolerability of treating children with primary and recurrent Clostridioides difficile infection (CDI) with fidaxomicin in a real-world, multicenter cohort.

STUDY DESIGN: We performed a multicenter, retrospective, observational study of fidaxomicin treatment for primary or recurrent CDI (rCDI) in children ages 12 months to 18 years old identified from 2013 to 2021 at 5 centers via electronic medical records. Outcomes included assessment of clinical response at day 14 after initiation of fidaxomicin treatment and clinical and microbiologic outcomes at day 60 after initiation of fidaxomicin treatment in the initial responders.

RESULTS: Of the 95 patients included in this study, 84 (88.4%) were treated with fidaxomicin for a rCDI, and 82 (86.3%) had at least one medical or surgical comorbidity. At the completion of fidaxomicin treatment (ie, by day 14 after initiation), 50 patients (52.6%) had a clinical cure and an additional 29 (30.5%) had improvement of symptoms. Among 79 patients who responded to fidaxomicin treatment, 17 (21.5%) had a clinical and microbiologically confirmed recurrence of CDI by day 60, likely representing relapse. Patients with inflammatory bowel disease (IBD) were less likely to achieve clinical cure at day 14 (OR 0.27 (95% CI 0.11, 0.70)), but 20 patients with IBD who had initial clinical cure or response did not have a demonstrable increased risk of recurrence at day 60. The most common adverse events reported during therapy were abdominal pain and nausea.

CONCLUSIONS: In this retrospective, real-world study, fidaxomicin for children with CDI appears to be well tolerated and is associated with low rates of treatment failure.},
}

@article {pmid40482640,
year = {2025},
author = {DeLeon, O and Mocanu, M and Tan, A and Sidebottom, AM and Koval, J and Ceccato, HD and Kralicek, S and Colgan, JJ and St George, MM and Lake, JM and Cooper, M and Xu, J and Moore, J and Su, Q and Xu, Z and Ng, SC and Chan, FKL and Tun, HM and Cham, CM and Liu, CY and Rubin, DT and Martinez-Guryn, K and Chang, EB},
title = {Microbiome mismatches from microbiota transplants lead to persistent off-target metabolic and immunomodulatory effects.},
journal = {Cell},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cell.2025.05.014},
pmid = {40482640},
issn = {1097-4172},
abstract = {Fecal microbiota transplant (FMT) is an increasingly used intervention, but its suitability to restore regional gut microbiota, particularly in the small bowel (SB), must be questioned because of its predominant anaerobic composition. In human subjects receiving FMT by upper endoscopy, duodenal engraftment of anaerobes was observed after 4 weeks. We hypothesized that peroral FMTs create host-microbe mismatches that impact SB homeostasis. To test this, antibiotic-treated specific-pathogen-free (SPF) mice were given jejunal, cecal, or fecal microbiota transplants (JMTs, CMTs, or FMTs, respectively) and studied 1 or 3 months later. JMT and FMT altered regional microbiota membership and function, energy balance, and intestinal and hepatic transcriptomes; JMT favored host metabolic pathways and FMT favored immune pathways. MTs drove regional intestinal identity (Gata4, Gata6, and Satb2) and downstream differentiation markers. RNA sequencing (RNA-seq) of metabolite-exposed human enteroids and duodenal biopsies post-FMT confirmed transcriptional changes in mice. Thus, regional microbial mismatches after FMTs can lead to unintended consequences and require rethinking of microbiome-based interventions.},
}

@article {pmid40481571,
year = {2025},
author = {Feng, Y and Zhao, Q and Zhao, Y and Ma, C and Tian, M and Hu, X and Chen, F and Li, D},
title = {Lactobacillus plantarum-derived extracellular vesicles from dietary barley leaf supplementation attenuate Citrobacter rodentium infection and intestinal inflammation.},
journal = {Journal of nanobiotechnology},
volume = {23},
number = {1},
pages = {426},
pmid = {40481571},
issn = {1477-3155},
support = {32371511 and 32001677//the National Natural Science Foundation of China/ ; 2020M680256//the China Postdoctoral Science Foundation/ ; },
mesh = {Animals ; *Citrobacter rodentium ; Mice ; *Enterobacteriaceae Infections/microbiology ; *Extracellular Vesicles/metabolism/chemistry ; *Lactobacillus plantarum/metabolism/chemistry ; *Hordeum/chemistry ; Gastrointestinal Microbiome/drug effects ; Colitis/microbiology ; *Plant Leaves/chemistry ; Mice, Inbred C3H ; *Dietary Supplements ; Male ; Inflammation ; },
abstract = {BACKGROUND: Inflammatory bowel disease (IBD) is a gastrointestinal inflammatory disorder characterized by disturbed interactions between gut microbiota and host immune response. Barley leaf (BL) is a traditional Chinese herb recorded to have health-promoting effects. However, little is known about the beneficial role of BL against enteric infection-induced intestinal inflammation. Here, we uncover that BL protects against Citrobacter rodentium (C. rodentium)-induced infectious colitis by improving host-microbiota interactions.

METHODS: C3H/HeN mice were fed a diet with/without BL and infected with C. rodentium. Transcriptome sequencing, anti-CD4 antibody treatment, and flow cytometry were conducted to investigate the mechanisms of T cell immune modulation. The intervention involved administering anti-CD4 antibody at 500 µg each time for three times before and during C. rodentium infection. Analysis of gut microbiota composition was performed by 16S rRNA gene sequencing on fecal samples. Fecal microbiota transplantation was conducted by administering microbiota from donor group to recipient group via oral gavage to investigate the role of intestinal microbiota in immune modulation.

RESULTS: BL ameliorated the severity of C. rodentium-induced colitis, and this effect was linked to improved gut homeostasis and enhanced mucosal barrier function. BL enriched the pathways of T helper 1 (Th1)/Th2 and Th17 cell differentiation in the colon, suggesting the involvement of CD4[+] T cells. Consistent with this, anti-CD4 antibody treatment abrogated the effect of BL and flow cytometry analysis revealed that BL mitigated C. rodentium-induced pro-inflammatory Th1 immune response. Moreover, the protective effect of BL was associated with alleviation of gut microbiota dysbiosis and increased abundance of Lactobacillus. Our in vivo studies further revealed that live Lactobacillus plantarum (L. plantarum) administration attenuated the pathogenic effects induced by C. rodentium infection, whereas heat-inactivated L. plantarum did not show the same results. Mechanistically, BL supplementation enriched L. plantarum, which subsequently released nanosized extracellular vesicles (EVs) that serve as a key mediator in alleviating C. rodentium-associated pathology and Th1 cell dysregulation.

CONCLUSIONS: Our work thus provides evidence for utilizing BL and L. plantarum-derived EVs to manage enteric infection-associated IBD.},
}

Animals
*Citrobacter rodentium
Mice
*Enterobacteriaceae Infections/microbiology
*Extracellular Vesicles/metabolism/chemistry
*Lactobacillus plantarum/metabolism/chemistry
*Hordeum/chemistry
Gastrointestinal Microbiome/drug effects
Colitis/microbiology
*Plant Leaves/chemistry
Mice, Inbred C3H
*Dietary Supplements
Male
Inflammation

@article {pmid40478639,
year = {2025},
author = {Bathobakae, L and Bashir, R and Koodirile, A and Villegas, K and Rajab, I and Perez, EW and Cavanagh, Y and El-Sedfy, A and Suh, JS},
title = {Clostridioides difficile enteritis: a targeted review of current literature.},
journal = {Scandinavian journal of gastroenterology},
volume = {},
number = {},
pages = {1-11},
doi = {10.1080/00365521.2025.2515423},
pmid = {40478639},
issn = {1502-7708},
abstract = {Clostridioides difficile enteritis (CDE) is a rare but clinically significant form of Clostridioides difficile infection (CDI) affecting the small intestine. CDE poses a diagnostic challenge owing to its rarity, complexity, and nonspecific presentation. The current data is retrospective in the form of case reports and conference proceedings. The lack of widespread awareness and limited literature on CDE often result in diagnostic delays, contributing to increased morbidity. This targeted narrative review sought to consolidate the current knowledge on the epidemiology, pathophysiology, clinical presentation, and management of CDE, addressing a critical gap in the existing literature. Electronic databases, including PubMed, Embase, and Web of Science, were searched for published cases from inception to April 2024. The initial search yielded 2,120 articles, which were filtered using study design, English language, and human subjects. After screening for duplicates and excluding irrelevant articles, 44 articles comprising 49 patients were included in the final review. Of the 49 individual cases reviewed, 25 (51%) were male and 24 (49%) were female. The patients' ages ranged from 16 to 91 years, with a mean age of 53.4 years. Abdominal pain and diarrhea were the chief complaints reported in 37/49 (76%) and 35/49 (71%) cases, respectively. About 42/49 (86%) cases were effectively treated with antibiotics, while some cases required fecal microbiota transplantation or surgical exploration. Given its grave course, CDE warrants prompt and appropriate treatment to prevent complications such as fulminant enteritis, compartment syndrome, and bowel perforation.},
}

@article {pmid40478172,
year = {2025},
author = {Lasagna, A},
title = {Mitigation strategies for gastrointestinal (GI) immune-related adverse events for patients with solid tumors receiving immunotherapy.},
journal = {Immunotherapy},
volume = {},
number = {},
pages = {1-9},
doi = {10.1080/1750743X.2025.2516995},
pmid = {40478172},
issn = {1750-7448},
abstract = {Over the past decade, immunotherapy has revolutionized the treatment algorithm for solid tumors. Immune checkpoint inhibitors (ICIs) demonstrated efficacy against several tumor types, but they can favor the development of immune-related adverse events (irAEs). IrAEs can sometimes be life-threatening. In this review, we will briefly analyze the main gastro-intestinal toxicities and focus on potential strategies for mitigating irAEs, particularly through the modification of gut microbiota (GM) composition. Finally, we will briefly dwell on the potential role of artificial intelligence (AI) in the prediction of irAEs.},
}

@article {pmid40475999,
year = {2025},
author = {Hwang, D and Chong, E and Li, Y and Li, Y and Roh, K},
title = {Deciphering the gut microbiome's metabolic code: pathways to bone health and novel therapeutic avenues.},
journal = {Frontiers in endocrinology},
volume = {16},
number = {},
pages = {1553655},
pmid = {40475999},
issn = {1664-2392},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Bone and Bones/metabolism ; Animals ; Probiotics/therapeutic use ; *Bone Remodeling/physiology ; *Osteoporosis/metabolism/microbiology/therapy ; Prebiotics ; Fecal Microbiota Transplantation ; Bone Diseases/metabolism/microbiology/therapy ; },
abstract = {The gut microbiome plays an important role in the protection against various systemic diseases. Its metabolic products profoundly influence a wide range of pathophysiological events, including the regulation of bone health. This review discusses the recently established connections between the gut microbiome and bone metabolism, focusing on the impact of microbiome-derived metabolites such as SCFAs, Bile Acids, and tryptophan to the control of bone remodeling and immunoreactions. Recent advances in metagenomics and microbiome profiling have unveiled new exciting therapeutic opportunities, ranging from the use of probiotics, prebiotics, engineered microbes, and to fecal microbiota transplantation. Understanding of the interplay among diet, microbiota, and bone health provides new avenues for tailored interventions aimed at reducing disease risk in osteoporosis and other related disorders. By drawing knowledge from microbiology, metabolism, and bone biology, this review highlights the potential of microbiome-targeted therapies to transform skeletal health and the management of bone diseases.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Bone and Bones/metabolism
Animals
Probiotics/therapeutic use
*Bone Remodeling/physiology
*Osteoporosis/metabolism/microbiology/therapy
Prebiotics
Fecal Microbiota Transplantation
Bone Diseases/metabolism/microbiology/therapy

@article {pmid40472289,
year = {2025},
author = {Lim, LWZ and Toh, KY and Cook, AR and Lee, JWJ and Lim, JFY},
title = {Public knowledge, awareness and perception of gut microbiome and faecal microbiota transplantation in Singapore: a survey study.},
journal = {Singapore medical journal},
volume = {},
number = {},
pages = {},
pmid = {40472289},
issn = {2737-5935},
abstract = {INTRODUCTION: Despite the exponential increase in microbiome research, knowledge and beliefs about the gut microbiome and faecal microbiota transplantation (FMT) remain unclear. The aim of this study was to identify the extent of knowledge, awareness and perception among the general public regarding the gut microbiome and FMT.

METHODS: An online questionnaire on knowledge and beliefs about the gut microbiome and FMT was administered to 1831 participants. Data analysis software was used to generate descriptive statistics and explore associations between knowledge and sociodemographic variables.

RESULTS: Even though only 33% of participants had heard of the gut microbiome, more than 92% had consumed probiotic drinks or supplements. While 85% had not heard of the FMT procedure, 72% of respondents would consider having FMT to treat Clostridioides difficile infection (CDI). Willingness to receive FMT depended mainly on recommendation from healthcare providers (77%). Knowledge and awareness regarding the gut microbiome and FMT were relatively low, despite most participants having prior gut health-related behaviours.

CONCLUSION: This study identified the public's perceptions of FMT and the potential barriers to its uptake. Insights from the study highlight the need for health education to enhance acceptance of FMT and the importance of using information supported by medical professionals to immunise the public against poorly validated science.},
}

@article {pmid40471587,
year = {2025},
author = {Wei, M and Huang, Q and Yu, F and Luo, YF and Feng, X and Liao, D and Li, J and Zhang, B and Liu, ZY and Xia, J},
title = {Elevated phenylacetylglutamine caused by gut dysbiosis associated with type 2 diabetes increases neutrophil extracellular traps formation and exacerbates brain infarction.},
journal = {Clinical science (London, England : 1979)},
volume = {},
number = {},
pages = {},
doi = {10.1042/CS20242943},
pmid = {40471587},
issn = {1470-8736},
support = {2022YFC3602400, 2022YFC3602401//National Key Research and Development Projects/ ; 82271369; 82301514; 82471365//National Natural Science Foundation of China/ ; 2021JJ31109; 2023JJ41018//Natural Science Foundation of Hunan Province/ ; },
abstract = {Type 2 diabetes (T2D) aggravates ischemic stroke. The association between gut microbiota-derived metabolite phenylacetylglutamine (PAGln) and ischemic stroke patients with T2D remains unclear. Therefore, we aimed to explore the change of gut microbiota and its metabolite, PAGln in ischemic stroke patients with T2D, as well as investigate the role of PAGln in this disease. We performed two clinical cohort studies to investigate the changes of gut microbiota and PAGln in ischemic stroke patients with T2D. Then, we transplanted fecal microbiota from patients into rats and established a middle cerebral artery occlusion model. Finally, an intraperitoneal injection of PAGln was administered to rats to test whether it exacerbates brain infarction. Plasma PAGln levels were significantly higher in stroke patients with T2D compared to those without T2D. There was a positive correlation of Plasma PAGln with NETs. Enterobacteriaceae, Verrucomicrobiota, and Klebsiella were enriched in stroke patients with T2D and showed a significant positive correlation with PAGln levels. The rats transplanted with fecal microbes from stroke patients with T2D developed a more severe brain injury and had higher levels of plasma PAGln and NETs compared to the rats transplanted with fecal microbes from stroke patients without T2D. Additionally, rats treated with PAGln exhibited more severe brain injury accompanied by increased systemic inflammation, oxidative stress and NET formation. Our results suggest elevated circulating PAGln levels, resulting from gut dysbiosis in stroke patients with T2D, may exacerbate brain infarction through NETs formation, systemic inflammation, and oxidative stress.},
}

@article {pmid40470286,
year = {2025},
author = {Hetterich, J and Pees, M},
title = {Case Report: Oral fecal microbiota transplantation in a Mediterranean spur-thighed tortoise (Testudo graeca) suffering from chronic gastrointestinal disease-procedure, clinical outcome and follow-up.},
journal = {Frontiers in veterinary science},
volume = {12},
number = {},
pages = {1560689},
pmid = {40470286},
issn = {2297-1769},
abstract = {INTRODUCTION: Fecal microbiota transplantation (FMT) is the process of transferring fecal microbiota from a healthy donor into the gastrointestinal tract of a recipient. Although many mechanisms of FMT are still not completely understood at present, it has been described that the treatment of various gastrointestinal diseases in different species, including humans, is significantly improved by FMT therapy. Since the first report on FMT therapy in veterinary medicine in small mammals numerous cases have been reported, but little information has been published on the therapeutic effects of FMT treatment in reptiles. The present case report describes the effects of orally administered fecal microbiota transplantation in a Mediterranean spur-thighed tortoise (Testudo graeca) suffering from chronic gastrointestinal disorders.

CASE PRESENTATION: A nine-year-old, 330 g, intact female Mediterranean spur-thighed tortoise (Testudo graeca) from the animal owner's own offspring was presented for consultation due to decreased general condition, anorexia and sialorrhea following oral intake of a lettuce species (Lactuca virosa) known for its poisonous plant ingredients (sesquiterpene lactones) 3 weeks prior to presentation. Pre-existing conditions were not reported. Clinical examination revealed sialorrhea and a reduced general condition. Diagnostic procedures included blood chemistry, radiography and ultrasonography. Despite repeated treatment attempts with various medical regimes over 158 days, the tortoise continued showing variable recurring gastrointestinal symptoms. An orally administered FMT was initiated and continued for a total of 3 weeks. Gastrointestinal signs improved rapidly within 1 week and resolved completely after 3 weeks. Over a follow up period of 9 months, no symptom recurrence or adverse effects were monitored.

CONCLUSION: This case report describes the first successful trial of fecal microbiota transplantation in chelonians. The outcome indicates that this therapeutic approach may be beneficial not only to small animals but also for the therapy of gastrointestinal disorders in reptiles, especially those cases with insufficient conventional therapy results.},
}

@article {pmid40469520,
year = {2025},
author = {Yu, L and Chen, Z and Yin, S and Guo, Q and Chen, Y and Li, J and Wang, Y and Liu, X and Xu, Z and Zhang, Y and Zhang, Y and Zheng, Z and Chen, K and Ding, Y and Fan, H and Liu, Z and Ding, Y},
title = {Gut-derived Lactobacillus from exceptional responders mitigates chemoradiotherapy-induced intestinal injury through methionine-driven epigenetic modulation.},
journal = {iMeta},
volume = {4},
number = {3},
pages = {e70043},
pmid = {40469520},
issn = {2770-596X},
abstract = {Acute chemoradiotherapy-induced intestinal injury (ACRIII) is a common and debilitating complication in patients with colorectal cancer, significantly impairing both quality of life and treatment outcomes. This study aimed to investigate the role of the gut microbiome in mitigating ACRIII. Through bioinformatics analysis of clinical fecal samples and fecal microbiota transplantation (FMT) experiments in mice, we identified a strong association between a high abundance of Lactobacillus species and the absence of ACRIII. From the fecal samples of rectal cancer patients who achieved complete remission without experiencing ACRIII during chemoradiotherapy, 10 novel Lactobacillus strains were isolated and characterized. Among these, Lacticaseibacillus rhamnosus DY801 exhibited a robust capacity to synthesize methionine through metB. This microbial methionine production modulated methionine metabolism in host gut lymphoid tissue inducer (Lti) cells, without diminishing the therapeutic efficacy of chemoradiotherapy. Supplementation with methionine increased intracellular levels of S-adenosylmethionine and enhanced histone H3 lysine 4 trimethylation (H3K4me3) in Lti cells. These epigenetic modifications led to the suppression of pro-inflammatory cytokines interleukin-17A (IL-17A) and interleukin-22 (IL-22), ultimately reducing ACRIII severity. Our findings suggest that specific Lactobacillus strains derived from patients with exceptional treatment responses may offer a novel therapeutic avenue for preventing or alleviating ACRIII. This microbiome-based approach holds significant potential for improving patient outcomes and enhancing the tolerability of chemoradiotherapy in colorectal cancer.},
}

@article {pmid40469517,
year = {2025},
author = {Zhang, F and Li, R and Liu, Y and Liang, J and Gong, Y and Xiao, C and Cai, J and Wang, T and You, Q and Zhang, J and Chen, H and Xiao, J and Zhang, Y and Yang, Y and Li, H and Yao, J and Zhang, Q and Zheng, J},
title = {Integrative cross-tissue analysis unveils complement-immunoglobulin augmentation and dysbiosis-related fatty acid metabolic remodeling during mammalian aging.},
journal = {iMeta},
volume = {4},
number = {3},
pages = {e70027},
pmid = {40469517},
issn = {2770-596X},
abstract = {Aging-related decline and adaptation are complex, multifaceted processes that affect various tissues and increase risk of chronic diseases. To characterize key changes in cross-tissue aging, we performed comprehensive proteomic and metabolomic analyses across 21 solid tissues and plasma samples, alongside shotgun metagenomic profiling of fecal microbial communities in young and aged mice. Our findings revealed widespread aging-rewired chronic inflammation, characterized by complement system activation in plasma and universal immunoglobulins accumulation across multiple solid tissues. This inflammatory remodeling significantly enhanced vulnerability to aging-related tissue injury. Moreover, we identified organ-specific and organ-enriched proteins with high functional specificity. Among these, aging-related proteins were closely linked to disorders arising from lipid metabolism dysfunction. Analysis of multi-tissue metabolomic and fecal metagenomic profiles revealed that aging significantly disrupted inter-tissue metabolic coupling, activities of polyunsaturated fatty acids metabolism, and gut microbiota homeostasis. Aged mice exhibited a marked decrease in Escherichia and an increase in Helicobacter, strongly correlating with alterations in omega-3 and omega-6 fatty acid abundances. Through multi-omics integration, we identified key molecular hubs driving organismal responses to aging. Collectively, our study uncovers extensive aging-associated alterations across tissues, emphasizing the interplay between systemic inflammation and dysbiosis-driven fatty acid remodeling. These findings provide deeper insights into the development of healthy aging from a cross-tissue perspective.},
}

@article {pmid40469413,
year = {2025},
author = {Shimizu, K and Ogura, H and Oda, J},
title = {Gut dysbiosis and its treatment in patients with critical illness.},
journal = {Acute medicine & surgery},
volume = {12},
number = {1},
pages = {e70068},
pmid = {40469413},
issn = {2052-8817},
abstract = {The gut is a target organ that functions as the "motor" of critical illness. In patients with critical illness, the disrupted gut microbiota following infection and injury could cause diarrhea, pneumonia, and systemic inflammation. For maintaining the gut microbiota, therapeutic approaches are required to modulate host responses and prevent systemic inflammation. Probiotics and synbiotics could maintain the gut microbiota and decrease not only the incidence of diarrhea but also that of ventilator-associated pneumonia. The effects of probiotics/synbiotics differ with the type of bacteria and disease severity. Adverse effects of probiotics have been reported; therefore, the selection of safe and effective probiotics/synbiotics is warranted. Refractory diarrhea with prolonged dysbiosis may require a novel intestinal therapy, such as fecal microbiota transplantation, to alleviate gut dysbiosis.},
}

@article {pmid40468650,
year = {2025},
author = {Cha, RR and Sonu, I},
title = {Fecal microbiota transplantation: present and future.},
journal = {Clinical endoscopy},
volume = {58},
number = {3},
pages = {352-359},
doi = {10.5946/ce.2024.270},
pmid = {40468650},
issn = {2234-2400},
support = {//Gyeongsang National University Fund/ ; },
abstract = {Fecal microbiota transplantation (FMT) involves transplanting fecal matter from healthy donors into patients with gut dysbiosis to restore microbial balance. It has been proven to be highly effective in treating recurrent Clostridioides difficile infection (CDI), and United States Food and Drug Administration-approved microbiome-based therapies, such as REBYOTA (fecal microbiota live-jslm) and VOWST (fecal microbiota spores live-brpk), offer promising treatment options. Although FMT is widely used to treat recurrent CDI, its use in gastrointestinal and metabolic diseases remains limited. Future research directions include optimizing donor selection, understanding microbial mechanisms, and exploring the potential of FMT for treating other diseases. Ongoing research not only aims to broaden its indications but also improves its safety and efficacy. Emerging therapies such as VE303 (Vedanta) are being studied to refine treatment approaches and expand the use of microbiota-based therapies. Further studies are needed to standardize guidelines, improve patient outcomes, and better define the role of FMT in the treatment of diseases beyond recurrent CDI.},
}

@article {pmid40466419,
year = {2025},
author = {Zhang, K and Dong, Y and Ding, Y and Wang, X and Liu, T and Zhong, W and Cao, H},
title = {Illuminating prospects of probiotic Akkermansia muciniphila in intestinal inflammation and carcinogenesis.},
journal = {Microbiological research},
volume = {299},
number = {},
pages = {128240},
doi = {10.1016/j.micres.2025.128240},
pmid = {40466419},
issn = {1618-0623},
abstract = {Akkermansia muciniphila (A. muciniphila) is portrayed as an advantageous enteric bacterium with a particular property of mucin utilization. Emerging data suggest A. muciniphila can reshape gut chronic inflammation, enhance intestinal epithelial tight junctions, and sensitize toll-like receptors 2 (TLR2) and TLR4 to restrain the infiltrating cytotoxic T lymphocytes and macrophages. As well, analogous role is detected in surface A. muciniphila-coated pili, outer-membrane protein Amuc_1100, β-galactosidase enzyme Amuc_2172, and extracellular vesicles. We rendered insights into empirical evidence on molecular mechanisms mediated by A. muciniphila in inflammatory bowel disease and intestinal cancers which include colitis-associated colorectal cancer and colorectal cancer. We discussed its potential preventive and therapeutic benefits on immune checkpoint inhibitors therapy. A. muciniphila supplementation through diet, probiotics-prebiotics, fecal microbiota transplantation, and certain drugs, would be a promising therapeutic strategy. Nevertheless, data profiles decipher A. muciniphila is linked to multiple sclerosis and Parkinson's disease occurrence and evolvement. Thus, how to avoid the deleterious effects triggered by A. muciniphila warrants further exploration. It ought to be considered to conduct a critical and cautious analysis of the next-generation beneficial microbe manipulation ahead of clinical application.},
}

@article {pmid40069438,
year = {2025},
author = {Park, M and Jung, J and Lee, JA and Lee, E and Lee, H and Eom, HS and Park, HJ},
title = {Understanding gut Microbiome changes in Korean children, adolescents, and young adults with hematologic malignancies.},
journal = {Annals of hematology},
volume = {104},
number = {5},
pages = {2947-2961},
pmid = {40069438},
issn = {1432-0584},
support = {2011500-1//National Cancer Center, Korea/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/drug effects ; Adolescent ; Child ; Male ; Female ; *Hematologic Neoplasms/therapy/microbiology/epidemiology ; Young Adult ; Republic of Korea/epidemiology ; Hematopoietic Stem Cell Transplantation ; Feces/microbiology ; Adult ; },
abstract = {We investigated whether changes in the gut microbiome composition are associated with infections and immunologic complications during the treatment of Korean children, adolescents, and young adults (AYAs) with hematologic malignancies. We analyzed stool samples from 26 patients and 10 healthy siblings using 16 S rRNA gene sequencing. At diagnosis, patients exhibited a lower abundance of Lachnospiraceae and a higher abundance of Enterococcaceae than their healthy siblings. Both the Chao1 and Shannon diversity indices declined from diagnosis to the end of induction chemotherapy. Patients with fever during induction had a lower baseline microbial diversity and higher Ruminococcus g4 abundance than those without fever. The use of either meropenem or piperacillin/tazobactam during induction was correlated with reduced richness and altered composition of the gut microbiome after induction. The Chao index and beta diversity of stool samples significantly differed before conditioning when compared with those of healthy siblings. During allogeneic hematopoietic stem cell transplantation, both the Chao1 and Shannon diversity indices significantly decreased on day 14 but recovered by day 60. Our study highlights the role of gut microbiome diversity and compositional structure in influencing treatment outcomes in children and AYA with hematologic malignancies, providing the information required to improve the gut microbiome configuration and treatment outcomes.},
}

Humans
*Gastrointestinal Microbiome/drug effects
Adolescent
Child
Male
Female
*Hematologic Neoplasms/therapy/microbiology/epidemiology
Young Adult
Republic of Korea/epidemiology
Hematopoietic Stem Cell Transplantation
Feces/microbiology
Adult

@article {pmid40464639,
year = {2025},
author = {Zhang, Q and Liu, Y and Li, Y and Bai, G and Pang, J and Wu, M and Li, J and Zhao, X and Xia, Y},
title = {Implications of gut microbiota-mediated epigenetic modifications in intestinal diseases.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2508426},
doi = {10.1080/19490976.2025.2508426},
pmid = {40464639},
issn = {1949-0984},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Epigenesis, Genetic ; Animals ; Dysbiosis/microbiology/therapy ; DNA Methylation ; Fecal Microbiota Transplantation ; Prebiotics/administration & dosage ; *Intestinal Diseases/microbiology/genetics/therapy ; Probiotics ; Inflammatory Bowel Diseases/microbiology/genetics/therapy ; Colorectal Neoplasms/microbiology/genetics ; },
abstract = {Intestinal diseases are highly prevalent, affecting millions worldwide and significantly contributing to global morbidity. The treatment of complex disorders, such as inflammatory bowel disease (IBD) and colorectal cancer (CRC), remains challenging due to multifactorial etiologies, diverse patient responses, and the limitations of current therapeutic strategies. Although the gut microbiota clearly plays a role in regulating the onset of intestinal diseases, few studies have explored the epigenetic factors by which the microbiota contributes to disease development. Here, the latest insights into the molecular mechanisms underlying the bidirectional influence between gut microbiota and epigenetic modifications are discussed, including DNA methylation, histone modifications, non-coding RNAs, and N6-methyladenosine (m[6]A). Importantly, mechanistic studies based on animal models or human cells have demonstrated that the gut microbiota, and other environmental factors, influence targeted gene expression and activate immune pathways through host epigenetic dysregulation, which are closely associated with the development of IBD and CRC. Furthermore, potential microbiome interventions, including probiotics, prebiotics and postbiotics, fecal microbiota transplantation (FMT), dietary modifications, and phage therapy, have been proposed as innovative therapeutic strategies to correct these abnormal epigenetic patterns associated with the diseases. Overall, addressing microbiome dysbiosis and its epigenetic consequences presents a promising frontier in the treatment of intestinal diseases, offering the potential to not only restore microbial balance but also provide more targeted and personalized therapeutic strategies for better patient outcomes.},
}

Humans
*Gastrointestinal Microbiome
*Epigenesis, Genetic
Animals
Dysbiosis/microbiology/therapy
DNA Methylation
Fecal Microbiota Transplantation
Prebiotics/administration & dosage
*Intestinal Diseases/microbiology/genetics/therapy
Probiotics
Inflammatory Bowel Diseases/microbiology/genetics/therapy
Colorectal Neoplasms/microbiology/genetics

@article {pmid40464558,
year = {2025},
author = {Ruan, Y and Zhu, T and Yang, R and Su, F and An, C and Hu, Z and Li, X and Li, Y and Chen, P and Shao, X and Qin, J and Chen, H and Chen, R},
title = {Donor-derived microbial engraftment and gut microbiota shifts associated with weight loss following fecal microbiota transplantation.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0012025},
doi = {10.1128/aem.00120-25},
pmid = {40464558},
issn = {1098-5336},
abstract = {Fecal microbiota transplantation (FMT) is a promising treatment for microbiota dysbiosis and may provide metabolic benefits for obesity. However, its mechanisms and variability in clinical outcomes remain poorly understood. This 12-week multicenter, single-arm study evaluated the efficacy of FMT for weight loss and explored the role of donor-derived microbial engraftment and functional shifts in mediating weight loss among overweight and obese individuals. Twenty-three participants (body mass index ≥24 kg/m[2]) without diabetes received three biweekly FMT sessions via a nasojejunal tube. Fecal samples from participants and donors were analyzed using metagenomic sequencing. By week 12, 52% of participants were classified as responders, achieving significant weight loss of ≥5% from baseline, with an average weight loss of 7.98 ± 2.69 kg (P < 0.001). In contrast, non-responders lost 2.90 ± 1.89 kg (P < 0.001). Responders exhibited a significantly higher proportion of donor-derived microbial strains post-FMT compared to non-responders (37.8% vs 15.2%, P = 0.020). Notably, key taxa, including Phascolarctobacterium (P = 0.034) and Acidaminococcaceae (P = 0.012), increased significantly in abundance in responders post-FMT, indicating successful microbial engraftment as a critical determinant of therapeutic success. These findings suggest that FMT is a viable intervention for weight loss in obese individuals. Successful donor-derived microbial engraftment strongly correlates with weight loss efficacy, highlighting the potential of microbiota-targeted therapies in obesity management and providing insights into the mechanisms underlying FMT outcomes.IMPORTANCEPrior research indicates that fecal microbiota transplantation (FMT) is a promising treatment for diseases related to microbiota imbalance, potentially providing metabolic benefits for obesity. However, the specific role of donor-derived microbial engraftment in driving clinical efficacy has remained unclear. In this study, we evaluated the efficacy of FMT in promoting weight loss and explored the role of donor-derived bacterial strains in this process. Our findings demonstrate that the successful engraftment of specific donor-derived taxa, such as Phascolarctobacterium and Acidaminococcaceae, is strongly associated with significant weight loss. This highlights the critical interplay between donor microbiota and recipient gut environment. These findings underscore the potential of microbiota-targeted therapies as a novel strategy for obesity management.CLINICAL TRIALSThis study is registered with the Chinese Clinical Trial Registry as ChiCTR1900024760.},
}

@article {pmid40463945,
year = {2025},
author = {Wu, C and Mi, Y and Song, J and Zhang, M and Wang, C},
title = {The Regulatory Effect of Human Umbilical Cord Mesenchymal Stem Cells on the Gut Microbiota in Diabetic Nephropathy Rats.},
journal = {Iranian journal of biotechnology},
volume = {23},
number = {1},
pages = {},
pmid = {40463945},
issn = {1728-3043},
abstract = {BACKGROUND: Chronic inflammation is increasingly recognized as a key factor in the progression of diabetic kidney disease (DKD). By discovering that the regulation of gut microbiota plays an important role in diabetic kidney disease, human umbilical cord mesenchymal stem cells (HU-MSCs) explore the mechanism of fibrosis in diabetic kidney disease through the regulation of chronic inflammation, providing new clinical insights for the prediction, diagnosis, and treatment of diabetic kidney disease.

OBJECTIVES: This study explores the regulatory effects of HU-MSCs on gut microbiota and their protective role on the intestinal barrier in diabetic nephropathy rats.

MATERIAL AND METHOD: Diabetic kidney disease (DKD) was induced in SD rats via intraperitoneal injection of streptozotocin. Three groups were established: control group, diabetic kidney disease (DKD) group, and treatment group (DKD+HU-MSCs) (10 rats each). After diabetic kidney disease (DKD) modeling, rats in the treatment group (DKD+HU-MSCs) received 2×10[6] HU-MSCs via tail vein injection weekly for four weeks. Blood, urine, kidney, and colon tissues were collected post-treatment. Pathological changes were observed microscopically; immunohistochemistry detected tight junction proteins ZO-1 and Occludin in colon tissues. DiR-labeled HU-MSCs distribution was assessed with in vivo imaging, and immunohistochemistry evaluated human mesenchymal stem cell markers CD44 and CD90. Fecal samples underwent metagenomic sequencing for gut microbiota analysis.

RESULTS: HU-MSCs transplantation significantly reduced Blood Urea Nitrogen (BUN), Serum Creatinine (SCr), and 24-hour urinary protein levels (all P < 0.05) and improved renal pathology. Markers CD44 and CD90 were present in DKD rat colon tissues. Tight junction proteins Occludin and ZO-1 were decreased in DKD rats but increased following HU-MSCs treatment. Metagenomic analysis showed enhanced abundance of beneficial bacteria (Bifidobacterium and Lactobacillus) with HU-MSCs. Urinary protein was positively correlated with Prevotella and negatively with Ligilactobacillus (p < 0.05).

CONCLUSIONS: HU-MSCs may improve intestinal barrier function in diabetic kidney disease (DKD) rats by restoring gut microbiota structure and increasing intestinal tight junction proteins, offering a potential pathway for enhancing renal function.},
}

@article {pmid40462220,
year = {2025},
author = {Chen, M and Pan, J and Song, Y and Liu, S and Sun, P and Zheng, X},
title = {Correction: Effect of inulin supplementation in maternal fecal microbiota transplantation on the early growth of chicks.},
journal = {Microbiome},
volume = {13},
number = {1},
pages = {138},
pmid = {40462220},
issn = {2049-2618},
}

@article {pmid40272189,
year = {2025},
author = {Zhang, L and Wang, H and Zhao, L and Zhang, J and Sun, W and Chu, J and Zhao, H and Yang, C and Yan, S and Chen, X and Xu, D},
title = {Unraveling the interplay between mesenchymal stem cells, gut microbiota, and systemic sclerosis: therapeutic implications.},
journal = {Microbiology spectrum},
volume = {13},
number = {6},
pages = {e0157624},
pmid = {40272189},
issn = {2165-0497},
support = {82171790//National Natural Science Foundation of China/ ; 82201925//National Natural Science Foundation of China/ ; 32000075//National Natural Science Foundation of China/ ; ZR2024QC071//Natural Science Foundation of Shandong Province/ ; ZR2024MH079//Natural Science Foundation of Shandong Province/ ; ZR2022QH203//Natural Science Foundation of Shandong Province/ ; },
mesh = {*Gastrointestinal Microbiome/physiology ; *Scleroderma, Systemic/therapy/chemically induced/microbiology/pathology ; Animals ; *Mesenchymal Stem Cells/physiology/metabolism ; Mice ; Humans ; *Mesenchymal Stem Cell Transplantation ; Disease Models, Animal ; Bacteria/classification/genetics/isolation & purification/metabolism ; Bleomycin ; Mice, Inbred C57BL ; Feces/microbiology ; Female ; },
abstract = {UNLABELLED: Systemic sclerosis (SSc) is an autoimmune disease with progressive fibrotic disorders in multiple organs. Mesenchymal stem cells (MSCs) have shown great potential in treating SSc, but the exact regulatory mechanism is not fully understood. In this study, we used human umbilical cord-derived MSCs (hUC-MSCs) to treat SSc mice induced by bleomycin. The gut microbiota composition and predicted functions were analyzed using 2bRAD sequencing of fecal samples from control, SSc, and MSCs-treated mice. Treatment with MSCs improved the bleomycin-induced SSc mice, characterized by significantly reduced collagen deposition and dermal thickness. The gut microbiota of SSc mice exhibited lower species evenness and was clearly separated from the control mice based on beta diversity. MSC treatment led to a significant reduction of conditionally pathogenic bacteria enriched in SSc, including Akkermansia muciniphila and Parasutterella excrementihominis. Conversely, the relative abundance of butyrate-producing bacteria, such as Roseburia, Butyricicoccus porcorum, and Gemmiger formicilis, was notably increased in MSCs-treated SSc mice. Additionally, the functional analysis revealed that MSCs intervention effectively enhanced sulfur metabolism, tryptophan metabolism, citrate cycle, RNA polymerase, and beta-lactam resistance. In summary, the findings in the present study have suggested the close association between gut microbiota and metabolic dysbiosis in mice with SSc. The administration of MSCs has been shown to regulate the disrupted metabolic pathways in SSc mice, thus restoring the normal function of the gut microbiota. This study provides valuable insights into the specific gut microbiota and metabolic pathways involved in the efficacy of MSC treatment, thereby proposing a novel therapeutic strategy for SSc.

IMPORTANCE: Human umbilical cord-derived mesenchymal stem cells (HUC‑MSCs) demonstrate efficacy in alleviating skin thickening and collagen deposition in systemic sclerosis (SSc) mice, which also regulate the gut microbiota composition and function. Specifically, MSC intervention leads to a notable increase in butyrate-producing bacteria, a decrease in Akkermansia muciniphila and Parasutterella excrementihominis, and a reversal of the dysregulated microbial function in SSc mice. These findings underscore the potential significance of gut microbiota in the therapeutic effects of MSCs in SSc.},
}

*Gastrointestinal Microbiome/physiology
*Scleroderma, Systemic/therapy/chemically induced/microbiology/pathology
Animals
*Mesenchymal Stem Cells/physiology/metabolism
Mice
Humans
*Mesenchymal Stem Cell Transplantation
Disease Models, Animal
Bacteria/classification/genetics/isolation & purification/metabolism
Bleomycin
Mice, Inbred C57BL
Feces/microbiology
Female

@article {pmid40462165,
year = {2025},
author = {Gao, H and Bai, H and Su, Y and Gao, Y and Fang, H and Li, D and Yu, Y and Lu, X and Xia, D and Mao, D and Luo, Y},
title = {Fecal microbiota transplantation from Helicobacter pylori carriers following bismuth quadruple therapy exacerbates alcohol-related liver disease in mice via LPS-induced activation of hepatic TLR4/NF-κB/NLRP3 signaling.},
journal = {Journal of translational medicine},
volume = {23},
number = {1},
pages = {627},
pmid = {40462165},
issn = {1479-5876},
support = {42377426//National Natural Science Foundation of China/ ; 42077382//National Natural Science Foundation of China/ ; 21JCYBJC01200//Tianjin Municipal Natural Science Foundation/ ; 2023220//Research Project on Integrated Traditional Chinese and Western Medicine of Tianjin Municipal Health Commission/ ; },
abstract = {BACKGROUND: Helicobacter pylori infection is common in patients with alcohol-related liver disease (ALD), and bismuth quadruple therapy (BQT) is widely used for eradication. However, its impact on ALD remains unclear. This study aims to characterize BQT-induced gut microbiota alterations in asymptomatic H. pylori carriers and evaluate their effect on an ALD mouse model.

METHODS: Metagenomic sequencing was conducted to assess the gut microbiota composition of individuals before and after BQT. Fecal microbiota transplantation (FMT) from these donors was performed in an ALD mouse model. Gut microbiota in mice was analyzed by 16S rRNA sequencing. Liver and intestinal parameters were assessed using western blot, RT-qPCR, histopathology, ELISA, and flow cytometry.

RESULTS: BQT treatment significantly altered the gut microbiota in H. pylori carriers, increasing the abundance of opportunistic pathogens, including Klebsiella pneumoniae, Escherichia coli, Klebsiella quasipneumoniae, and Klebsiella variicola, while decreasing beneficial bacteria such as Bifidobacterium, Eubacterium, Bacteroides, Faecalibacterium, and Blautia. In ALD mice receiving FMT from post-BQT donors, exacerbated gut dysbiosis was observed, marked by an enrichment of Enterobacteriaceae and Escherichia-Shigella. These microbiota changes were associated with impairment of intestinal barrier integrity, as evidenced by reduced levels of mucins, tight junction proteins, and antimicrobial peptides, along with a decrease in Treg cells and an increase in Th17 and Th1 cells. Additionally, this dysbiosis led to elevated serum lipopolysaccharide (LPS) levels, which activated the hepatic NLRP3 inflammasome pathway and subsequently increased IL-18 and IL-1β levels. Furthermore, liver function and oxidative stress markers, including ALT, AST, MDA, GSSG/GSH ratio, and SOD, were significantly elevated, indicating severe liver dysfunction and increased oxidative stress. Finally, probiotic supplementation effectively mitigated the negative effects of BQT-induced gut microbiota remodeling on ALD in mice.

CONCLUSIONS: BQT markedly alters the gut microbiota in H. pylori carriers, promoting dysbiosis that exacerbates ALD in mice via LPS-mediated activation of hepatic inflammatory pathways. These findings highlight the need for careful consideration of BQT use in ALD patients.},
}

@article {pmid40461622,
year = {2025},
author = {Ferreira, J},
title = {Fecal microbiota transplantation therapy.},
journal = {Lab animal},
volume = {54},
number = {6},
pages = {133},
doi = {10.1038/s41684-025-01564-x},
pmid = {40461622},
issn = {1548-4475},
}

@article {pmid40461059,
year = {2025},
author = {Laiola, M and Koppe, L and Larabi, A and Thirion, F and Lange, C and Quinquis, B and David, A and Le Chatelier, E and Benoit, B and Sequino, G and Chanon, S and Vieille-Marchiset, A and Herpe, YE and Alvarez, JC and Glorieux, G and Krukowski, H and Geert, HRB and Raes, J and Fouque, D and Massy, ZA and Ehrlich, SD and Stengel, B and Wagner, S and , },
title = {Toxic microbiome and progression of chronic kidney disease: insights from a longitudinal CKD-Microbiome Study.},
journal = {Gut},
volume = {},
number = {},
pages = {},
doi = {10.1136/gutjnl-2024-334634},
pmid = {40461059},
issn = {1468-3288},
abstract = {BACKGROUND: The gut microbiota has been linked to non-communicable diseases, including chronic kidney disease (CKD). However, the relationships between gut microbiome composition changes, uraemic toxins (UTs) accumulation, and diet on CKD severity and progression remain underexplored.

OBJECTIVE: To characterise relationships between gut microbiome composition and functionality, UTs diet, and CKD severity and progression, as well as assess microbial contributions to UTs accumulation through mice faecal microbiota transplantation (FMT).

DESIGN: This study profiled the gut microbiome of 240 non-dialysis patients with CKD (CKD-REIN cohort) using shotgun metagenomics, with follow-up in 103 patients after 3 years, with comparisons with healthy volunteers from the Milieu Intérieur cohort. A multiomics approach identifies features associated with CKD severity (and progression), with validation in an independent Belgian cohort. Experimental models used FMT to test CKD gut microbiome effects on UTs and kidney fibrosis. Changes in gut microbiome over time were evaluated, and the impact of diet on these changes was assessed.

RESULTS: Compared with matched healthy controls, patients with CKD exhibited gut microbiota alteration, with enrichment of UT precursor-producing species. Patients with severe CKD exhibited higher UT levels and greater enrichment of UT (precursor)-producing species in the microbiota than patients with moderate CKD. Over time, UT (precursor)-producing species increased, and a plant-based low protein diet appeared to mitigate these changes. FMT from patients with CKD to antibiotic-treated CKD model mice increased serum UT levels and exacerbated kidney fibrosis.

CONCLUSIONS: This study highlights the role of the microbiome and UTs in CKD, suggesting a potential therapeutic target to slow disease progression.},
}

@article {pmid40460824,
year = {2025},
author = {Gogokhia, L and Tran, N and Grier, A and Nagayama, M and Xiang, G and Funez-dePagnier, G and Lavergne, A and Ericsson, C and Ben Maamar, S and Zhang, M and Battat, R and Scherl, E and Lukin, DJ and Longman, RS},
title = {Donor composition and fiber promote strain engraftment in a randomized controlled trial of fecal microbiota transplant for ulcerative colitis.},
journal = {Med (New York, N.Y.)},
volume = {},
number = {},
pages = {100707},
doi = {10.1016/j.medj.2025.100707},
pmid = {40460824},
issn = {2666-6340},
abstract = {BACKGROUND: Fecal microbiota transplantation (FMT) is an emerging treatment for ulcerative colitis (UC), but the impact of prebiotic fiber on FMT efficacy for UC is unclear. We performed a randomized, double-blind, placebo-controlled clinical trial to examine the efficacy of FMT with and without dietary fiber supplementation in patients with UC.

METHODS: 27 patients with mild to moderate UC were randomized to receive a single FMT or placebo with or without psyllium fiber supplementation for 8 weeks. The primary outcome was clinical response at week 8, and secondary outcomes included endoscopic improvement and clinical remission. Metagenomic sequencing of fecal DNA was analyzed to determine taxonomic profiles and donor strain engraftment.

FINDINGS: The trial was terminated early due to manufacturer discontinuation of FMT product. FMT induced clinical response, remission, and endoscopic improvement in UC patients compared to placebo (p < 0.05), but fiber did not improve clinical outcomes of FMT. Recipient microbiome composition post-FMT shifted toward donor composition in responders and non-responders, but the durability of this change was stronger in responders. Clinical response and durable change in microbiome composition following FMT was donor dependent. Strain tracking analysis also demonstrated a donor-dependent variability in the rate of successful engraftment and identified a consortium of engrafted bacteria associated with treatment response or fiber supplementation.

CONCLUSIONS: Single-dose FMT demonstrated clinical efficacy for mild to moderate UC compared to placebo but revealed no benefit of fiber supplementation. These results highlight proof of concept that donor selection and prebiotic fiber can shape strain-level engraftment. This study was registered at ClinicalTrials.gov: NCT03998488.

FUNDING: National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK128257, to R.S.L.).},
}

@article {pmid40458824,
year = {2025},
author = {Huang, Y and Huang, J and Li, Y and Xu, T and Quan, G and Xu, P and Yang, X and Liu, Z and Xie, W},
title = {Therapeutic efficacy of fecal microbiota transplantation in severe food intolerance: a case report.},
journal = {Frontiers in nutrition},
volume = {12},
number = {},
pages = {1594022},
pmid = {40458824},
issn = {2296-861X},
abstract = {This report presents the first documented application of fecal microbiota transplantation (FMT) for the management of extensive multi-food intolerance involving 52 specific foods in a pediatric patient with autism spectrum disorder (ASD). A 7 years-old autistic child was diagnosed with food intolerance to 52 items, presenting with generalized rashes, diarrhea, and malnutrition (BMI of 12.9) upon exposure or ingestion of the implicated foods. The child received oral fecal microbiota capsule treatment, with a daily dose of nine capsules (a total of 120 capsules per course) for two consecutive treatment courses. The rashes resolved, the child regained tolerance to previously intolerable foods, nutritional status improved, and stool consistency normalized. This case suggests that FMT may hold therapeutic potential for managing food intolerance in autistic patients.},
}

@article {pmid40457025,
year = {2025},
author = {Elkrief, A and Pidgeon, R and Maleki Vareki, S and Messaoudene, M and Castagner, B and Routy, B},
title = {The gut microbiome as a target in cancer immunotherapy: opportunities and challenges for drug development.},
journal = {Nature reviews. Drug discovery},
volume = {},
number = {},
pages = {},
pmid = {40457025},
issn = {1474-1784},
abstract = {The gut microbiome has a critical role in shaping the patient's immune response and influencing the efficacy of anticancer immunotherapy. Emerging evidence suggests that modulating the gut microbiome through interventions such as faecal microbiota transplantation, probiotics, prebiotics and lifestyle modifications may enhance therapeutic outcomes. Consequently, drug development efforts in immuno-oncology have expanded to explore microbiome-based therapeutic strategies. In this Review, we examine the rationale for targeting the microbiome in cancer treatment, highlighting key advances in clinical microbiome characterization and their implications for immunotherapy. We discuss findings from recent clinical trials evaluating microbiome-based interventions and address the challenges associated with translating these approaches into clinical practice. Finally, we outline future directions for the development and integration of microbiome-targeted therapies in oncology, with a focus on optimizing efficacy, safety and patient stratification strategies.},
}

@article {pmid40456559,
year = {2025},
author = {Hu, Y and Wang, Y and Gao, H and Yang, G and Xie, J and He, Z and Lv, S and Gu, F and Huang, C and Hu, W},
title = {Piperine Improves DSS-Induced Colitis in Mice via Inhibition of Inflammation and Modulation of Gut Microbiota.},
journal = {Phytotherapy research : PTR},
volume = {},
number = {},
pages = {},
doi = {10.1002/ptr.8491},
pmid = {40456559},
issn = {1099-1573},
support = {ZDYF2024XDNY177//Hainan Province Science and Technology Special Fund/ ; 2023YFD1600200//National Key Research and Development Program of China/ ; 1630012025119//China Central Public-Interest Scientific Institution Basal Research Fund/ ; },
abstract = {Inflammatory bowel disease (IBD) is a global health concern with limited therapeutic options. Previous studies have demonstrated that piperine exhibited anti-inflammatory effects both in vitro and in vivo. However, its potential to ameliorate colitis in mice through modulation of gut microbiota has not been explored. This study aimed to investigate the role of gut microbiota in the protective effects of piperine against colitis using a dextran sulfate sodium (DSS)-induced mouse model. Mice were administered piperine (12.5 and 25 mg/kg) prior to DSS exposure. Fecal microbiota transplantation (FMT) was then performed, after which we evaluated colitis symptoms, inflammation levels, and intestinal barrier function. Subsequently, 16S rDNA-based high-throughput sequencing was employed to analyze the microbial composition of the mouse cecal contents. Piperine administration increased the colon length, decreased the spleen index, and improved colon histopathology. Furthermore, piperine modulated inflammatory responses by inhibiting NF-κB signaling, thereby reducing the release of pro-inflammatory cytokines and mediators. It also enhanced intestinal barrier integrity by increasing the expression of claudin-1, claudin-3, ZO-1, occludin, and mucin 2. Notably, the 16S rDNA sequencing results revealed that piperine increased the abundance of Dubosiella in the gut. Piperine effectively protected mice from DSS-induced colitis, suppressed inflammation, and improved poor intestinal barrier function. It reshaped the intestinal microbiota, ultimately alleviating DSS-induced colitis in mice. Our research highlighted the significant role of gut microbiota in the piperine-mediated alleviation of intestinal damage and suggested its therapeutic potential for promoting gut health and reducing the risk of colitis.},
}

@article {pmid40455241,
year = {2025},
author = {Yi, LT and Wang, XY and Zhou, L and Cheng, J and Xu, GH and Zhu, JX},
title = {Polysaccharides from Black Mulberry Attenuate Colitis through Gut Microbiota Mediated TNF-α/pNF-κB/ICAM-1 Signaling Pathway.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c01870},
pmid = {40455241},
issn = {1520-5118},
abstract = {Colitis is characterized by immune dysregulation and gut microbiota imbalance. This study investigates the therapeutic effects of polysaccharides from black mulberry (PBM) on dextran sulfate sodium-induced colitis in mice. PBM administration significantly alleviated colitis symptoms, including body weight loss, histological damage, and inflammation, while enhancing antioxidant capacity and strengthening tight junction protein expression. PBM modulated gut microbiota composition, notably increasing Weissella spp., which correlated with elevated short-chain fatty acids (SCFAs) and decreased pro-inflammatory markers. Colonic RNA sequencing revealed the role of PBM in attenuating colitis via the TNF-α/NF-κB/ICAM-1 signaling pathway. Fecal microbiota transplantation (FMT) from PBM-treated mice confirmed that microbiota modulation from PBM contributed to these therapeutic effects. These findings suggest PBM as a natural therapeutic agent for colitis, offering a multifaceted approach to restoring gut homeostasis through microbiota modulation and inflammatory pathway regulation. This study provides new insights into dietary polysaccharides as potential adjunctive therapies for colitis.},
}

@article {pmid40454811,
year = {2025},
author = {Millard, SA and Vendrov, KC and Young, VB and Seekatz, AM},
title = {Host origin of microbiota drives functional recovery and Clostridioides difficile clearance in mice.},
journal = {mBio},
volume = {},
number = {},
pages = {e0110825},
doi = {10.1128/mbio.01108-25},
pmid = {40454811},
issn = {2150-7511},
abstract = {UNLABELLED: Colonization resistance provided by the gut microbiota is essential for resisting both initial Clostridioides difficile infection (CDI) and potential recurrent infection (rCDI). Although fecal microbiota transplantation (FMT) has been successful in treating rCDI by restoring microbial composition and function, mechanisms underlying the efficacy of standardized stool-derived products remain poorly understood. Using a combination of 16S rRNA gene-based and metagenomic sequencing alongside metabolomics, we investigated microbiome recovery following FMT from human and murine donor sources in a mouse model of rCDI. We found that a human-derived microbiota was less effective in clearing C. difficile compared to a mouse-derived microbiota, despite recovery of taxonomic diversity, compositional changes, and bacterial functions typically associated with clearance. Metabolomic analysis revealed deficits in secondary metabolites compared to those that received murine FMT, suggesting a functional remodeling between human microbes in their new host environment. Collectively, our data revealed additional environmental, ecological, or host factors to consider in FMT-based recovery from rCDI.

IMPORTANCE: Clostridioides difficile is a significant healthcare-associated pathogen, with recurrent infections presenting a major treatment challenge due to further disruption of the microbiota after antibiotic administration. Despite the success of fecal microbiota transplantation (FMT) for the treatment of recurrent infection, the mechanisms mediating its efficacy remain underexplored. This study reveals that the effectiveness of FMT may be compromised by a mismatch between donor microbes and the recipient environment, leading to deficits in key microbial metabolites. These findings highlight additional factors to consider when assessing the efficacy of microbial-based therapeutics for C. difficile infection (CDI) and other conditions.},
}

@article {pmid40454495,
year = {2025},
author = {Bjørklund, G and Butnariu, M and Dadar, M and Semenova, Y},
title = {The Gut Microbiota-anxiety Connection: Evidence, Mechanisms, and Therapeutic Strategies.},
journal = {Current medicinal chemistry},
volume = {},
number = {},
pages = {},
doi = {10.2174/0109298673356125250409182218},
pmid = {40454495},
issn = {1875-533X},
abstract = {The gut-brain axis (GBA), a bidirectional communication system between the gut and the brain, has emerged as a critical player in mental health. The interest in the connection between anxiety disorders (AD) and the gut microbiota is growing. This paper provides an overview of gut microbiota's role in dysregulation in anxiety, including alterations in gut microbiota (dysbiosis), leaky gut, metabolic endotoxemia, and the effect of antipsychotic medications. The mechanisms underlying the gut microbiota-anxiety (GMA) connection, such as neurotransmitter production, immune dysregulation, and GBA communication, are discussed. Furthermore, the paper explores gut microbiota- based therapeutic strategies, including probiotics, prebiotics, symbiotics, fecal microbiota transplantation, and dietary interventions, as potential approaches for anxiety management. This research field's clinical implications and future directions are also examined, underscoring that more studies are needed on gut microbiota's role in anxiety disorders. The conclusion highlights the importance of this ongoing research and the potential for personalized therapeutic interventions, instilling hope and optimism for the future of anxiety management and providing reassurance about the potential for personalized therapeutic interventions in this field.},
}

@article {pmid40454186,
year = {2025},
author = {Sharma, VK},
title = {Diabetes-induced depression: unravelling the role of gut dysbiosis.},
journal = {Journal of diabetes and metabolic disorders},
volume = {24},
number = {1},
pages = {129},
pmid = {40454186},
issn = {2251-6581},
abstract = {Depression is a prevalent yet often underdiagnosed neuropsychiatric comorbidity of type 2 diabetes mellitus (T2DM), significantly complicating disease management, treatment adherence, and overall well-being. Emerging evidence suggests that gut microbiota dysbiosis plays a pivotal role in linking T2DM and depression through mechanisms such as epithelial barrier dysfunction, systemic inflammation, neurotransmitter imbalances, hypothalamic-pituitary-adrenal (HPA) axis dysregulation, and impaired neurogenesis. This review aims to explore the mechanistic pathways through which diabetes-induced dysbiosis contributes to depression and to appraise the therapeutic potential of microbiota-targeted interventions, including probiotics, prebiotics, and fecal microbiota transplantation, in mitigating depressive symptoms and improving metabolic outcomes. Understanding this gut-brain interplay may provide novel insights into therapeutic strategies for managing the dual burden of diabetes and depression.},
}

@article {pmid40448308,
year = {2025},
author = {Gu, BH and Jung, HY and Rim, CY and Kim, TY and Lee, SJ and Choi, DY and Park, HK and Kim, M},
title = {Comparative Colonisation Ability of Human Faecal Microbiome Transplantation Strategies in Murine Models.},
journal = {Microbial biotechnology},
volume = {18},
number = {6},
pages = {e70173},
pmid = {40448308},
issn = {1751-7915},
support = {2024-ER2113-00//the Korea National Institute of Health (KNIH) research project/ ; 20019505//the Ministry of Trade, Industry & Energy (MOTIE, Korea)/ ; },
mesh = {Animals ; *Fecal Microbiota Transplantation/methods ; Humans ; Mice ; *Gastrointestinal Microbiome ; *Feces/microbiology ; Disease Models, Animal ; *Bacteria/classification/growth & development/isolation & purification/genetics ; Dysbiosis/therapy/microbiology ; Male ; Models, Animal ; },
abstract = {The gut microbiome plays a crucial role in maintaining intestinal homeostasis and influencing immune-mediated diseases. Human faecal microbiota transplantation (FMT) is often employed in murine models to investigate the role of human microbes in disease regulation, but methods for effective colonisation require refinement. This study aimed to assess the colonisation efficiency of human microbiota in a murine model using FMT with human faeces, focusing particularly on the impact of gut microbiota depletion via polyethylene glycol (PEG) and comparing oral-gastric gavage with enema administration routes. Our findings revealed that PEG-induced depletion enhanced human microbiome colonisation in mice. Oral-gastric gavage prolonged colonisation, while enema administration facilitated quicker resolution of dysbiosis, both inducing selective human microbial colonisation in a time-dependent manner. Notably, genera such as Bacteroides, Blautia, Medicaternibacter and Bifidobacteria were successfully colonised, whereas Roseburia, Anaerostipes, Anaerobutyricum and Faecalibacterium failed to establish in the murine gut post-FMT. These findings highlight the challenges of replicating human gut microbiota in murine models and underscore the importance of selecting appropriate FMT methods based on desired outcomes. This study provides valuable insights into the colonisation dynamics of human microbiota in mice, contributing to the development of more effective FMT strategies for disease treatment.},
}

Animals
*Fecal Microbiota Transplantation/methods
Humans
Mice
*Gastrointestinal Microbiome
*Feces/microbiology
Disease Models, Animal
*Bacteria/classification/growth & development/isolation & purification/genetics
Dysbiosis/therapy/microbiology
Male
Models, Animal

@article {pmid40448218,
year = {2025},
author = {Gao, ZK and Fan, CY and Zhang, BW and Geng, JX and Han, X and Xu, DQ and Arshad, M and Sun, HX and Li, JY and Jin, X and Mu, XQ},
title = {Cardiac function of colorectal cancer mice is remotely controlled by gut microbiota: regulating serum metabolites and myocardial cytokines.},
journal = {Animal microbiome},
volume = {7},
number = {1},
pages = {53},
pmid = {40448218},
issn = {2524-4671},
support = {NSFC81903631//The National Natural Science Foundation of China/ ; },
abstract = {Several studies have indicated that the dysregulation of microbial metabolites and the inflammatory environment resulting from microbial dysbiosis may contribute to the occurrence and progression of cardiovascular diseases. Therefore, restoring the disordered gut microbiota in patients with colorectal cancer by fecal microbiota transplantation (FMT) has the potential to reduce the incidence of cardiac disease. In this study, we identified cardiac dysfunction in azomethane and dextran sodium sulfate-induced colorectal cancer mice. Intestinal microbes from healthy mice were transferred to colorectal cancer mice, which vastly reversed the disorder of the gut microbiota and effectively alleviated cardiac dysfunction. Moreover, FMT regulated the expression of serum metabolites such as uridine triphosphate (UTP), tiamulin, andrographolide, and N-Acetyl-D-glucosamine, as well as cytokines like TGF-β, IRF5, and β-MHC in the heart. These findings uncover that the disturbed gut microbiota causes cardiac dysfunction in colorectal cancer mice by modulating the expression of serum metabolites and cytokines, which could be alleviated by treatment with FMT.},
}

@article {pmid39752608,
year = {2025},
author = {Holtan, SG and Bolaños-Meade, J and Al Malki, MM and Wu, J and Kitko, CL and Reshef, R and Rezvani, AR and Shaffer, BC and Solh, MM and Yao, JM and Runaas, L and Elmariah, H and Larkin, KT and El Jurdi, N and Gooptu, M and Loren, AW and Hall, AC and Alousi, AM and Jamy, O and Clark, W and Kean, L and Bhatt, AS and Perales, MA and Applegate, K and Efebera, YA and Leifer, E and Jones, RJ and Horowitz, MM and Mattila, D and Saber, W and Hamadani, M and Martens, MJ},
title = {Improved Patient-Reported Outcomes With Post-Transplant Cyclophosphamide: A Quality-of-Life Evaluation and 2-Year Outcomes of BMT CTN 1703.},
journal = {Journal of clinical oncology : official journal of the American Society of Clinical Oncology},
volume = {43},
number = {8},
pages = {912-918},
pmid = {39752608},
issn = {1527-7755},
support = {U10 HL069294/HL/NHLBI NIH HHS/United States ; U24 CA076518/CA/NCI NIH HHS/United States ; U24 HL138660/HL/NHLBI NIH HHS/United States ; UG1 HL138645/HL/NHLBI NIH HHS/United States ; },
mesh = {Humans ; *Cyclophosphamide/therapeutic use/administration & dosage/adverse effects ; *Patient Reported Outcome Measures ; *Graft vs Host Disease/prevention & control ; *Quality of Life ; *Bone Marrow Transplantation/adverse effects ; Female ; Male ; Middle Aged ; Adult ; *Immunosuppressive Agents/therapeutic use ; Methotrexate/administration & dosage/therapeutic use ; Tacrolimus/administration & dosage/therapeutic use ; Mycophenolic Acid/administration & dosage/therapeutic use/analogs & derivatives ; Aged ; Treatment Outcome ; },
abstract = {The BMT CTN 1703 phase III trial confirmed that graft-versus-host disease (GVHD) prophylaxis with post-transplantation cyclophosphamide (PTCy), tacrolimus (Tac), and mycophenolate mofetil (MMF) results in superior GVHD-free, relapse-free survival (GRFS) compared with Tac/methotrexate (MTX) prophylaxis. This companion study assesses the effect of these regimens on patient-reported outcomes (PROs). Using the Lee Chronic GVHD Symptom Score and PROMIS subscales (physical function, GI symptoms, social role satisfaction) as primary end points and hemorrhagic cystitis symptoms and Lee subscales as secondary end points, responses from English and Spanish speakers were analyzed at baseline and days 100, 180, and 365 after transplant. PRO scores were compared between the arms using inverse probability weighted-independent estimating equation models. The PTCy arm had significantly lower scores on the Lee Chronic GVHD Symptom Scale (P = .01), indicating lower GVHD symptom burden. Lee Scale nutrition and mouth subscores were also better in the PTCy arm compared with the Tac/MTX arm (P < .01 for both). Older participants (age >65 years) reported better Lee Scale psychological subscores than younger participants (P = .003). No significant differences were identified in hemorrhagic cystitis or in the PROMIS subscales between treatment arms. The updated clinical end points at 2 years for the parent trial confirmed that PTCy/Tac/MMF maintained a significant advantage over Tac/MTX in GRFS (42.4% v 28.8%, P = .001). In addition to improved GRFS, patients randomly assigned to the PTCy arm reported lower symptom burden during the first year after transplant.},
}

Humans
*Cyclophosphamide/therapeutic use/administration & dosage/adverse effects
*Patient Reported Outcome Measures
*Graft vs Host Disease/prevention & control
*Quality of Life
*Bone Marrow Transplantation/adverse effects
Female
Male
Middle Aged
Adult
*Immunosuppressive Agents/therapeutic use
Methotrexate/administration & dosage/therapeutic use
Tacrolimus/administration & dosage/therapeutic use
Mycophenolic Acid/administration & dosage/therapeutic use/analogs & derivatives
Aged
Treatment Outcome

@article {pmid40447159,
year = {2025},
author = {Jeong, SH and Vasavada, SP and Lashner, B and Werneburg, GT},
title = {Fecal microbiota transplant is associated with resolution of recurrent urinary tract infection.},
journal = {Urology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.urology.2025.05.052},
pmid = {40447159},
issn = {1527-9995},
abstract = {OBJECTIVE: To investigate the association of fecal microbiota transplant (FMT) therapy, an effective treatment for recurrent C. difficile colitis, with resolution of recurrent UTI (rUTI).

METHODS: A prospectively accrued database of patients who underwent FMT for recurrent Clostridoides difficile colitis was retrospectively reviewed for individuals with rUTI in the two years prior to FMT. Recurrent UTI status (defined as two UTI episodes in six months or three UTI episodes in one year) and UTI frequency in the two years prior to the FMT were compared to those in the two year follow up period after FMT using the two-tailed Wilcoxin matched pairs signed rank test. A p-value <0.05 was considered statistically significant.

RESULTS: Of 11 patients who had rUTI in the two years preceding FMT, no patient had rUTI over the follow up period following FMT (p=0.001). The average number of UTIs in the two years prior to FMT was 3.7 (range 2-6), and the average number of UTIs in the follow up period was 0.27 (range 0-1) (p=0.001). The Kaplan-Meier estimate, the median time to UTI recurrence, was 19.6 months (95% CI: 15.2 - 23.9). There was no marked difference in antibiotic susceptibility profiles before and after FMT.

CONCLUSIONS: FMT was associated with resolution of rUTI and reduction in UTI frequency in this cohort. The results of this study support the hypothesis that modulation of the gut microbiome may reduce rUTI risk, and support a clinical trial to further assess the safety and efficacy of FMT for rUTI.},
}

@article {pmid40446472,
year = {2025},
author = {Chen, L and Ahmad, M and Li, J and Li, J and Yang, Z and Hu, C},
title = {Gut microbiota manipulation to mitigate the toxicities of environmental pollutants.},
journal = {Aquatic toxicology (Amsterdam, Netherlands)},
volume = {285},
number = {},
pages = {107425},
doi = {10.1016/j.aquatox.2025.107425},
pmid = {40446472},
issn = {1879-1514},
abstract = {The gut microbiome, commonly termed as a "super organ", plays a crucial role in the modulation of various biological functions associated with metabolism, endocrinology, immunology, and neurology. However, gut microbiome is extremely susceptible to the risks of environmental pollutants, which will drive gut microbial community to dysbiosis. Simultaneously, restoring healthy gut microbiome can protect the hosts from the health hazards of pollutants. It is increasingly verified that probiotics, prebiotics, and fecal microbiota transplantation (FMT) are efficacious measures to manipulate and remediate gut microecosystem. Among various probiotic strains, lactic acid bacteria are the most extensively applied in toxicity mitigation, which is characterized by shaping gut microbiota structure and metabolism, increasing gut epithelial barrier integrity, promoting fecal elimination of pollutants, suppressing inflammation symptoms, and then improving host systemic physiology. Prebiotics are dietary fibers that cannot be digested by the host, but can be fermented by specific gut bacteria to produce short chain fatty acids, which are identified as the key effect molecules in the manifestation of prebiotic toxicity mitigation actions. In addition, by transplanting the entire community of healthy gut microbiota, FMT also shows effective performances in counteracting the adverse effects of environmental pollutants and recovering host animal health. Intriguingly, FMT from young donors is even found to inhibit the toxic disturbances in healthy aging progression. Based on current evidence, this review summarized the findings about using probiotics, prebiotics, and FMT to manipulate gut microbiota and alleviate the health impairment of environmental pollutants. Key mechanistic insights into the interactive behaviors were underlined. Furthermore, the challenges and future directions in harnessing gut microbiota manipulation as a novel therapeutic approach to mitigate pollutant-induced toxicities were postulated. This review is expected to advocate comprehensive scientific research and literally favor the application of health intervention strategies.},
}

@article {pmid40446358,
year = {2025},
author = {Porcari, S and Ng, SC and Zitvogel, L and Sokol, H and Weersma, RK and Elinav, E and Gasbarrini, A and Cammarota, G and Tilg, H and Ianiro, G},
title = {The microbiome for clinicians.},
journal = {Cell},
volume = {188},
number = {11},
pages = {2836-2844},
doi = {10.1016/j.cell.2025.04.016},
pmid = {40446358},
issn = {1097-4172},
mesh = {Humans ; *Microbiota ; Clinical Trials as Topic ; },
abstract = {Despite promising evidence in diagnostics and therapeutics, microbiome research is not yet implemented into clinical medicine. Several initiatives, including the standardization of microbiome research, the refinement of microbiome clinical trial design, and the development of communication between microbiome researchers and clinicians, are crucial to move microbiome science toward clinical practice.},
}

Humans
*Microbiota
Clinical Trials as Topic

@article {pmid40444969,
year = {2025},
author = {Xie, J and Kim, T and Liu, Z and Panier, H and Bokoliya, S and Xu, M and Zhou, Y},
title = {Young gut microbiota transplantation improves the metabolic health of old mice.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0160124},
doi = {10.1128/msystems.01601-24},
pmid = {40444969},
issn = {2379-5077},
abstract = {UNLABELLED: The gut microbiota evolves over a lifetime and significantly impacts the aging process. Targeting the gut microbiota represents a novel avenue to delay aging and aging-related physical and mental decline. However, the underlying mechanism by which the microbiota modulates the aging process, particularly age-related physical and behavioral changes is not completely understood. We conducted fecal microbiota transplantation (FMT) from young or old male donor mice to the old male recipients. Old recipients with young microbiota had a higher alpha diversity than the old recipients with old microbiota. Compared to FMT with old microbiota, FMT with young microbiota reduced body weight and prevented fat accumulation in the old recipients. FMT with young microbiota also lowered frailty, increased grip strength, and alleviated depression and anxiety-like behavior in the old recipients. Consistent with observed physical changes, untargeted metabolomic analysis of serum and stools revealed that FMT with young microbiota lowered age-related long-chain fatty acid levels and increased amino acid levels in the old recipients. Bulk RNAseq analysis of the amygdala of the brain showed that FMT with young microbiota downregulated inflammatory pathways and upregulated oxidative phosphorylation in the old recipients. Our results demonstrate that FMT with young microbiota has substantial positive influences on age-related body composition, frailty, and psychological behaviors. These effects are associated with changes in host lipid and amino acid metabolism in the periphery and transcriptional regulation of neuroinflammation and energy utilization in the brain.

IMPORTANCE: The gut microbiome is a key hallmark of aging. Fecal microbiota transplantation (FMT) using young microbiota represents a novel rejuvenation strategy to delay aging. Our study provides compelling evidence that transplanting microbiota from young mice significantly improved grip strength, frailty, and body composition in aged recipient mice. At the molecular level, FMT improved aging-related metabolic markers in the gut and circulation. Additionally, FMT from young microbiota rejuvenated the amygdala of the aged brain by downregulating inflammatory pathways. This study highlights the importance of metabolic reprogramming via young microbiota FMT in improving physical and metabolic health in elderly recipients.},
}

@article {pmid40443229,
year = {2025},
author = {Lee, MA and Slead, T and Suchodolski, J and Tolbert, MK and Marsilio, S},
title = {Adverse events after fecal microbiota transplantation in nine cats: a case series.},
journal = {Journal of feline medicine and surgery},
volume = {27},
number = {5},
pages = {1098612X251337274},
doi = {10.1177/1098612X251337274},
pmid = {40443229},
issn = {1532-2750},
mesh = {Animals ; Cats ; *Cat Diseases/therapy ; *Fecal Microbiota Transplantation/veterinary/adverse effects ; Female ; Male ; Diarrhea/veterinary/therapy ; },
abstract = {This case series describes nine cases of fecal microbiota transplantation in cats and associated adverse events (AEs) from two tertiary referral hospitals. AEs were graded according to criteria established by the Veterinary Cooperative Oncology Group's Common Terminology Criteria for Adverse Events (VCOG-CTCAE v2) for clinical trials. Cats received 5-6 g/kg donor feces 2-6 times for chronic enteropathy (n = 4) or therapy-resistant diarrhea (n = 5). AEs included lethargy (n = 7), vomiting (n = 5), diarrhea (n = 5), weight loss (n = 5), inappetence (n = 5), dehydration (n = 5), abdominal pain (n = 2), gastroenterocolitis based on ultrasound (n = 2) and anorexia (n = 1). Temperatures of up to 103.4°F were noted but did not meet the criteria for AEs (>103.5°F). Cats responded to antimicrobials (metronidazole, marbofloxacin), anthelmintics (fenbendazole), supportive care with fluids, ondansetron and mirtazapine (n = 5), gabapentin (n = 2), pradofloxacin (n = 1) or self-resolved (n = 1). Positive response to fecal microbiota transplantation for the presenting complaint was seen in eight cats (seven complete, one partial and transient).Relevance and novel informationFecal microbiota transplantation is increasing in usage among companion animals. Fecal microbiota transplantations in cats have been rarely described in the literature as have AEs after administration. This case series represents the first description of AEs after fecal microbiota transplantation in cats.},
}

Animals
Cats
*Cat Diseases/therapy
*Fecal Microbiota Transplantation/veterinary/adverse effects
Female
Male
Diarrhea/veterinary/therapy

@article {pmid40443227,
year = {2025},
author = {Green, GBH and Cox-Holmes, AN and Marlow, GH and Potier, ACE and Wang, Y and Zhou, L and Chen, D and Morrow, CD and McFarland, BC},
title = {Human microbiota influence the immune cell composition and gene expression in the tumor environment of a murine model of glioma.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2508432},
doi = {10.1080/19490976.2025.2508432},
pmid = {40443227},
issn = {1949-0984},
mesh = {Animals ; *Glioma/immunology/microbiology/genetics ; Mice ; Humans ; *Gastrointestinal Microbiome/immunology ; Disease Models, Animal ; *Tumor Microenvironment/immunology/genetics ; *Brain Neoplasms/immunology/microbiology/genetics ; Cell Line, Tumor ; Feces/microbiology ; Programmed Cell Death 1 Receptor/antagonists & inhibitors/immunology ; RNA, Ribosomal, 16S/genetics ; Bacteria/classification/genetics/isolation & purification ; Mice, Inbred C57BL ; },
abstract = {BACKGROUND: Immunotherapy has shown success against other cancers but not glioblastoma. Previous data has revealed that microbiota influences anti-PD-1 efficacy. We have previously found that, when using gnotobiotic mice transplanted with human fecal microbiota, the gut microbial composition influenced the response to anti-PD-1 in a mouse model of glioma. However, the role of the human microbiota in influencing the mouse immune cells in the glioma microenvironment and anti-PD-1 response was largely unknown. Using two distinct humanized microbiome (HuM) lines, we used single-cell RNA sequencing (scRNA-seq) to determine how gut microbiota affect immune infiltration and gene expression in a murine glioma model.

METHODS: 16S rRNA sequencing was performed on fecal samples from HuM1 (H1) and HuM2 (H2) mice. Mice were intracranially injected with murine glioma cells (GL261), and on day 13 treated with one dose of isotype control or anti-PD1. Mice were euthanized on day 14 for analysis of all immune cells in the tumors by scRNA-seq.

RESULTS: HuM1 and HuM2 mice had different microbial populations, with HuM1 being primarily dominated via Alistipes, and HuM2 being primarily composed of Odoribacter. Sc-RNA-seq of the tumor immune cells revealed 21 clusters with significant differences between H1 and H2 samples with a larger population of M1 type macrophages in H1 samples. Gene expression analysis revealed higher expression of inflammatory markers in the M1 population in H2 mice treated with anti-PD-1.

CONCLUSIONS: Microbial gut communities influence the presence and gene activation patterns of immune cells in the brain tumors of mice both under control (isotype) and following anti-PD-1 treatment.},
}

Animals
*Glioma/immunology/microbiology/genetics
Mice
Humans
*Gastrointestinal Microbiome/immunology
Disease Models, Animal
*Tumor Microenvironment/immunology/genetics
*Brain Neoplasms/immunology/microbiology/genetics
Cell Line, Tumor
Feces/microbiology
Programmed Cell Death 1 Receptor/antagonists & inhibitors/immunology
RNA, Ribosomal, 16S/genetics
Bacteria/classification/genetics/isolation & purification
Mice, Inbred C57BL

@article {pmid40441587,
year = {2025},
author = {Luo, M and Du, Y and Liu, X and Zhang, S and Zhu, W and Liu, K and Ren, X and Zhang, N},
title = {Fecal Microbiota Transplantation Alleviates Cirrhotic Portal Hypertension in Rats via Butyrate-Mediated HDAC3 Inhibition and PI3K/Akt/eNOS Signaling Regulation.},
journal = {European journal of pharmacology},
volume = {},
number = {},
pages = {177781},
doi = {10.1016/j.ejphar.2025.177781},
pmid = {40441587},
issn = {1879-0712},
abstract = {BACKGROUND: Portal hypertension (PHT) is a severe complication of liver cirrhosis, with limited therapeutic options. Despite emerging evidence linking gut microbiota dysbiosis to PHT progression, the mechanisms by which microbial metabolites modulate liver sinusoidal endothelial cells (LSECs) dysfunction and the therapeutic efficacy of fecal microbiota transplantation (FMT) remain poorly understood. This study investigated the potential of FMT to alleviate PHT in cirrhotic rats, exploring the underlying mechanisms involving butyrate-mediated HDAC3 inhibition and PI3K/Akt/eNOS signaling regulation in LSECs.

METHODS: Cirrhosis with PHT was induced in Sprague-Dawley rats via intraperitoneal carbon tetrachloride injection, followed by FMT or butyrate supplementation via oral gavage. Analyses included portal hemodynamic measurements, gut microbiota sequencing, serum SCFA metabolomics profiling, HDAC3 activity assays, NO level quantification, and assessments of liver fibrosis, liver function, and LSEC ultrastructure. LSECs were isolated for PI3K/Akt/eNOS signaling analysis via qRT-PCR, Western blotting, and immunofluorescence staining.

RESULTS: A two-week FMT intervention in cirrhotic rats with PHT enriched butyrate-producing bacteria and increased serum butyrate levels, which were associated with reduced portal pressure and intrahepatic vascular resistance, without affecting liver fibrosis, function, or LSEC ultrastructure. FMT reduced HDAC3 activity by 2.17-fold and increased Akt and eNOS phosphorylation in primary LSECs by 1.69-fold and 1.25-fold, respectively, elevating plasma NO levels by 1.66-fold compared to untreated controls. In vitro experiments with primary LSECs confirmed these butyrate-mediated effects.

CONCLUSION: FMT alleviates cirrhotic PHT through butyrate-mediated HDAC3 inhibition and subsequent PI3K/Akt/eNOS signaling activation in LSECs, highlighting the therapeutic potential of targeting the gut-liver axis via microbial metabolites for PHT management.},
}

@article {pmid40441086,
year = {2025},
author = {Sharma, P and Das, S and Rituraj, R and Bhagyashree, B},
title = {Understanding oncobiosis in ovarian cancer: Emerging concepts in tumor progression.},
journal = {Pathology, research and practice},
volume = {271},
number = {},
pages = {156026},
doi = {10.1016/j.prp.2025.156026},
pmid = {40441086},
issn = {1618-0631},
abstract = {Ovarian cancer is a leading cause of gynecologic cancer mortality and has recently been linked to microbial dysbiosis or oncobiosis. Tumorigenesis is a highly complex process, and recent research has revealed numerous new mechanisms showing how tumors interact with their surrounding microenvironment. The inclusion of microbiome studies has significantly advanced this field revealing the important role microbes play, not only in maintaining normal physiological functions of the human body but also in influencing oncogenic pathways. This expanding knowledge is deepening our understanding of tumor pathophysiology and is helping to create new diagnostic, prognostic, therapeutic and preventive strategies for specific cancers. This review explores the role of the microbiome in ovarian carcinogenesis, focusing on its interaction with the tumor microenvironment (TME) and its influence on inflammation, immune regulation and metabolic signaling. This review studied dysbiosis in several anatomical compartments such as the gut, oral cavity, lower and upper genital tracts and ovarian tissues, in relation to ovarian oncobiosis. Emerging clinical implications of these studies include the use of microbial profiles as diagnostic or prognostic biomarkers. Therapeutic strategies such as fecal microbiota transplantation and probiotics are also discussed for their ability to restore microbial balance and enhance treatment efficacy. This review highlights the importance of continued research to explore causal relationships between the microbiome and tumorigenesis, positioning microbiome studies as promising tools in ovarian cancer management and improving patient care.},
}

@article {pmid40438840,
year = {2025},
author = {Saleem, MM and Masood, S and Rahmatullah, MM and Ayesha Imdad, I and Mohammed Aslam Sange, A and Nasr, D},
title = {Gut Microbiota Dysbiosis and Its Role in the Development of Irritable Bowel Syndrome.},
journal = {Cureus},
volume = {17},
number = {4},
pages = {e83084},
pmid = {40438840},
issn = {2168-8184},
abstract = {The gut microbiota refers to the diverse community of symbiotic and pathogenic microorganisms inhabiting the host digestive tract. This microbiome plays a vital role in maintaining the integrity of the digestive system. Irritable bowel syndrome (IBS) is a functional gastrointestinal disorder (FGID) characterized by chronic abdominal pain and altered bowel habits. Although the pathophysiology of IBS remains unclear, recent studies suggest that the disruption of the gut microbiota (dysbiosis) may play a significant role. This study aims to examine the role of the gut microbiota in the development of IBS, analyze factors influencing the gut microbiome, and explore the potential for microbiota-targeted therapies. Relevant literature published from 2014 until 2024 was sourced from Google Scholar, PubMed, and Scopus using the keywords "microbiome", "irritable bowel syndrome", "dysbiosis", "faecal transplantation", and "probiotics". This review revealed consistent evidence of gut microbiota dysbiosis in individuals with IBS, characterized by altered microbial diversity, composition, and metabolic function. Contributing factors included a reduced abundance of beneficial commensals, overgrowth of potentially pathogenic species, and disrupted host-microbiota interactions. This dysbiosis was also frequently associated with symptom severity and specific IBS subtypes. Emerging evidence further highlights the role of diet, stress, and genetic factors in modulating gut microbiota and influencing IBS development. The growing body of research supports a strong link between dysbiosis and the pathogenesis and symptomatology of IBS. Understanding the microbial underpinnings of IBS opens avenues for potential diagnostic biomarkers and innovative therapeutic interventions aimed at restoring a balanced gut microbiota. However, further research is needed to elucidate the underlying mechanisms and translate these insights into effective clinical strategies for the management of IBS. This review underscores the significance of gut microbiota in IBS and its potential as a target for future therapeutic interventions.},
}

@article {pmid40438215,
year = {2025},
author = {Hanna, A and Abbas, H and Yassine, F and AlBush, A and Bilen, M},
title = {Systematic review of gut microbiota composition, metabolic alterations, and the effects of treatments on PCOS and gut microbiota across human and animal studies.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1549499},
pmid = {40438215},
issn = {1664-302X},
abstract = {INTRODUCTION: Polycystic ovary syndrome (PCOS) is an endocrine disorder affecting around 12% of women globally, associated with infertility and various comorbidities. Emerging evidence suggests a crucial role of gut microbiota in PCOS pathophysiology, prompting research to investigate alterations in gut microbial composition in patients with PCOS.

METHODS: This systematic review aims to analyze human and animal studies that compare gut microbiota composition, gut-derived metabolites, and treatment interventions in PCOS patients versus healthy controls. A comprehensive literature search was conducted using PubMed, Scopus, and Web of Science, yielding studies examining gut microbiota, metabolomic shifts, and treatment responses in PCOS models and human populations.

RESULTS: Our analysis revealed decreases in alpha diversity in PCOS patients, with more pronounced changes in beta diversity in animal models. Specific bacterial taxa, such as Bacteroides vulgatus, Escherichia-Shigella and Lactobacillus, showed implication in PCOS pathogenesis, suggesting potential microbial markers. Furthermore, discrepancies between human and animal studies show the need for humanized mouse models to bridge this gap. Interventions like probiotics and fecal microbiota transplantation (FMT) showed varying levels of efficacy, with FMT emerging as a more promising but invasive option, offering live bacteriotherapy as a potential therapeutic alternative. Alterations in gut-derived metabolites, including short-chain fatty acids and bile acids, highlighted the multifaceted nature of PCOS, with implications extending to metabolic, hormonal, and gut-brain axis disruptions.

DISCUSSION: In conclusion, PCOS exhibits complex interactions between gut microbiota and metabolic pathways, necessitating further research with standardized methods and larger sample sizes to elucidate the microbiome's role in PCOS.},
}

@article {pmid40437401,
year = {2025},
author = {Unrug-Bielawska, K and Sandowska-Markiewicz, Z and Pyśniak, K and Piątkowska, M and Czarnowski, P and Goryca, K and Mróz, A and Żeber-Lubecka, N and Wójcik-Trechcińska, U and Bałabas, A and Dąbrowska, M and Surynt, P and Radkiewicz, M and Mikula, M and Ostrowski, J},
title = {Western Diet and fecal microbiota transplantation alter phenotypic, liver fatty acids, and gut metagenomics and metabolomics in Mtarc2 knockout mice.},
journal = {Genes & nutrition},
volume = {20},
number = {1},
pages = {13},
pmid = {40437401},
issn = {1555-8932},
support = {2018/29/B/NZ7/00809//Narodowe Centrum Nauki/ ; },
}

@article {pmid40436727,
year = {2025},
author = {Qingsong, L},
title = {Comment on "Alteration of gut microbial composition associated with the therapeutic efficacy of fecal microbiota transplantation in Clostridium difficile infection".},
journal = {Journal of the Formosan Medical Association = Taiwan yi zhi},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jfma.2025.05.033},
pmid = {40436727},
issn = {0929-6646},
}

@article {pmid40433559,
year = {2025},
author = {Zhang, J and Chen, K and Chen, F},
title = {Exploring the impact of the liver-intestine-brain axis on brain function in non-alcoholic fatty liver disease.},
journal = {Journal of pharmaceutical analysis},
volume = {15},
number = {5},
pages = {101077},
pmid = {40433559},
issn = {2214-0883},
abstract = {This study investigates the molecular complexities of non-alcoholic fatty liver disease (NAFLD)-induced brain dysfunction, with a focus on the liver-intestine-brain axis and potential therapeutic interventions. The main objectives include understanding critical microbiota shifts in NAFLD, exploring altered metabolites, and identifying key regulatory molecules influencing brain function. The methods employed encompassed 16S ribosomal RNA (rRNA) sequencing to scrutinize stool microbiota in NAFLD patients and healthy individuals, non-targeted metabolomics using LC-MS to uncover elevated levels of deoxycholic acid (DCA) in NAFLD mice, and single-cell RNA sequencing (scRNA-seq) to pinpoint the pivotal gene Hpgd in microglial cells and its downstream Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway. Behavioral changes and brain function were assessed in NAFLD mice with and without Fecal microbiota transplantation (FMT) treatment, utilizing various assays and analyses. The results revealed significant differences in microbiota composition, with increased levels of Bacteroides in NAFLD patients. Additionally, elevated DCA levels were observed in NAFLD mice, and FMT treatment demonstrated efficacy in ameliorating liver function and brain dysfunction. Hpgd inhibition by DCA activated the JAK2/STAT3 pathway in microglial cells, leading to inflammatory activation, inhibition of mitochondrial autophagy, induction of neuronal apoptosis, and reduction in neuronal action potentials. This study elucidates the intricate molecular mechanisms underlying the liver-gut-brain axis in NAFLD, and the identification of increased DCA and the impact of JAK2/STAT3 signaling on microglial cells highlight potential therapeutic targets for addressing NAFLD-induced brain dysfunction.},
}

@article {pmid40431274,
year = {2025},
author = {Schiavone, N and Isoldi, G and Calcagno, S and Rovida, E and Antiga, E and De Almeida, CV and Lulli, M},
title = {Exploring the Gut Microbiota-Retina Axis: Implications for Health and Disease.},
journal = {Microorganisms},
volume = {13},
number = {5},
pages = {},
doi = {10.3390/microorganisms13051101},
pmid = {40431274},
issn = {2076-2607},
abstract = {The gut microbiota represents a rich and adaptive microbial network inhabiting the gastrointestinal tract, performing key functions in nutrient processing, immune response modulation, intestinal wall protection, and microbial defense. Its composition remains highly personalized and responsive to external influences, including lifestyle patterns, physical activity, body composition, and nutritional intake. The interactions of the gut microbiota with bodily systems are conventionally interpreted as broad systemic impacts on organ balance. Yet, emerging research-exemplified by the gut microbiota-brain axis-suggests the potential existence of more targeted and direct communication mechanisms. Dysbiosis, characterized by microbial ecosystem disturbance, generates multiple metabolic compounds capable of entering systemic circulation and reaching distant tissues, notably including ocular structures. This microbial imbalance has been associated with both systemic and localized conditions linked to eye disorders. Accumulating scientific evidence now supports the concept of a gut-retina axis, underscoring the significant role of microbiota disruption in generating various retinal pathologies. This review comprehensively investigates gut microbiota composition, functional dynamics, and dysbiosis-induced alterations, with specific focus on retinal interactions in age-related macular degeneration, diabetic retinopathy, glaucoma, and retinal artery occlusion. Moreover, the review explores microbiota-targeted therapeutic strategies, including precision nutritional interventions and microbial transplantation, as potential modulators of retinal disease progression.},
}

@article {pmid40431196,
year = {2025},
author = {Harder, JW and Ma, J and Collins, J and Alard, P and Jala, VR and Bodduluri, H and Kosiewicz, MM},
title = {Characterization of Sex-Based Differences in Gut Microbiota That Correlate with Suppression of Lupus in Female BWF1 Mice.},
journal = {Microorganisms},
volume = {13},
number = {5},
pages = {},
doi = {10.3390/microorganisms13051023},
pmid = {40431196},
issn = {2076-2607},
support = {Target Identification in Lupus Grant//Alliance for Lupus Research/ ; R01AR067188/NH/NIH HHS/United States ; },
abstract = {Systemic lupus erythematosus (SLE) is more prevalent in female mice and humans and is associated with microbiota dysbiosis. We analyzed the fecal microbiota composition in female and male NZBxNZWF1 (BWF1) mice, a model of SLE, using 16S RNA gene sequencing. Composition of gut microbiota differed between adult disease-prone female (pre-disease) and disease-resistant male mice. Transfer of male cecal contents by gavage into female mice suppressed kidney disease (decreased proteinuria) and improved survival. After our mouse colony was moved to a new barrier facility with similar housing, male cecal transplants failed to suppress disease in female recipients. After two years, the protective phenotype reemerged: male cecal transplants once again suppressed disease in female mice. We compared the gut microbiota composition in female and male BWF1 mice for the three different periods, during which the male microbiota either protected or failed to protect female recipients. In female vs. male mice and in female mice receiving male cecal transplants, we found Bacteroides was high, Clostridium was low (high Bacteroides/Clostridium ratio), and Alistipes was present during periods when male cecal transplants suppressed disease. These data suggest that specific bacterial populations may have opposing effects on disease suppression in a model of microbiota transplantation.},
}

@article {pmid40431182,
year = {2025},
author = {Matsumoto, H and Gu, T and Yo, S and Sasahira, M and Monden, S and Ninomiya, T and Osawa, M and Handa, O and Umegaki, E and Shiotani, A},
title = {Fecal Microbiota Transplantation Using Donor Stool Obtained from Exercised Mice Suppresses Colonic Tumor Development Induced by Azoxymethane in High-Fat Diet-Induced Obese Mice.},
journal = {Microorganisms},
volume = {13},
number = {5},
pages = {},
doi = {10.3390/microorganisms13051009},
pmid = {40431182},
issn = {2076-2607},
support = {JP 19K11484//Japanese Grant-in-Aid Scientific Reserach/ ; },
abstract = {The gut microbiota plays an important role in the development of colorectal tumors. However, the underlying mechanisms remain unclear. In this study, we examined the effects of fecal microbiota transplantation (FMT) on azoxymethane (AOM)-induced colorectal tumors in obese mice. We divided the study subjects into the following five groups: high-fat diet (HFD), normal diet (ND), ND+exercise (Ex), HFD+FMT from ND-alone donor (HFD+FMT(ND alone)), and HFD+FMT from ND+Ex donor (HFD+FMT(ND+Ex)). The Ex group performed treadmill exercise for 15 weeks. Thereafter, fecal and colonic mucus samples were extracted for microbiome analysis. The deoxyribonucleic acid sample was collected from the feces and colonic mucosa, and V3-V4 amplicon sequencing analysis of the 16S rRNA gene was performed using MiSeq. The number of polyps was significantly lower in the ND (6.0 ± 1.6) and ND+Ex (1.8 ± 1.3) groups than in the HFD group (11.4 ± 1.5). The ND+Ex group had significantly fewer polyps than the ND group. The HFD+FMT(ND alone) (5.2 ± 0.8) and HFD+FMT(ND+Ex) (2.8 ± 2.6) groups also had significantly fewer polyps than the HFD group. The IL-15 mRNA levels in the colonic tissues were significantly higher in the HFD+FMT(ND alone) group than in the ND group. Fecal ω-muricholic acid concentrations were significantly higher in the HFD+FMT(ND alone) group than in the ND group and in the HFD+FMT(ND+Ex) group than in the ND+Ex group. The ND, ND+Ex, HFD+FMT(ND alone), and HFD+FMT(ND+Ex) groups had a significantly higher abundance of Lacyobacillaceae than the HFD group. In the FMT group, Erysipelotrichaceae and Tannerellaceae were significantly less abundant. Compared with the HFD group, the ND, ND+Ex, HFD+FMT(ND alone), and HFD+FMT(ND+Ex) groups had a significantly higher abundance of Muribaculaceae and a significantly higher abundance of Lactobacillaceae and Rikenellaceae in common among the ND and ND+Ex groups. The common and significantly less common species were Bacteroidaceae in the FMT group and Lactobacillaceae and Rikenellaceae in the ND alone and ND+Ex groups. Bacteroidaceae and Lachnospiraceae were significantly less common in the FMT group. We found that FMT inhibited AOM-induced colorectal tumorigenesis in obese mice. Furthermore, the fecal concentrations of short-chain fatty acids, bile acids, microbiota, and mucosa-associated microbiota differed between the FMT and diet/EX groups, suggesting that the inhibitory effect of FMT on colorectal tumorigenesis may be due to mechanisms different from those of ND alone and ND+Ex.},
}

@article {pmid40430481,
year = {2025},
author = {Zhou, Q and Yang, C and Jia, M and Qu, Q and Peng, X and Ren, W and Li, G and Xie, Y and Li, B and Shi, X},
title = {Gut Microbiota-Targeted Intervention of Hyperlipidemia Using Monascus-Fermented Ginseng.},
journal = {Pharmaceuticals (Basel, Switzerland)},
volume = {18},
number = {5},
pages = {},
doi = {10.3390/ph18050661},
pmid = {40430481},
issn = {1424-8247},
support = {82174093//National Natural Science Foundation of China/ ; },
abstract = {Background/Objectives: Hyperlipidemia (HLP) encompasses a spectrum of poorly understood lipid metabolism disorders that are frequently overlooked or misdiagnosed, potentially leading to multiple complications. While the gut microbiota has been implicated in HLP pathogenesis, the causal relationships and molecular mechanisms remain elusive. This study aimed to investigate the therapeutic mechanisms of Monascus-fermented ginseng (MFG) on HLP through gut microbiota modulation and explore treatment potential via fecal microbiota transplantation (FMT). Methods: The MFG-modulated gut microbiota was transplanted into HLP mice. Systemic evaluations, including serum biochemical parameter detection, histopathological section analysis, 16S rRNA sequencing, and fecal metabolomics, were conducted to assess therapeutic efficacy and identify associated metabolic pathways. Results: FMT significantly improved lipid profiles, reduced body weight, and attenuated hepatic lipid accumulation in HLP mice. Mechanistically, it enhanced cholesterol excretion and fatty acid β-oxidation while suppressing lipogenic regulators, concurrently promoting primary-to-secondary bile acid conversion. Gut microbiota analysis revealed that the MFG intervention effectively normalized the Firmicutes/Bacteroidetes ratio and enriched beneficial microbiota. Conclusions: These findings demonstrate FMT's therapeutic value in HLP management and provide new perspectives on utilizing fermented herbal medicines for metabolic disorders via gut microbiota reprogramming.},
}

@article {pmid40428769,
year = {2025},
author = {Datkhayeva, Z and Iskakova, A and Mireeva, A and Seitaliyeva, A and Skakova, R and Kulniyazova, G and Shayakhmetova, A and Koshkimbayeva, G and Sarmuldayeva, C and Nurseitova, L and Koshenova, L and Imanbekova, G and Maxutova, D and Yerkenova, S and Shukirbayeva, A and Pernebekova, U and Dushimova, Z and Amirkhanova, A},
title = {The Multifactorial Pathogenesis of Endometriosis: A Narrative Review Integrating Hormonal, Immune, and Microbiome Aspects.},
journal = {Medicina (Kaunas, Lithuania)},
volume = {61},
number = {5},
pages = {},
doi = {10.3390/medicina61050811},
pmid = {40428769},
issn = {1648-9144},
mesh = {Humans ; *Endometriosis/physiopathology/microbiology/immunology/etiology ; Female ; *Gastrointestinal Microbiome/physiology/immunology ; Estrogens/metabolism ; Dysbiosis/complications ; Inflammation ; },
abstract = {Endometriosis (EM) is a common estrogen-dependent chronic inflammatory disorder affecting reproductive-aged women, yet its pathogenesis remains incompletely understood. Recent evidence suggests that the gut microbiota significantly influence immune responses, estrogen metabolism, and systemic inflammation, potentially contributing to EM progression. This narrative review explores the relationship between the gut microbiota and EM, emphasizing microbial dysbiosis, inflammation, estrogen regulation, and potential microbiome-targeted therapies. Studies published within the last 30 years were included, focusing on the microbiota composition, immune modulation, estrogen metabolism, and therapeutic interventions in EM. The selection criteria prioritized peer-reviewed articles, clinical trials, meta-analyses, and narrative reviews investigating the gut microbiota's role in EM pathophysiology and treatment. Microbial dysbiosis in EM is characterized by a reduced abundance of beneficial bacteria (Lactobacillus, Bifidobacterium, and Ruminococcaceae) and an increased prevalence of pro-inflammatory taxa (Escherichia/Shigella, Streptococcus, and Bacteroides). The gut microbiota modulate estrogen metabolism via the estrobolome, contributing to increased systemic estrogen levels and lesion proliferation. Additionally, lipopolysaccharides (LPS) from Gram-negative bacteria activate the TLR4/NF-κB signaling pathway, exacerbating inflammation and EM symptoms. The interaction between the gut microbiota, immune dysregulation, and estrogen metabolism suggests a critical role in EM pathogenesis. While microbiota-targeted interventions offer potential therapeutic benefits, further large-scale, multi-center studies are needed to validate microbial biomarkers and optimize microbiome-based therapies for EM. Integrating microbiome research with precision medicine may enhance the diagnostic accuracy and improve the EM treatment efficacy.},
}

Humans
*Endometriosis/physiopathology/microbiology/immunology/etiology
Female
*Gastrointestinal Microbiome/physiology/immunology
Estrogens/metabolism
Dysbiosis/complications
Inflammation

@article {pmid40427529,
year = {2025},
author = {Daude, N and Machado, I and Arce, L and Yang, J and Westaway, D},
title = {Microbial Composition, Disease Trajectory and Genetic Background in a Slow Onset Model of Frontotemporal Lobar Degeneration.},
journal = {Biomolecules},
volume = {15},
number = {5},
pages = {},
doi = {10.3390/biom15050636},
pmid = {40427529},
issn = {2218-273X},
support = {N/A//Nanostring AD panel/ ; N/A//SynAD ADRD/ ; 16308/CAPMC/CIHR/Canada ; 173286/CAPMC/CIHR/Canada ; NIF 21633//Canada Foundation for Innovation/ ; NIF 39588//Canada Foundation for Innovation/ ; N/A//Campus Alberta Neuroscience/ ; APRIIEP201600033//Alberta Prion Research Institute/ ; N/A//Hope for Tomorrow/ ; },
mesh = {Animals ; Mice ; Mice, Transgenic ; Disease Models, Animal ; tau Proteins/metabolism/genetics ; *Frontotemporal Lobar Degeneration/genetics/microbiology/pathology/metabolism ; Mice, Inbred C57BL ; *Gastrointestinal Microbiome/genetics ; Genetic Background ; Humans ; Male ; },
abstract = {Slow-onset neurodegenerative disease in a low-expresser 2N4R P301L transgenic (Tg) mouse model is marked by neuroinflammation and by differing patterns of CNS deposition and accumulation of tau conformers, with such heterogeneities present even within inbred backgrounds. Gut microbial genotypes were notably divergent within C57BL6/Tac or 129SvEv/Tac congenic (Cg) sublines of TgTau[P301L] mice, and these sublines differed when challenged with antibiotic treatment and fecal microbial transplantation. Whereas aged, transplanted Cg 129SvEv/Tac TgTau[P301L] mice had neuroanatomical deposition of tau resembling controls, transplanted Cg C57BL6/Tac TgTau[P301L] mice had different proportions of rostral versus caudal tau accumulation (p = 0.0001). These data indicate the potential for environmental influences on tau neuropathology in this model. Furthermore, Cg C57BL6/Tac TgTau[P301L] cohorts differed from 129SvEv/Tac counterparts by showing 28% versus 9% net intercurrent loss (p = 0.0027). While the origin of this phenomenon is not established, it offers a parallel to differing patterns of frailty observed in C57BL6 versus 129 SvEv Tg mice expressing the 695 amino acid isoform of human amyloid precursor protein. We infer that generalized responses to protein aggregation might account for similar reductions in viability even when expressing different human proteins in the same inbred strain background.},
}

Animals
Mice
Mice, Transgenic
Disease Models, Animal
tau Proteins/metabolism/genetics
*Frontotemporal Lobar Degeneration/genetics/microbiology/pathology/metabolism
Mice, Inbred C57BL
*Gastrointestinal Microbiome/genetics
Genetic Background
Humans
Male

@article {pmid40427424,
year = {2025},
author = {Golenia, A and Olejnik, P},
title = {The Role of Oxidative Stress in Ischaemic Stroke and the Influence of Gut Microbiota.},
journal = {Antioxidants (Basel, Switzerland)},
volume = {14},
number = {5},
pages = {},
doi = {10.3390/antiox14050542},
pmid = {40427424},
issn = {2076-3921},
abstract = {Ischaemic stroke is the most prevalent stroke subtype, accounting for 80-90% of all cases worldwide, and remains a leading cause of morbidity and mortality. Its pathophysiology involves complex molecular cascades, with oxidative stress playing a central role. During cerebral ischaemia, reduced blood flow deprives neurons of essential oxygen and nutrients, triggering excitotoxicity, mitochondrial dysfunction, and excessive production of reactive oxygen and nitrogen species (RONS). Not only do these species damage cellular components, but they also activate inflammatory pathways, particularly those mediated by the transcription factor nuclear factor kappa-B (NF-κB). The pro-inflammatory milieu intensifies neuronal damage, compromises blood-brain barrier integrity, and exacerbates reperfusion-induced damage. Recent findings highlight the importance of the gut microbiota in modulating stroke outcomes, primarily through metabolic and immunological interactions along the gut-brain axis. Dysbiosis, characterised by reduced microbial diversity and an imbalance between beneficial and harmful strains, has been linked to increased systemic inflammation, oxidative stress, and worse prognoses. Specific gut-derived metabolites, including short-chain fatty acids (SCFAs) and trimethylamine N-oxide (TMAO), appear to either mitigate or intensify neuronal injury. SCFAs may strengthen the blood-brain barrier and temper inflammatory responses, whereas elevated TMAO levels may increase thrombotic risk. This narrative review consolidates both experimental and clinical data demonstrating the central role of oxidative stress in ischaemic stroke pathophysiology and explores the gut microbiota's ability to modulate these damaging processes. Therapeutic strategies targeting oxidative pathways or rebalancing gut microbial composition, such as antioxidant supplementation, dietary modulation, probiotics, and faecal microbiota transplantation, present promising paradigms for stroke intervention. However, their widespread clinical implementation is hindered by a lack of large-scale, randomised trials. Future efforts should employ a multidisciplinary approach to elucidate the intricate mechanisms linking oxidative stress and gut dysbiosis to ischaemic stroke, thereby paving the way for novel, mechanism-based therapies for improved patient outcomes.},
}

@article {pmid40426604,
year = {2025},
author = {Xia, YM and Zhang, MX and Ma, XY and Tan, LL and Li, T and Wu, J and Li, MA and Zhao, WJ and Qiao, CM and Jia, XB and Shen, YQ and Cui, C},
title = {Intranasal Transplantation of Microbiota Derived from Parkinson's Disease Mice Induced Astrocyte Activation and Neurodegenerative Pathology from Nose to Brain.},
journal = {Brain sciences},
volume = {15},
number = {5},
pages = {},
doi = {10.3390/brainsci15050433},
pmid = {40426604},
issn = {2076-3425},
support = {82171429//National Natural Science Foundation of China/ ; },
abstract = {BACKGROUND: Parkinson's disease (PD) is characterized by early-onset olfactory dysfunction preceding motor symptoms, yet its mechanisms remain elusive. Based on the studies on microbiota-gut-brain axis, the microbiota-nose-brain axis might be involved in the pathogenesis of PD. However relative studies are rare.

METHODS: By consecutive 14-days intranasally transplanting bacteria, we established mice models exhibiting nasal microbiota dysbiosis (NMD), including animal group received intranasal drops of fecal bacterial suspension from normal mice (NB group) and animal group received intranasal drops of fecal bacterial suspension from PD mice (PB group), with animals that only received anesthesia used as the control group. Then we analyzed the nasal microbiota composition via 16S rRNA sequencing, evaluated the olfactory and motor functions through behavioral experiments, including buried food test, open field test, pole descent test, and traction test. The neuropathology in olfactory-related and PD-related brain regions, including olfactory bulb, pyriform cortex, hippocampus, substantia nigra and striatum, was also detected by western blotting, immunofluorescence and immunohistochemical experiments using the antibodies of NeuN, TH and GFAP.

RESULTS: 16S rRNA sequencing revealed that PB mice were primarily characterized by an increase in bacteria associated with inflammation and PD. Behavioral assessments revealed that mice with NMD demonstrated impairments in the buried food test and pole descent test, indicative of olfactory and motor dysfunction. By detecting NeuN and GFAP expression, we identified neuronal loss and astrocytes activation in olfactory-related brain regions and adjacent structures, including the olfactory bulb, pyriform cortex, hippocampus, substantia nigra and striatum of both NMD groups, which may contribute to the observed functional disorders. Notably, animals exposed to PD-derived bacteria exhibited more pronounced changes in nasal bacteria, with more severe neuropathology.

CONCLUSIONS: We present evidence supporting the microbiota-nose-brain axis, and the NMD-induced astrocyte activation and neurodegenerative pathology along the olfactory pathway may serve as a link between nose and brain.},
}

@article {pmid40424882,
year = {2025},
author = {Huang, YY and Qin, SM and Nguyen, MT and Chen, W and Si, XM and Huang, YQ and Zhang, HY},
title = {The protective effects of dietary resistant starch against post-antibiotic bone loss in meat ducks associated with the recovery of caecal microbiota dysbiosis.},
journal = {Poultry science},
volume = {104},
number = {8},
pages = {105238},
doi = {10.1016/j.psj.2025.105238},
pmid = {40424882},
issn = {1525-3171},
abstract = {Compromised bone quality increases the risk of fractures in domesticate birds, resulting in pain and altered behaviour. Although dietary resistant starch (RS) supplementation show promise for improving inferior bone mass, the diet-mediated gut microbiota alterations as a potential mechanism underlying RS positive roles in bone remains uncertain. With a post-antibiotic model and faecal microbiota transplantation (FMT), this study investigated the effects of a RS diet on antibiotic-induced bone loss and gut microbial composition in meat ducks. Ducklings were assigned to 4 treatments with 6 replicate pens until 21 d, including the control group (Ctrl, feeding a basal diet) and the RS-fed group, and post-antibiotic treatment following the gavage of phosphate-buffered saline (Post-anti-PBS) or faecal microbiota transplantation (Post-anti-FMT). The RS diet increased the proportion of Firmicutes, improved intestinal integrity, and reduced inflammation-induced bone resorption, all of which contributed to an increase in tibial bone volume (P < 0.05). Post-antibiotic treatment was found to reduce tibial quality by stimulating bone resorption and inhibiting bone formation, accompanied by gut microbiota dysbiosis, increased intestinal permeability (P = 0.059), and inflammatory flare compared to control birds. FMT from RS-fed ducks into the antibiotic-treated birds reversed bone loss by primarily blocking osteoclastic frequency and activity. Furthermore, FMT increased the ratio of Firmicutes to Bacteroidetes (P < 0.05) and suppressed the release of pro-osteoclastogenic cytokines such as tumour necrosis factor-α (P = 0.062) and interleukin-1β (P < 0.05) in the bone marrow. These results demonstrated the involvement of gut microbiota in improving bone quality of meat ducks by RS, and FMT of RS-fed birds corrected the imbalance of ceca microbiota and attenuated bone loss in meat ducks with enhanced bone resorption.},
}

@article {pmid40335381,
year = {2025},
author = {Vuyk, W and Bobholz, M and Emmen, I and Lail, A and Minor, N and Bhimalli, P and Eickhoff, JC and Ries, HJ and Machkovech, H and Wei, W and Weiler, A and Richardson, A and DePagter, C and VanSleet, G and Bhasin, M and Kamal, S and Wolf, S and Virdi, A and Bradley, T and Gifford, A and Benito, M and Shipe, A and Mohamed, R and Smith, J and Wilson, N and Friedrich, TC and O'Connor, DH and Garonzik-Wang, J},
title = {Longitudinal Assessment of Solid Organ Transplant Recipients With SARS-CoV-2 Infection.},
journal = {Transplantation proceedings},
volume = {57},
number = {5},
pages = {922-930},
doi = {10.1016/j.transproceed.2025.04.004},
pmid = {40335381},
issn = {1873-2623},
mesh = {Humans ; *COVID-19/diagnosis/virology/epidemiology/immunology ; Middle Aged ; *SARS-CoV-2/genetics/isolation & purification ; Male ; *Organ Transplantation/adverse effects ; *Immunocompromised Host ; Female ; Virus Shedding ; *Transplant Recipients ; Prospective Studies ; Adult ; RNA, Viral ; Longitudinal Studies ; Viral Load ; Aged ; Feces/virology ; },
abstract = {BACKGROUND: Compared with immunocompetent individuals, those who are immunocompromised, including solid organ transplant (SOT) recipients, have higher SARS-CoV-2-related morbidity and mortality. We determined the duration of SARS-CoV-2 RNA positivity to evaluate viral persistence in SOT recipients.

METHODS: This study prospectively followed SOT recipients who recently tested positive for SARS-CoV-2. The duration of viral RNA shedding in nasal swabs and stool samples was tracked, and viral genome sequencing was performed where possible. Persistent infection was defined as a positive nucleic acid amplification test (NAAT) for SARS-CoV-2 at 28 days or later after initial infection. This duration was chosen based on the U.S. Centers for Disease Control and Prevention (CDC) recommendation that immunocompromised individuals isolate for at least 20 days [1], compared with 10 days for non-immunocompromised individuals.

RESULTS: Of 30 SOT recipients, 12 (40%) had positive SARS-CoV-2 RNA in nasal swabs or stool (cycle threshold [Ct] < 40) at 28 or more days after the first positive SARS-CoV-2 test. Immunocompromised (IC) subject 015 had high viral loads (Ct < 30) at 28 days, with continued detection for 54 days.

CONCLUSIONS: In 12 of 30 SOT subjects, SARS-CoV-2 RNA was detected at or beyond 28 days post-detection (dpd), despite vaccination and antibody and/or antiviral treatment in most participants. Three subjects tested positive for SARS-CoV-2 RNA past 50 dpd. Viral persistence in the setting of host immune suppression, coupled with exposure to antiviral treatments, raises concern about the selection of unusual viral variants.},
}

Humans
*COVID-19/diagnosis/virology/epidemiology/immunology
Middle Aged
*SARS-CoV-2/genetics/isolation & purification
Male
*Organ Transplantation/adverse effects
*Immunocompromised Host
Female
Virus Shedding
*Transplant Recipients
Prospective Studies
Adult
RNA, Viral
Longitudinal Studies
Viral Load
Aged
Feces/virology

@article {pmid40422666,
year = {2025},
author = {Gaspar, BS and Roşu, OA and Enache, RM and Manciulea Profir, M and Pavelescu, LA and Creţoiu, SM},
title = {Gut Mycobiome: Latest Findings and Current Knowledge Regarding Its Significance in Human Health and Disease.},
journal = {Journal of fungi (Basel, Switzerland)},
volume = {11},
number = {5},
pages = {},
doi = {10.3390/jof11050333},
pmid = {40422666},
issn = {2309-608X},
abstract = {The gut mycobiome, the fungal component of the gut microbiota, plays a crucial role in health and disease. Although fungi represent a small fraction of the gut ecosystem, they influence immune responses, gut homeostasis, and disease progression. The mycobiome's composition varies with age, diet, and host factors, and its imbalance has been linked to conditions such as inflammatory bowel disease (IBD) and metabolic disorders. Advances in sequencing have expanded our understanding of gut fungi, but challenges remain due to methodological limitations and high variability between individuals. Emerging therapeutic strategies, including antifungals, probiotics, fecal microbiota transplantation, and dietary interventions, show promise but require further study. This review highlights recent discoveries on the gut mycobiome, its interactions with bacteria, its role in disease, and potential clinical applications. A deeper understanding of fungal contributions to gut health will help develop targeted microbiome-based therapies.},
}

@article {pmid40421334,
year = {2025},
author = {Ponce Alencastro, JA and Salinas Lucero, DA and Solis, RP and Herrera Giron, CG and Estrella López, AS and Anda Suárez, PX},
title = {Molecular Mechanisms and Emerging Precision Therapeutics in the Gut Microbiota-Cardiovascular Axis.},
journal = {Cureus},
volume = {17},
number = {4},
pages = {e83022},
pmid = {40421334},
issn = {2168-8184},
abstract = {A microbiome in the gut plays a significant role in cardiovascular health and disease. Dysbiosis is an imbalance in the gut microbiome, leading to multiple cardiovascular diseases (CVD) such as atherosclerosis, hypertension, and heart failure. Gut microbe-derived metabolites such as trimethylamine-N-oxide (TMAO) and short-chain fatty acids (SCFAs) are important mediators of the gut-heart axis. Evaluation of the relationship between the gut microbiome and host biomarkers with CVD requires the integration of metagenomics and metabolomics with meta-omics approaches. The literature review found that microbes and metabolic signatures are associated with the risk and progression of CVD. The development of precision therapeutic approaches for targeting gut microbiota includes preventing adverse microbial effects using probiotics, prebiotics, and the drug-as-bug approach to inhibit harmful metabolites of microbiomes, and fecal microbiota transplantation (FMT). However, the implication and practice of these findings in clinical settings face challenges due to the heterogeneity of study designs, difficulty in the determination of causality, and the impact of confounding factors such as diet, medication, and potential inter-individual gut microbiome variability. Future researchers are recommended to conduct longitudinal studies to further establish both gut microbiome associations with CVD and develop successful precision therapeutics approaches based on the microbiome for the treatment of CVD.},
}

@article {pmid40420583,
year = {2025},
author = {He, X and Luthuli, S and Wen, Q and Wang, C and Ding, J and Cui, B and Zhang, F},
title = {Washed microbiota transplantation for ribotype 027 Clostridioides difficile infection in a pregnant woman with two-year follow-up: a case report.},
journal = {Journal of biomedical research},
volume = {},
number = {},
pages = {1-4},
doi = {10.7555/JBR.39.20250063},
pmid = {40420583},
issn = {1674-8301},
abstract = {Clostridioides difficile (C. difficile) is one of the major causes of nosocomial infections. The pregnant women, who were considered at low risk for C. difficile infection (CDI), have attracted attention with increasing reports. Oral vancomycin, the only first-line treatment for the pregnant women infected with C. difficile, came with the problem of increasing strains resistance that was associated with decreased efficacy. Fecal microbiota transplantation (FMT) is recommended for severe, fulminant and recurrent CDI, while it is avoided in the pregnant women due to safety concerns. We reported a pregnant woman case with primary ribotype 027 CDI, who got a successful outcome with washed microbiota transplantation (WMT), an improved FMT, via enema. The specific strain of ribotype 027 was related to severe outcomes but was not reported in the pregnant women. The follow-up lasted two years, the patient's diarrhea was fully alleviated without recurrence. The baby had normal growth and development and no adverse events were recorded in both of them. This case provides evidence for the efficacy and safety of WMT in the pregnant women infected with C. difficile, indicating that WMT via enema may be a strategy for this population in treating CDI.},
}

@article {pmid40419682,
year = {2025},
author = {Nishinarita, Y and Miyoshi, J and Kuronuma, S and Wada, H and Oguri, N and Hibi, N and Takeuchi, O and Akimoto, Y and Lee, STM and Matsuura, M and Kobayashi, T and Hibi, T and Hisamatsu, T},
title = {Characteristic gene expression profile of intestinal mucosa early in life promotes bacterial colonization leading to healthy development of the intestinal environment.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {18437},
pmid = {40419682},
issn = {2045-2322},
support = {19K23977//Japan Society for the Promotion of Science/ ; 21K07900//Japan Society for the Promotion of Science/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/genetics ; Mice ; *Intestinal Mucosa/microbiology/metabolism ; Fecal Microbiota Transplantation ; *Bacteria/genetics/growth & development/classification ; Germ-Free Life ; *Transcriptome ; Male ; Gene Expression Profiling ; Female ; Feces/microbiology ; Mice, Inbred C57BL ; },
abstract = {The gut microbiome early in life plays a crucial role in development of the host and affects health throughout life. The definition of a healthy microbiome early in life has not been established, and the underlying mechanism of how a young host selects appropriate microbes for colonization remains unclear. Understanding the mechanism may provide insights into novel preventive and therapeutic strategies by correcting dysbiosis early in life. We employed germ-free mice early in life (4 weeks of age) and later in life (10 weeks of age) for fecal microbiota transfer (FMT) from specific pathogen-free mice. We performed age-unmatched FMT between recipients early in life and donors early or later in life, in addition to common age-matched FMT. Age-matched FMT resulted in significantly different bacterial compositions between recipients early vs. later in life. When the gut microbiome from donors early or later in life was transferred to recipients early in life, bacterial compositions of recipients from donors later in life were similar to those of recipients from donors early in life. This finding suggests that the host early in life has mechanisms to select microbes appropriate for age from the exposed microbiome. We hypothesized that the age-specific intestinal environment promotes age-appropriate intestinal microbiome colonization and examined gene expression in the intestinal mucosa of germ-free mice. We observed that gene expression profiles were different between early vs. later in life. Correlation analysis demonstrated that genera Lachnospiraceae NK4A136 group and Roseburia were positively correlated to genes expressed predominantly early in life, but negatively with genes expressed predominantly later in life. We confirmed that the relative abundance of these genera was significantly higher in specific pathogen-free mice early in life compared with mice later in life. The characteristic gene expression of the intestinal mucosa early in life might play roles in selecting specific bacteria in the intestinal microbiome early in life.},
}

Animals
*Gastrointestinal Microbiome/genetics
Mice
*Intestinal Mucosa/microbiology/metabolism
Fecal Microbiota Transplantation
*Bacteria/genetics/growth & development/classification
Germ-Free Life
*Transcriptome
Male
Gene Expression Profiling
Female
Feces/microbiology
Mice, Inbred C57BL

@article {pmid40419041,
year = {2025},
author = {Chen, L and Zhao, S and Chen, Q and Luo, P and Li, X and Song, Y and Pan, S and Wu, Q and Zhang, Y and Shen, X and Chen, Y},
title = {Poria cocos polysaccharides ameliorate AOM/DSS-induced colorectal cancer in mice by remodeling intestinal microbiota composition and enhancing intestinal barrier function.},
journal = {International journal of biological macromolecules},
volume = {},
number = {},
pages = {144477},
doi = {10.1016/j.ijbiomac.2025.144477},
pmid = {40419041},
issn = {1879-0003},
abstract = {Colorectal cancer (CRC) remains a leading cause of cancer-related mortality, necessitating the development of novel therapeutic strategies. Poria cocos polysaccharides (PCP), bioactive components of the traditional medicinal fungus Poria cocos, exhibit significant anticancer potential. This study investigates the protective effects of PCP against azoxymethane/dextran sulfate sodium (AOM/DSS)-induced CRC in mice, with a focus on its impact on intestinal microbiota composition, intestinal barrier integrity, and inflammatory responses. PCP treatment significantly reduced tumor incidence, tumor size, and tumor burden while improving histopathological features and inhibiting Ki67-positive cell proliferation. Mechanistically, PCP enhanced intestinal barrier function by restoring tight junction proteins (E-cadherin, ZO-1, Claudin-3) and mucin secretion (MUC2), thereby reducing intestinal permeability and systemic lipopolysaccharide (LPS) levels. Furthermore, PCP exhibited potent anti-inflammatory effects by downregulating pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) and upregulating the anti-inflammatory cytokine IL-10. 16S rRNA sequencing results revealed that PCP modulated the intestinal microbiota, decreasing pathogenic bacteria such as Helicobacter and Eisenbergiella while promoting beneficial taxa including Limosilactobacillus, Paraprevotella, and Muribaculum. Fecal microbiota transplantation (FMT) further confirmed the microbiota-mediated protective effects of PCP, as FMT from PCP-treated donors significantly suppressed tumorigenesis, restored intestinal barrier integrity, and alleviated inflammation in CRC mice. Additionally, PCP demonstrated a favorable safety profile, with no adverse effects on major organs. These findings highlight PCP as promising natural agents for CRC prevention and therapy, acting through modulation of the intestinal microbiota, enhancement of intestinal barrier function, and suppression of inflammation.},
}

@article {pmid40415934,
year = {2025},
author = {Liu, L and Zhao, W and Zhang, H and Shang, Y and Huang, W and Cheng, Q},
title = {Relationship between pediatric asthma and respiratory microbiota, intestinal microbiota: a narrative review.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1550783},
pmid = {40415934},
issn = {1664-302X},
abstract = {Pediatric asthma is a common chronic airway inflammatory disease that begins in childhood and its impact persists throughout all age stages of patients. With the continuous progress of detection technologies, numerous studies have firmly demonstrated that gut microbiota and respiratory microbiota are closely related to the occurrence and development of asthma, and related research is increasing day by day. This article elaborates in detail on the characteristics, composition of normal gut microbiota and lung microbiota at different ages and in different sites, as well as the connection of the gut-lung axis. Subsequently, it deeply analyzes various factors influencing microbiota colonization, including host factor, delivery mode, maternal dietary and infant feeding patterns, environmental microbial exposure and pollutants, and the use of antibiotics in early life. These factors are highly likely to play a crucial role in the onset process and disease progression of asthma. Research shows that obvious changes have occurred in the respiratory and gut microbiota of asthma patients, and these microbiomes exhibit different characteristics according to the phenotypes and endotypes of asthma. Finally, the article summarizes the microbiota-related treatment approaches for asthma carried out in recent years, including the application of probiotics, nutritional interventions, and fecal microbiota transplantation. These treatment modalities are expected to become new directions for future asthma treatment and bring new hope for solving the problem of childhood asthma.},
}

@article {pmid40415928,
year = {2025},
author = {Karimianghadim, R and Satokari, R and Yeo, S and Arkkila, P and Kao, D and Pakpour, S},
title = {Prolonged effect of antibiotic therapy on the gut microbiota composition, functionality, and antibiotic resistance genes' profiles in healthy stool donors.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1589704},
pmid = {40415928},
issn = {1664-302X},
abstract = {INTRODUCTION: Fecal microbiota transplantation (FMT) is highly effective in preventing Clostridioides difficile recurrence by restoring gut microbiota composition and function. However, the impact of recent antibiotic use, a key exclusion criterion for stool donors, on gut microbiota recovery is poorly understood.

METHODS: We investigated microbial recovery dynamics following antibiotic use in three long-term stool donors from Canada and Finland. Using longitudinal stool sampling, metagenomic sequencing, and qPCR, we assessed changes in bacterial diversity, community composition, microbial functions, the gut phageome, and the risk of transmitting antibiotic-resistant genes (ARGs).

RESULTS: Antibiotics caused lasting disruption to bacterial communities, significantly reducing important taxa like Bifidobacterium bifidum, Blautia wexlerae, Akkermansia muciniphila, Eubacterium sp. CAG 180, and Eubacterium hallii, with effects persisting for months. Functional analyses revealed alterations in housekeeping genes critical for energy production and biosynthesis, with no direct links to key health-related pathways. Antibiotics also disrupted viral populations, decreasing diversity and increasing crAssphage abundance, reflecting disrupted host-bacteriophage dynamics. No significant increase in clinically important ARGs was detected.

DISCUSSION: These findings highlight the unpredictable and complex recovery of gut microbiota post-antibiotics. Individualized suspension periods in donor programs, guided by metagenomic analyses, are recommended to optimize FMT outcomes in various indications by considering antibiotic spectrum, duration, and host-specific factors.},
}

@article {pmid40414934,
year = {2025},
author = {Jan, A and Bayle, P and Mohellibi, N and Lemoine, C and Pepke, F and Béguet-Crespel, F and Jouanin, I and Tremblay-Franco, M and Laroche, B and Serror, P and Rigottier-Gois, L},
title = {A consortium of seven commensal bacteria promotes gut microbiota recovery and strengthens ecological barrier against vancomycin-resistant enterococci.},
journal = {Microbiome},
volume = {13},
number = {1},
pages = {129},
pmid = {40414934},
issn = {2049-2618},
support = {COOPERATE project (2021-2022)//Poc'UP program of SATT Paris-Saclay/ ; COOPERATE project (2021-2022)//Poc'UP program of SATT Paris-Saclay/ ; COOPERATE project (2021-2022)//Poc'UP program of SATT Paris-Saclay/ ; COOPERATE project (2021-2022)//Poc'UP program of SATT Paris-Saclay/ ; COOPERATE project (2021-2022)//Poc'UP program of SATT Paris-Saclay/ ; COOPERATE project (2021-2022)//Poc'UP program of SATT Paris-Saclay/ ; COOPERATE project (2021-2022)//Poc'UP program of SATT Paris-Saclay/ ; COOPERATE project (2021-2022)//Poc'UP program of SATT Paris-Saclay/ ; COOPERATE project (2021-2022)//Poc'UP program of SATT Paris-Saclay/ ; COOPERATE project (2021-2022)//Poc'UP program of SATT Paris-Saclay/ ; PhD scholarship AJ (2020-2023)//INRAE Metaprogram HOLOFLUX and doctoral school ABIES at University Paris-Saclay/ ; Travel grants from Graduate schools Life sciences and Health (LSH) and Biosphera from University Paris-Saclay//France 2030 program "ANR-11-IDEX-0003"/ ; REMOVE project (2018-2019)//INRAE MICA division/ ; REMOVE project (2018-2019)//INRAE MICA division/ ; REMOVE project (2018-2019)//INRAE MICA division/ ; REMOVE project (2018-2019)//INRAE MICA division/ ; REMOVE project (2018-2019)//INRAE MICA division/ ; Key action MIND (2017)//INRAE Metaprogram MEM/ ; Key action MIND (2017)//INRAE Metaprogram MEM/ ; Key action MIND (2017)//INRAE Metaprogram MEM/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome ; *Vancomycin-Resistant Enterococci/growth & development ; Mice ; Symbiosis ; Dysbiosis/microbiology/chemically induced ; Anti-Bacterial Agents ; *Gram-Positive Bacterial Infections/microbiology ; Feces/microbiology ; *Bacteria/classification/genetics/isolation & purification ; Mice, Inbred C57BL ; },
abstract = {BACKGROUND: Vancomycin-resistant enterococci (VRE) often originate from the gastrointestinal tract, where their proliferation precedes dissemination into the bloodstream, and can lead to systemic infection. Uncovering the actors and mechanisms reducing the intestinal colonisation by VRE is essential to control infection. We aimed to identify commensal bacteria that interfere with VRE gut colonisation or act as an ecological barrier.

RESULTS: We performed a 3-week longitudinal analysis of the gut microbiota composition and VRE carriage levels during microbiota recovery in mice colonised with VRE after antibiotic-induced dysbiosis. By combining biological data and mathematical modelling, we identified 15 molecular species (OTUs) that negatively correlated with VRE overgrowth. Six strains representative of these OTUs were collected, cultivated and used in mixture with a seventh strain (Mix7) in two different mouse lines challenged with VRE. Of the seven strains, three belonged to Lachnospiraceae, one to Muribaculaceae, one to Ruminococcaceae and two to Lactobacillaceae. We found that Mix7 led to a better recovery of the gut microbiota composition and reduced VRE carriage. Differences in the effect of Mix7 were observed between responder and non-responder mice. These differences were associated with variations in the composition of the initial microbiota and during recovery and represent potential biomarkers for predicting response to Mix7. In a mouse model of alternative stable state of dysbiosis, response to Mix7 was associated with higher concentrations of short-chain fatty acids (acetate, propionate, butyrate) and a range of metabolites including bile acids, reflecting the recovery of the microbiota back to initial state. Furthermore, Muribaculum intestinale strain was required to obtain the Mix7 effect on VRE reduction in vivo, but the presence of at least one of the other six strains was needed. None of the supernatant of the seven strains, alone or in combination, inhibited VRE growth in vitro. Interestingly, five strains belong to species shared among humans and mice, and the other two have human functional equivalents.

CONCLUSIONS: An innovative approach based on mathematical modelling of the microbiota composition permitted to identify a mixture of commensal bacterial strains, which improves the ecological barrier effect against VRE. The mechanisms are dependent on the recovery and initial composition of the microbiota. Ultimately, this work will enable a move towards a personalised medicine by targeting predisposed patients presenting a risk of infection, such as neutropenic or bone-marrow transplant patients, and likely to respond to supplementation with commensal strains, providing new live biotherapeutic products and biomarkers to predict response to supplementation. Video Abstract.},
}

Animals
*Gastrointestinal Microbiome
*Vancomycin-Resistant Enterococci/growth & development
Mice
Symbiosis
Dysbiosis/microbiology/chemically induced
Anti-Bacterial Agents
*Gram-Positive Bacterial Infections/microbiology
Feces/microbiology
*Bacteria/classification/genetics/isolation & purification
Mice, Inbred C57BL

@article {pmid40414635,
year = {2025},
author = {Kumar, R and Kumar, R},
title = {Intestinal dysbiosis leads to the reduction in neurochemical production in Parkinson's disease (PD).},
journal = {International review of neurobiology},
volume = {180},
number = {},
pages = {25-56},
doi = {10.1016/bs.irn.2025.03.004},
pmid = {40414635},
issn = {2162-5514},
mesh = {Humans ; *Dysbiosis/metabolism/therapy ; *Parkinson Disease/metabolism/therapy/physiopathology/microbiology ; *Gastrointestinal Microbiome/physiology ; Animals ; },
abstract = {Parkinson's Disease (PD) is a neurodegenerative disorder characterized by motor and non-motor symptoms, with emerging research suggesting a critical link between intestinal dysbiosis and PD progression. This review explores the pathophysiological mechanisms underlying PD, such as alpha-synuclein aggregation, mitochondrial dysfunction, neuroinflammation, and oxidative stress, while focusing on the impact of gut dysbiosis on intestinal barrier function and its role in reduced neurochemical production. The clinical features of PD, including dopamine, serotonin, and GABA deficiencies, are examined, with a focus on how dysbiosis contributes to neurotransmitter depletion. Current treatments of PD, such as levodopa and dopamine agonists, are discussed alongside gut health therapies such as probiotics, prebiotics, and Fecal Microbiota Transplantation (FMT). Future therapeutic directions, including synbiotics, engineered microbes, phage therapy, and the integration of machine learning (ML) and artificial intelligence (AI), are explored. The chapter also considers preventive strategies, such as lifestyle adjustments and early gut health monitoring using modern diagnostic tools and biosensors. Furthermore, a strong need for continued research into the gut-brain axis (GBA) to develop more effective, gut-targeted therapies for managing PD is discussed.},
}

Humans
*Dysbiosis/metabolism/therapy
*Parkinson Disease/metabolism/therapy/physiopathology/microbiology
*Gastrointestinal Microbiome/physiology
Animals

@article {pmid40414634,
year = {2025},
author = {Singh, S and Saini, V and Jha, HC},
title = {The role of secondary genomes in neurodevelopment and co-evolutionary dynamics.},
journal = {International review of neurobiology},
volume = {180},
number = {},
pages = {245-297},
doi = {10.1016/bs.irn.2025.03.008},
pmid = {40414634},
issn = {2162-5514},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Neurodevelopmental Disorders/genetics/microbiology ; *Biological Evolution ; Animals ; *Brain/growth & development ; },
abstract = {This chapter examines how human biology and microbial "secondary genomes" have co-evolved to shape neurodevelopment through the gut-brain axis. Microbial communities generate metabolites that cross blood-brain and placental barriers, influencing synaptogenesis, immune responses, and neural circuit formation. Simultaneously, Human Accelerated Regions (HARs) and Endogenous Retroviruses (ERVs) modulate gene expression and immune pathways, determining which microbes thrive in the gut and impacting brain maturation. These factors converge to form a dynamic host-microbe dialogue with significant consequences for neurodevelopmental disorders (NDD), including autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder (ADHD), and schizophrenia. Building on evolutionary perspectives, the chapter elucidates how genetic and immune mechanisms orchestrate beneficial and pathological host-microbe interactions in early brain development. It then explores therapeutic strategies, such as probiotics, prebiotics, fecal microbiota transplantation, and CRISPR-driven microbial engineering, targeting gut dysbiosis to mitigate or prevent neurodevelopmental dysfunctions. Furthermore, innovative organ-on-chip models reveal mechanistic insights under physiologically relevant conditions, offering a translational bridge between in vitro experiments and clinical applications. As the field continues to evolve, this work underscores the translational potential of manipulating the microbiome to optimize neurological outcomes. It enriches our understanding of the intricate evolutionary interplay between host genomes and the microbial world.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Neurodevelopmental Disorders/genetics/microbiology
*Biological Evolution
Animals
*Brain/growth & development

@article {pmid40414573,
year = {2025},
author = {Yu, F and Ji, JL and Wang, Y and Liu, YD and Lian, YM and Wang, MZ and Cai, ZX},
title = {Anti-epileptic and Gut-protective Effects of Trioctanoin and the Critical Role of Gut Microbiota in a Mouse Model of Epilepsy.},
journal = {Brain research bulletin},
volume = {},
number = {},
pages = {111401},
doi = {10.1016/j.brainresbull.2025.111401},
pmid = {40414573},
issn = {1873-2747},
abstract = {Gut microbiota structure and function affect metabolism, gut health, and behavioral responses and are regulated by dietary factors. Recent research suggests the association of the gut-brain axis with epilepsy pathogenesis, thus offering potential new therapeutic targets. This study evaluated the anti-epileptic effect of trioctanoin and explored the potential role of the gut microbiota in a chronic pentylentetrazol (PTZ)-induced seizure mouse model. Behavioral assessments, electroencephalogram monitoring, immunofluorescence staining, neurotransmitter detection, gut microbiota sequencing, intestinal barrier function tests, and Fecal Microbiota Transplantation (FMT) were performed to systematically study the anti-epileptic effects of trioctanoin and the potential role of microbiota. Trioctanoin significantly restored glial cell proliferation to normal levels in chronic PTZ mice. Moreover, trioctanoin reduced elevated glutamate levels in the hippocampus of PTZ mice and improved gut microbiota imbalance and gut health by restoring the abundance of Dubosiella and Faecalibaculum genera, upregulating tight junction protein expression in the colon, and decreasing elevated levels of the inflammatory markers. Antibiotics(Abx) pre-treatment abolished the anticonvulsant protective effect of Trioctanoin. Although the FMT experiment did not transfer the anticonvulsant protection to the Abx+PTZ group mice, the results suggest that FMT still partially restored the gut microbiota imbalance in the chronic PTZ-induced epilepsy mouse model. These results provide new insights into dietary and gut microbiota-based therapeutic strategies for epilepsy.},
}

@article {pmid40413728,
year = {2025},
author = {Kousgaard, SJ and Dall, SM and Albertsen, M and Nielsen, HL and Thorlacius-Ussing, O},
title = {Fecal microbiota transplantation from a healthy pouch donor for chronic pouchitis: a proof-of-concept study.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2510464},
doi = {10.1080/19490976.2025.2510464},
pmid = {40413728},
issn = {1949-0984},
mesh = {Humans ; *Pouchitis/therapy/microbiology ; *Fecal Microbiota Transplantation/adverse effects/methods ; Male ; Female ; Adult ; Middle Aged ; Feces/microbiology ; Quality of Life ; Chronic Disease/therapy ; Gastrointestinal Microbiome ; Proof of Concept Study ; Treatment Outcome ; Tissue Donors ; Denmark ; },
abstract = {Chronic pouchitis is a common complication after ileal pouch-anal anastomosis (IPAA) with limited treatment options. In this case series, we aimed to investigate clinical and microbiome changes, as well as adverse events, associated with using fecal microbiota transplantation (FMT) from a donor with a normal functioning IPAA to induce remission in patients with chronic pouchitis. Methods The study was a case-series including a 4-week intervention period and 12-month follow-up. Patients with chronic pouchitis who met the inclusion criteria were recruited from the Department of Gastrointestinal Surgery at Aalborg University Hospital, Denmark. Participants received FMT derived from a donor with a normal functioning IPAA. Treatment was administered by enema daily for two weeks, then every other day for two more weeks. Disease severity and quality of life (QoL) were accessed at baseline and 30-day follow-up. Clinical remission was defined as Pouchitis Disease Activity Index (PDAI) <7. Fecal samples from participants, healthy donors, and the IPAA donor were analyzed using shotgun metagenomic sequencing. Results Three patients with chronic pouchitis were included and completed the treatment protocol and follow-up visits. At the 30-day follow-up, all participants achieved clinical remission with reduced endoscopic inflammation. The median total PDAI score decreased from 8 (range 10-8) at baseline to 6 (range 6-5) at 30 days. Two participants reported improved QoL, while one reported no change. Few mild, self-limited adverse events were reported by all participants during treatment, with no serious events. Principal component analysis of fecal samples distinguished two clusters: healthy donors and the IPAA donor, with participant samples forming a separate cluster Conclusion We observed that all participants achieved clinical remission with reduced endoscopic inflammation following a 4-week FMT intervention. Adverse events were mild and self-limited. Metagenomic analysis revealed distinct microbiome clusters between IPAA donor and recipients, both of which differed from those of healthy donors.},
}

Humans
*Pouchitis/therapy/microbiology
*Fecal Microbiota Transplantation/adverse effects/methods
Male
Female
Adult
Middle Aged
Feces/microbiology
Quality of Life
Chronic Disease/therapy
Gastrointestinal Microbiome
Proof of Concept Study
Treatment Outcome
Tissue Donors
Denmark

@article {pmid40413726,
year = {2025},
author = {Zhang, DY and Li, D and Chen, SJ and Zhang, LJ and Zhu, XL and Chen, FD and Chen, C and Wang, Q and Du, Y and Xiong, JX and Huang, SM and Zhang, XD and Lv, YT and Zeng, F and Chen, RX and Huang, X and Mao, F and Zhou, S and Yao, Q and Huang, Y and Chen, R and Mo, Y and Xie, Y and Jiang, YH and Chen, Z and Mo, CY and Chen, JJ and Bai, FH},
title = {Bacteroides uniformis-generated hexadecanedioic acid ameliorates metabolic-associated fatty liver disease.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2508433},
doi = {10.1080/19490976.2025.2508433},
pmid = {40413726},
issn = {1949-0984},
mesh = {Humans ; Gastrointestinal Microbiome ; Animals ; *Bacteroides/metabolism/genetics ; Mice ; Male ; Female ; Middle Aged ; Feces/microbiology ; Liver/metabolism ; *Fatty Liver/microbiology/metabolism ; Fecal Microbiota Transplantation ; Prospective Studies ; Adult ; Metabolomics ; Mice, Inbred C57BL ; },
abstract = {Gut microbiota exerts a pivotal influence on the development of Metabolic Associated Fatty Liver Disease (MAFLD), although the specific contributions of individual bacterial strains and their metabolites remain poorly defined. We conducted stool shotgun metagenomic sequencing and plasma untargeted metabolomics in a large prospective cohort comprising 120 MAFLD patients and 120 matched healthy controls. The mechanisms and microbial-derived metabolites involved in MAFLD were further investigated through multi-omics analyses in vitro and in vivo. Distinct differences were identified in both the microbial community structure and metabolomic profiles between MAFLD patients and healthy controls. Bacteroides uniformis (B. uniformis) was the most significantly depleted species in MAFLD and negatively correlated with hepatic steatosis and BMI. MAFLD was characterized by marked disruptions in fatty acid and amino acid metabolism. Combined analysis of metabolomic and metagenomic data achieved high diagnostic accuracy for MAFLD and hepatic steatosis severity (AUC = 0.93). Transplantation of fecal microbiota from MAFLD subjects into ABX mice led to the onset of MAFLD-like symptoms, whereas B. uniformis administration alleviate disease progression by inhibiting intestinal fat absorption, FFA from eWAT influx into liver via the gut-liver axis, and IRE1α-XBP1s-mediated flipogenesis and ferroptosis, as confirmed by hepatic transcriptomic and proteomic analyses. Hexadecanedioic acid (HDA), potentially identified as a key metabolite produced by B. uniformis, ameliorated MAFLD symptoms. Mechanistically, B. uniformis-derived HDA also inhibited fat absorption and transported, and entered the liver via the portal vein to suppress IRE1α-XBP1s-mediated flipogenesis and ferroptosis. B. uniformis and its potential putative metabolite HDA may contribute to MAFLD progression modulation, through regulation of the IRE1α-XBP1s axis. This study provides new insights into the gut-liver axis in MAFLD and offers promising therapeutic targets based on specific microbes and their metabolites.},
}

Humans
Gastrointestinal Microbiome
Animals
*Bacteroides/metabolism/genetics
Mice
Male
Female
Middle Aged
Feces/microbiology
Liver/metabolism
*Fatty Liver/microbiology/metabolism
Fecal Microbiota Transplantation
Prospective Studies
Adult
Metabolomics
Mice, Inbred C57BL

@article {pmid40412060,
year = {2025},
author = {Lin, Z and Wang, J and Luo, H and Huang, L and Pan, Z and Yang, S and Zhong, C and Shan, NC and Ye, Z and Tan, H and Yang, X and Zhang, B and Huang, C and Zhang, H},
title = {Changdiqing decoction (CDQD) ameliorates colitis via suppressing inflammatory macrophage activation and modulating gut microbiota.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {143},
number = {},
pages = {156856},
doi = {10.1016/j.phymed.2025.156856},
pmid = {40412060},
issn = {1618-095X},
abstract = {BACKGROUND: Ulcerative colitis (UC) is a non-specific inflammatory bowel disease. Unlike any single form of cell death reported previously, macrophage PANoptosis, a unique programmed cell death characterized by inflammation and necrosis, plays a crucial role in the pathogenesis of colitis. Changdiqing Decoction (CDQD), an empirical hospital prescription enema, has been used to treat UC for decades. This study aimed to investigate the multi-target anti-colitic effects of CDQD by examining its impact on intestinal homeostasis and its anti-inflammatory properties.

METHODS: A dextran sulfate sodium (DSS)-induced mouse model of acute colitis was employed. Interferon-gamma (IFN-γ) and KPT-330 were used to induce macrophage PANoptosis. Ultra-high-performance liquid chromatography-high-resolution mass spectrometry (UHPLCHRMS) was utilized to identify the chemical constituents of CDQD. Multi-omics analysis and fecal microbiota transplantation (FMT) were used to explore the therapeutic targets and gut microbiota alterations induced by CDQD.

RESULTS: CDQD treatment significantly alleviated colitis symptoms in mice, with a dose-dependent therapeutic effect. The decoction mitigated PANoptosis in colon tissues and bone marrow-derived macrophages (BMDMs). 16S rRNA sequencing analysis and metabonomics revealed that CDQD administration significantly altered the gut microbiota composition and metabolite profiles. Notably, CDQD-modulated gut microbiota exhibited anti-colitic effects through FMT. Integrated transcriptomics and network pharmacology analysis revealed that CDQD significantly downregulated the PI3K/Akt signaling pathway in colitis. This finding was further validated using the inhibitors LY294002 and MK2206.

CONCLUSIONS: CDQD alleviates colitis by suppressing inflammatory macrophage activation and modulating the gut microbiota. Our research provides a novel traditional Chinese medicine strategy for the treatment of UC via enema administration.},
}

@article {pmid40411710,
year = {2025},
author = {Chen, L and Chen, C and Bai, Y and Li, C and Wei, C and Wei, R and Luo, R and Li, R and Ma, Q and Geng, Y},
title = {Evaluation of the effects of different formulations of protectants on the preservation of the microbiota in fecal microbiota transplantation.},
journal = {International microbiology : the official journal of the Spanish Society for Microbiology},
volume = {},
number = {},
pages = {},
pmid = {40411710},
issn = {1618-1905},
abstract = {BACKGROUND: With the increasing indications for fecal microbiota transplantation for the treatment of diseases, there is a growing demand for the preparation of frozen or lyophilized fecal microbiota products that are viable and can stably colonize the recipient. The addition of protective agents plays an important role in the preparation. However, there has been no systematic evaluation of the protective agents used in fecal microbiota sample transplantation preparation for transplantation.

METHODS: We were used the donor bacterial flora containing 10 different formulations of protective agents were frozen, lyophilized, and stored. Plate counting, CCK8 assay, flow cytometry after LIVE/DEAD staining, and fluorescence intensity were used to assess viable bacteria in vitro. In addition, the donor bacterial flora samples containing different formulations protective agents were transplanted into antibiotic-treated SPF mice, with 3 mice in each group and a total of 5 groups. Fecal samples were collected for metagenomic sequencing to observe the colonization of the bacterial flora in the recipient mice.

RESULTS: The preliminary screening results showed that the survival rate of bacteria in the 5% trehalose (T) groups, and 5% sucrose, 5% inulin, and 1% cysteine hydrochloride (SI) groups was slightly higher than that in the other groups. SI groups tended to be more protective against anaerobes than T groups. The donor gut microbiota containing the SI groups protective agent exhibited the best colonization of the recipient mice. The protective effects of different formulations of protective agents on the colonized probiotic strains and the metabolic function of the bacterial flora in recipient mice were found to be species specific.

CONCLUSIONS: SI groups can not only better protect the activity of anaerobic bacteria in the intestine, but also effectively promote the effective colonization of donor intestinal bacteria in the recipient mice, and the effect of frozen storage method is less, and can be used at the same time as frozen and freeze-dried preparation. It can be used as a reference for the selection of protective agents in the preparation of fecal microbiota transplantation samples.},
}

@article {pmid39581509,
year = {2025},
author = {Chen, S and Wen, Q and Zhang, F},
title = {An Unusual Cause of Diarrhea and Hematochezia.},
journal = {Gastroenterology},
volume = {168},
number = {6},
pages = {1066-1070},
doi = {10.1053/j.gastro.2024.11.007},
pmid = {39581509},
issn = {1528-0012},
}

@article {pmid40411629,
year = {2025},
author = {Nezhadi, J and Lahouty, M and Rezaee, MA and Fadaee, M},
title = {Clostridium difficile as a potent trigger of colorectal carcinogenesis.},
journal = {Discover oncology},
volume = {16},
number = {1},
pages = {910},
pmid = {40411629},
issn = {2730-6011},
abstract = {Clostridium difficile, traditionally recognized as a cause of antibiotic-associated colitis, has emerged as a potential oncogenic factor in colorectal cancer (CRC). This article explores the mechanisms by which C. difficile toxins, TcdA and TcdB, contribute to CRC pathogenesis through epithelial barrier disruption, DNA damage, and chronic inflammation via NF-κB and STAT3 activation. Dysbiosis further exacerbates tumorigenesis by altering microbial metabolites. Understanding these interactions highlights potential therapeutic strategies, including toxin-neutralizing antibodies, fecal microbiota transplantation, and anti-inflammatory interventions, to mitigate CRC risk associated with C. difficile.},
}

@article {pmid40410854,
year = {2025},
author = {Fan, L and Chen, J and Zhang, Q and Ren, J and Chen, Y and Yang, J and Wang, L and Guo, Z and Bu, P and Zhu, B and Zhao, Y and Wang, Y and Liu, X and Wang, W and Chen, Z and Gao, Q and Zheng, L and Cai, J},
title = {Fecal microbiota transplantation for hypertension: an exploratory, multicenter, randomized, blinded, placebo-controlled trial.},
journal = {Microbiome},
volume = {13},
number = {1},
pages = {133},
pmid = {40410854},
issn = {2049-2618},
support = {82300564//National Natural Science Foundation of China/ ; 81630014//National Natural Science Foundation of China/ ; BRWEP2024W012060100//Beijing Research Ward Excellence Program/ ; BRWEP2024W012060100//Beijing Research Ward Excellence Program/ ; 2024ZD0526804//National Science and Technology Major Project for the Prevention and Treatment of Cancer, Cardiovascular and Cerebrovascular Diseases, Respiratory Diseases and Metabolic Diseases/ ; 2024ZD0526800//National Science and Technology Major Project for the Prevention and Treatment of Cancer, Cardiovascular and Cerebrovascular Diseases, Respiratory Diseases and Metabolic Diseases/ ; BRWEP2024W012060105//Beijing Research Ward Excellence Program，BRWEP/ ; CIFMS, 2021-I2M-1-007//CAMS Innovation Fund for Medical Sciences/ ; 81825002//National Outstanding Youth Science Fund Project of National Natural Science Foundation of China/ ; BJJWZYJH01201910023029//Beijing Outstanding Young Scientist Program/ ; Z231100004623009//Beijing Municipal Science & Technology Commission/ ; CI2021A00920//Key project of Science and Technology Innovation Project of China Academy of Chinese Medical Sciences/ ; ZLRK202511//Beijing Hospitals Authority Clinical medicine Development of special funding support/ ; L248105//Beijing Natural Science Foundation/ ; },
mesh = {Humans ; *Fecal Microbiota Transplantation/methods/adverse effects ; Male ; Female ; *Hypertension/therapy/microbiology ; Adult ; *Gastrointestinal Microbiome/physiology ; Middle Aged ; Feces/microbiology ; Blood Pressure ; China ; Treatment Outcome ; },
abstract = {BACKGROUND: On the basis of the contribution of the gut microbiota to hypertension development, a novel strategy involving fecal microbiota transplantation (FMT) has been proposed to treat hypertension, but its efficacy has not been investigated in the clinic.

METHODS: In a randomized, blinded, placebo-controlled clinical trial (2021/03-2021/12, ClinicalTrials.gov, NCT04406129), hypertensive patients were recruited from seven centers in China, and received FMT or placebo capsules orally at three visits. The patients were randomized at a 1:1 ratio in blocks of four and stratified by center by an independent statistician. The intention-to-treat principle was implemented, as all randomized participants who received at least one intervention were included. The primary outcome was the decrease in office systolic blood pressure (SBP) from baseline to the day 30 visit. Adverse events (AEs) were recorded through the 3-month follow-up to assess safety measures. Alterations in BP, the fecal microbiome, and the plasma metabolome were assessed via exploratory analyses.

RESULTS: This study included 124 patients (mean age 43 years, 73.4% men) who received FMT (n = 63) or placebo (n = 61) capsules. The numbers of participants who experienced AEs (13 (20.6%) vs. 9 (14.8%), p = 0.39) and the primary outcome (6.28 (11.83) vs. 5.77 (10.06) mmHg, p = 0.62) were comparable between the groups. The FMT group presented a decrease in SBP after 1 week of FMT, with a between-arm difference of - 4.34 (95% CI, - 8.1 to - 0.58; p = 0.024) mmHg, but this difference did not persist even after repeated intervention. After FMT, shifts in microbial richness and structure were identified and the abundance of the phyla Firmicutes and Bacteroidetes was altered. Decreases in the abundances of Eggerthella lenta, Erysipelatoclostridium ramosum, Anaerostipes hadrus, Gemella haemolysans, and Streptococcus vestibularis and increases in the abundances of Parabacteroides merdae, Prevotella copri, Bacteroides galacturonicus, Eubacterium sp. CAG 180, Desulfovibrio piger, Megamonas hypermegale, Collinsella stercoris, Coprococcus catus, and Allisonella histaminiformans were identified and correlated with office SBP. Those species were also correlated with responding and inversely office SBP-associated metabolites including tyrosine, glutamine, aspartate, phenylalanine, methionine, serine, sarcosine, and/or asparagine.

CONCLUSIONS: Safety but unsustainable BP reduction was observed in the first trial of the effects of FMT on hypertension. Additional intervention studies on specific microbes with metabolite-targeting and BP-modulating features are needed. Video Abstract.},
}

Humans
*Fecal Microbiota Transplantation/methods/adverse effects
Male
Female
*Hypertension/therapy/microbiology
Adult
*Gastrointestinal Microbiome/physiology
Middle Aged
Feces/microbiology
Blood Pressure
China
Treatment Outcome

@article {pmid40409520,
year = {2025},
author = {Sen, U},
title = {Gut microbiota and well-being: a comprehensive summary of the special issue.},
journal = {Pharmacological research},
volume = {},
number = {},
pages = {107791},
doi = {10.1016/j.phrs.2025.107791},
pmid = {40409520},
issn = {1096-1186},
abstract = {Gut microbes play an immense role in digesting ingested food, providing nutrients to the host, and producing several bioactive metabolites that not only help maintain health but can also elicit disease during dysbiotic conditions. The bioactive compounds derived from gut microbiota metabolites include trimethylamine-N-oxide (TMAO), uremic toxins, short chain fatty acids (SCFAs), phytoestrogens, anthocyanins, bile acids, lipopolysaccharide - to name a few. Once these compounds enter the host cells, tissues, and organs they can cause diseases such as epigenetic, metabolic, neurodegenerative, psychiatric, cardiovascular, hypertension, respiratory, gastrointestinal, kidney, bone, cancer, and others. Regulating healthy gut microbiota thus provides a potential option for the prevention, reversal, or even treatment of these diseases. Towards this end, various interventional strategies are postulated in this field of emerged and rapidly expanding health research arena that includes fecal microbiota transplantation, prebiotics, and probiotics, and to introduce the concept that correcting gut dysbiosis can ameliorate disease symptoms, thus offering a new approach towards dysbiosis-related disease mitigation and treatment. In the special issue of Pharmacological Research titled "Gut Microbiota and Well-Being," several outstanding research findings and review articles are published, covering a broad spectrum of topics related to the influence of gut microbiota on health and disease. This editorial summarizes each of these contributions, prioritizing research findings before discussing the review articles. The summaries are restructured abstracts of relevant articles focusing on major findings or thematic topics.},
}

@article {pmid40409481,
year = {2025},
author = {Chen, E and Zhou, W},
title = {Immunotherapy in Microsatellite-Stable Colorectal Cancer: Strategies to Overcome Resistance.},
journal = {Critical reviews in oncology/hematology},
volume = {},
number = {},
pages = {104775},
doi = {10.1016/j.critrevonc.2025.104775},
pmid = {40409481},
issn = {1879-0461},
abstract = {Colorectal cancer (CRC) is among the foremost causes of cancer-related mortality worldwide; however, individuals with microsatellite-stable (MSS) disease-who constitute most CRC diagnoses-derive limited benefit from existing immunotherapeutic approaches. Here, we outline emerging methods designed to address the inherent resistance of MSS CRC to immune checkpoint inhibitors (ICIs). Recent findings emphasize how the immunosuppressive tumor microenvironment (TME) in MSS CRC, marked by diminished immunogenicity and high levels of regulatory T cells and myeloid-derived suppressor cells, restricts effective antitumor immune activity. Combination regimens that merge ICIs with chemotherapy, anti-angiogenic agents, or targeted blockade of pathways such as TGF-β and VEGF have shown encouraging early outcomes, including enhanced antigen presentation and T-cell penetration. Novel immunomodulatory platforms-such as epigenetic modifiers, oncolytic viruses, and engineered probiotic vaccines-are under assessment to further reprogram the TME and boost therapeutic efficacy. Concurrently, progress in adoptive cell therapies (for example, chimeric antigen receptor (CAR) T cells) and the development of cancer vaccines targeting tumor-associated and neoantigens promise to extend immune control over MSS CRC. In parallel, improving patient selection through predictive biomarkers-from circulating tumor DNA (ctDNA) to gene expression signatures and specific molecular subtypes-could refine individualized treatment strategies. Finally, interventions that alter the gut microbiome, including probiotics and fecal transplantation, serve as complementary tools to strengthen ICI responses. Taken together, these insights and combined treatment strategies lay the foundation for more successful immunotherapeutic interventions in MSS CRC, ultimately aiming to provide sustained clinical benefits to a broader spectrum of patients.},
}

@article {pmid40406094,
year = {2025},
author = {Eslami, M and Naderian, R and Bahar, A and Babaeizad, A and Rezanavaz Gheshlagh, S and Oksenych, V and Tahmasebi, H},
title = {Microbiota as diagnostic biomarkers: advancing early cancer detection and personalized therapeutic approaches through microbiome profiling.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1559480},
pmid = {40406094},
issn = {1664-3224},
mesh = {Humans ; Precision Medicine/methods ; *Gastrointestinal Microbiome/immunology ; *Neoplasms/diagnosis/therapy/microbiology ; *Early Detection of Cancer/methods ; *Biomarkers, Tumor ; Animals ; Fecal Microbiota Transplantation ; },
abstract = {The important function of microbiota as therapeutic modulators and diagnostic biomarkers in cancer has been shown by recent developments in microbiome research. The intricate interplay between the gut microbiota and the development of cancer, especially in colorectal and breast cancers, emphasizes how microbial profiling may be used for precision treatment and early diagnosis. Important microbial signatures, including Bacteroides fragilis and Fusobacterium nucleatum, have been linked to the development and progression of cancer, providing important information on the processes behind carcinogenesis. Additionally, the influence of microbiota on the effectiveness of treatments such as immunotherapy and chemotherapy highlights its dual function in improving treatment outcomes and reducing side effects. To optimize treatment results, strategies including dietary changes and fecal microbiota transplantation (FMT) are being investigated. Despite these developments, there are still issues, such as individual variations in microbial composition, a lack of standardized procedures, and the requirement for reliable biomarkers. Integrating microbiome-based diagnostics with conventional approaches, such as liquid biopsies and machine learning algorithms, could revolutionize cancer detection and management. This review provides an overview of the current understanding of the host-microbe immunological axis and discusses emerging therapeutic strategies centered on microbiota modulation to support human health. Further research is essential to overcome existing challenges and fully realize the promise of microbiota-driven innovations in oncology.},
}

Humans
Precision Medicine/methods
*Gastrointestinal Microbiome/immunology
*Neoplasms/diagnosis/therapy/microbiology
*Early Detection of Cancer/methods
*Biomarkers, Tumor
Animals
Fecal Microbiota Transplantation

@article {pmid40402463,
year = {2025},
author = {Li, L and Hu, M and Zhu, X and Huang, X and Chen, H},
title = {Microbiota Transplantation in Tumor Immunology Studies.},
journal = {Methods in molecular biology (Clifton, N.J.)},
volume = {2930},
number = {},
pages = {295-306},
pmid = {40402463},
issn = {1940-6029},
mesh = {*Neoplasms/immunology/therapy/microbiology/pathology ; *Fecal Microbiota Transplantation/methods ; *Gastrointestinal Microbiome/immunology ; Animals ; Humans ; Mice ; Feces/microbiology ; },
abstract = {This protocol outlines the standardized procedures for utilizing fecal microbiota transplantation (FMT) in tumor immunology studies. FMT, the process of transferring gut microbiota from a healthy donor to a recipient, has shown potential in modulating the immune response against tumors. This protocol details the selection criteria for donors and recipients, preparation and processing of fecal material, and the administration routes for transplantation. Additionally, it describes the pre- and posttransplantation monitoring of microbiota composition, immune parameters, and tumor progression. By following this protocol, researchers can systematically investigate the impact of microbiota on tumor growth and immune modulation, contributing to the development of microbiota-based therapeutic strategies in oncology.},
}

*Neoplasms/immunology/therapy/microbiology/pathology
*Fecal Microbiota Transplantation/methods
*Gastrointestinal Microbiome/immunology
Animals
Humans
Mice
Feces/microbiology

@article {pmid40401951,
year = {2025},
author = {Huang, J and Qiao, H and Li, Q and Zhang, Y and Zhang, C and Su, H and Sun, X},
title = {Osteopontin protects from ovalbumin-induced asthma by preserving the microbiome and the intestinal barrier function.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0038925},
doi = {10.1128/msystems.00389-25},
pmid = {40401951},
issn = {2379-5077},
abstract = {UNLABELLED: The gut and lung microbiota are associated with asthma. Osteopontin (OPN) is an important cytokine associated with several inflammatory diseases. The potential role of OPN in the asthma-associated microbiome remains poorly understood. Here, we investigated whether OPN could moderate asthma by affecting the gut and lung microbiota. Our results showed that compared with wild-type (WT) mice, Spp1[-/-] mice exhibited immune cell infiltration in the lung, OVA-specific IgG1, increased levels of Th2- and Th17-related inflammatory factors, and decreased levels of Th1-related inflammatory factors and forkhead box P3 (FOXP3) expression, resulting in a Th1/Th2 and Th17/Treg imbalance. In addition, gut structure was impaired, and expression of tight junction-related proteins was reduced in Spp1[-/-] mice, which disrupted gut barrier function. Importantly, OPN-deficient significantly aggravated gut and lung microbiota dysbiosis in OVA-induced asthmatic mice. The results of high-throughput 16S rRNA sequencing demonstrated that OPN-deficient mice showed a substantial reduction in beneficial gut and lung bacteria (Bacteroidetes, Lactobacillus, Allobaculum), and an OVA-induced increase in the abundance of bacteria associated with potentially pathogenic gut and lung (Epsilonbacteraeota, Helicobacter, Desulfovibrio, Oscillibacter)-associated bacteria was elevated in abundance. Allobaculum was negatively correlated with interleukin-4 and GATA-3 and was positively correlated with interferon gamma and FOXP3. Moreover, through fecal microbiota transplantation, we found that OVA-induced IgE and IgG1 levels were reduced in OPN-deficient asthmatic mice, Th1/Th2 and Th17/Treg balance was maintained, gut barrier function was improved, and microbiome changes in OPN-deficient mice were compensated for, with an elevated abundance of Allobaculum and reduced abundance of Desulfovibrio and Oscillibacter. We further discovered that OPN deficiency reduces FOXP3 expression and decreases Lactobacillus colonization through activation of the PD-1/PD-L1 pathway in the intestine and lung. The present study suggests that OPN may moderate OVA-induced asthma by modulating the gut and lung microbiota.

IMPORTANCE: Osteopontin deficiency exacerbated asthmatic airway inflammation, an effect associated with microbiota dysbiosis, impaired intestinal barrier function, and increased PD-1/PD-L1 expression and thus decreased Treg cell function. The study provides clinicians with new insights into asthma mechanisms and can also lead to new ideas for asthma treatment.},
}

@article {pmid40401932,
year = {2025},
author = {McMullen, BN and Chen See, J and Baker, S and Wright, JR and Anderson, SLC and Yochum, G and Koltun, W and Portolese, A and Jeganathan, NA and Lamendella, R},
title = {Metatranscriptomic analysis of colonic mucosal samples exploring the functional role of active microbial consortia in complicated diverticulitis.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0243124},
doi = {10.1128/spectrum.02431-24},
pmid = {40401932},
issn = {2165-0497},
abstract = {In this study, we investigated complicated diverticulitis, an inflammatory condition associated with abscesses, fistulas, intestinal obstructions, perforations, and primarily affects adults over the age of 60. Although the exact etiology remains unclear, the gut microbiome has been suggested as a contributing factor. Previous studies have used 16S rRNA gene analysis from patient fecal samples, which is limited to identifying the bacterial communities present. Herein, we employed shotgun metatranscriptomics on 40 patient-matched samples of diseased and adjacent normal colonic mucosal tissues from 20 patients with complicated diverticulitis to gain a more comprehensive understanding of active microbial taxa and gene expression patterns that may be involved in this disease state. Our findings revealed distinct beta diversity and a conglomerate of pathogenic microbiota in the diseased tissues, including Staphylococcus cohnii, Corynebacterium jeikeium, Kineococcus, Talaromyces rugulosus, Campylobacteraceae, and Ottowia, among others. The adjacent normal tissues were a stark contrast, harboring anti-inflammatory taxa such as Streptococcus salivarius and housekeeping genes and pathways such as the ABC-2 type transport system ATP-binding protein. These results align with previous amplicon sequencing studies and provide novel functional insights that may be crucial for understanding the etiology of complicated diverticulitis.IMPORTANCEComplicated diverticulitis is a virulent condition with no clear cause other than the association with colonic diverticulosis. We assessed the microbial gene expression in complicated diverticulitis patients using colonic tissue samples, revealing microbes in the diseased tissue known to exacerbate the diverticular condition and to live in extreme places, and microbes in patients' normal tissue known to maintain normal bodily functions. This functional information is therefore important for understanding what microbial taxa are present and what they are doing. It is possible clinicians could someday harness this information to more effectively treat complicated diverticulitis symptoms. For example, clinicians may suggest dietary changes and prescribe probiotics to increase beneficial bacteria. Clinicians may also prescribe targeted antibiotics or consider the emerging treatment option of fecal transplants in complicated diverticulitis patients. While not curing complicated diverticulitis, each potential treatment option mentioned addresses balancing out dysbiosis of the gut microbiome, therefore alleviating associated symptoms.},
}

@article {pmid40400677,
year = {2025},
author = {Men, J and Cui, C and Li, H and Li, Z and Zhang, Y and Liu, Z and Wang, Q and Liu, P and Zou, S and Yu, Z and Zhang, Y and Wu, S and Zhu, G and Wang, P and Huang, X},
title = {Cold water swimming reshapes gut microbiome to improve high-fat diet-induced obesity.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1589902},
pmid = {40400677},
issn = {1664-302X},
abstract = {Hypothermia and swimming have been shown to alleviate high-fat diet (HFD)-induced obesity, with effects linked to the gut microbiota (GM). However, whether the effects of cold water swimming (CWS) on GM can be effectively transferred through fecal microbiota transplantation (FMT) has not been investigated. This study established mice models of obesity, CWS and FMT to investigate the mechanism by which CWS reshapes GM to improve HFD-induced obesity. Additionally, we analyzed the relationship between obesity phenotypes, GM composition, gene expression and CWS. The study found that HFD induced obesity phenotypes and GM dysbiosis in mice, while CWS produced opposite effects. The FMT results confirmed that CWS effectively alleviated HFD-induced lipid accumulation, metabolic disorders, and chronic inflammatory responses, which are associated with increased GM diversity, enrichment of beneficial bacteria, and the repair of intestinal barrier damage. Furthermore, these beneficial effects can be effectively transferred via FMT. The evidence from this study suggests that GM plays a critical role in the anti-obesity effects of CWS, with intestinal barrier repair emerging as a potential therapeutic target. This also provides scientific evidence for the feasibility of FMT as a strategy to combat obesity.},
}

@article {pmid40399878,
year = {2025},
author = {Qian, S and Su, Z and Lin, J and Hou, Q and Wang, X and Li, Y and Wang, J and Huang, C and Wang, Z and Cubero, FJ and Wang, X and Liao, L},
title = {Inhibition of Farnesoid-x-receptor signaling during abdominal sepsis by dysbiosis exacerbates gut barrier dysfunction.},
journal = {Cell communication and signaling : CCS},
volume = {23},
number = {1},
pages = {236},
pmid = {40399878},
issn = {1478-811X},
support = {81971814//the National Natural Science Foundation of China/ ; 81971814//the National Natural Science Foundation of China/ ; 81971814//the National Natural Science Foundation of China/ ; 81971814//the National Natural Science Foundation of China/ ; 20192BAB205013//the Natural Science Foundation of Jiangxi Province/ ; 20192BAB205013//the Natural Science Foundation of Jiangxi Province/ ; 20192BAB205013//the Natural Science Foundation of Jiangxi Province/ ; PWRd2020-06//Academic medicine leader's training Program in health systems of Pudong New Area/ ; PWYgf2021-03//Shanghai Pudong New Area Summit (emergency medicine and critical care) construction project/ ; 23Y11908300//Medical Innovation Research Special Project of Shanghai 2023 Science and Technology Innovation Action Plan/ ; 2020PJD050//Shanghai Pujiang Program/ ; },
mesh = {Animals ; *Receptors, Cytoplasmic and Nuclear/metabolism/agonists ; *Sepsis/metabolism/pathology/microbiology ; *Signal Transduction ; *Dysbiosis/metabolism/pathology ; Mice ; Myeloid Differentiation Factor 88/metabolism ; Fibroblast Growth Factors/metabolism ; Mice, Inbred C57BL ; Gastrointestinal Microbiome ; Male ; *Intestinal Mucosa/metabolism ; Liver/metabolism ; Bile Acids and Salts/metabolism ; },
abstract = {BACKGROUND AND AIMS: Bacterial translocation and intestinal dysbiosis due to gut barrier dysfunction are widely recognized as major causes of the initiation and development of intra-abdominal sepsis. Systemic bacterial translocation and hepatic activation of the myeloid differentiation primary response gene 88 (Myd88) can disturb bile acids (BAs) metabolism, further exacerbating intestinal dysbiosis. The farnesoid X receptor (FXR) and fibroblast growth factor (FGF) 15/19 are well known to be involved in the control of BAs synthesis and enterohepatic circulation. However, the influence of intestinal microbiota on intestinal Myd88 signaling, the FXR/FGF15 axis, as well as gut-liver crosstalk during sepsis remains unclear. The present study aims to decipher the role of intestinal Myd88 in abdominal sepsis, its impact on intestinal FXR signaling and FGF15-mediated gut-liver crosstalk.

METHODS: Expression levels of FXR and FGF15 in the liver and intestines, alongside assessments of gut barrier function, were evaluated in septic wild-type (WT) mice 24 h post-cecal ligation and puncture (CLP) surgery. Subsequently, the FXR agonist INT-747 was administered to explore the relationship between FXR activation and gut barrier function. Further investigations involved Myd88-deficient mice with specific deletion of Myd88 in intestinal epithelial cells (Myd88[△IEC]), subjected to CLP to examine the interplay among intestinal Myd88, FXR, gut barrier function, microbiota, and BA composition. Additionally, fecal microbiota transplantation (FMT) from septic mice to Myd88[△IEC] mice was conducted to study the impact of dysbiosis on intestinal Myd88 expression during sepsis, using floxed (Myd88[fl/fl]) mice as controls. Finally, the effects of the probiotic intervention on gut barrier function and sepsis outcomes in CLP mice were investigated.

RESULTS: Induction of sepsis via CLP led to hepatic cholestasis, suppressed FXR-FGF15 signaling, altered gut microbiota composition, and compromised gut barrier function. Administration of INT-747 increased intestinal FXR and FGF15 expression, strengthened gut barrier function, and enhanced barrier integrity. Interestingly, Myd88[△IEC] mice exhibited partial reversal of sepsis-induced changes in FXR signaling, BA metabolism, and intestinal function, suggesting enhanced FXR expression upon Myd88 knockdown. Moreover, FMT from septic mice activated intestinal Myd88, subsequently suppressing FXR-FGF15 signaling, exacerbating cholestasis, and ultimately compromising gut barrier function. Probiotic treatment during abdominal sepsis mitigated flora disturbances, reduced Myd88 activation in the intestinal epithelium, increased FXR expression, alleviated cholestasis, and consequently reduced barrier damage.

CONCLUSIONS: This study highlights the critical role of Myd88/FXR signaling in intestinal epithelial cells as a pivotal mediator of the detrimental effects induced by sepsis-related intestinal dysbiosis on barrier function and bile acid metabolism. In summary, disordered intestinal flora in septic mice specifically triggers intestinal epithelial Myd88 activation, inhibit the FXR-FGF15 axis, and then worsen intestinal barrier function impairment.},
}

Animals
*Receptors, Cytoplasmic and Nuclear/metabolism/agonists
*Sepsis/metabolism/pathology/microbiology
*Signal Transduction
*Dysbiosis/metabolism/pathology
Mice
Myeloid Differentiation Factor 88/metabolism
Fibroblast Growth Factors/metabolism
Mice, Inbred C57BL
Gastrointestinal Microbiome
Male
*Intestinal Mucosa/metabolism
Liver/metabolism
Bile Acids and Salts/metabolism

@article {pmid40339798,
year = {2025},
author = {Gîlcă-Blanariu, GE and Pakpour, S and Kao, D},
title = {More questions than answers? Predicting faecal microbiota transplantation outcomes for 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.2025.04.036},
pmid = {40339798},
issn = {1469-0691},
}

@article {pmid40398680,
year = {2025},
author = {Zhou, Y and Komnick, MR and Sepulveda, F and Liu, G and Nieves-Ortiz, E and Meador, K and Ndatabaye, O and Fatkhullina, A and Bozicevich, A and Juengel, B and Wu-Woods, NJ and Naydenkov, PM and Kent, J and Christiansen, N and Madariaga, ML and Witkowski, P and Ismagilov, RF and Esterházy, D},
title = {Inducible, but not constitutive, pancreatic REG/Reg isoforms are regulated by intestinal microbiota and pancreatic diseases.},
journal = {Mucosal immunology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.mucimm.2025.05.003},
pmid = {40398680},
issn = {1935-3456},
abstract = {The REG/Reg gene locus encodes a conserved family of potent antimicrobial but also pancreatitis-associated proteins. Here we investigated whether REG/Reg family members differ in their baseline expression levels and abilities to be regulated in the pancreas and gut upon perturbations. We found, in humans and mice, the pancreas and gut differed in REG/Reg isoform levels and preferences, with the duodenum most resembling the pancreas. Pancreatic acinar cells and intestinal enterocytes were the dominant REG producers. Intestinal symbiotic microbes regulated the expression of the same, select Reg members in gut and pancreas. These Reg members had the most STAT3-binding sites close to the transcription start sites and were partially IL-22 dependent. We thus categorized them as "inducible" and others as "constitutive". Indeed, in pancreatic ductal adenocarcinoma and pancreatitis models, only inducible Reg members were upregulated in the pancreas. While intestinal Reg expression remained unchanged upon pancreatic perturbation, pancreatitis altered the microbial composition of the duodenum and feces shortly after disease onset. Our study reveals differential usage and regulation of REG/Reg isoforms as a mechanism for tissue-specific innate immunity, highlights the intimate connection of pancreas and duodenum, and implies a gut-to-pancreas communication axis resulting in a coordinated Reg response.},
}

@article {pmid40398524,
year = {2025},
author = {He, X and Wei, X and He, Z and Yao, C and Nie, M and Ma, X and Chen, Q and Guo, DA},
title = {Biotransformation of artemisinin by human intestinal fungi and cytotoxicity against breast cancer cells of its metabolites.},
journal = {Phytochemistry},
volume = {},
number = {},
pages = {114551},
doi = {10.1016/j.phytochem.2025.114551},
pmid = {40398524},
issn = {1873-3700},
abstract = {Artemisinin widely exists in the Artemisia annua L. and is the front-line of antimalarial drugs. In this study, microbial transformation of artemisinin was performed based on seventeen human intestinal fungal species. Our findings revealed that isomerization and deoxygenation were the most prevalent metabolic pathways in fungi. Incubation of artemisinin with Rhizopus microspores (PT2906) and Candida boidinii (M7017B) afforded three new compounds (P3, P5 and P6) along with seven known metabolites which were elucidated by extensive spectroscopic data analysis. All metabolites were evaluated for their cytotoxicity against MCF-7 cells, and the results showed that 3β-hydroxydeoxyartemisinin (P5) suppressed the growth of MCF-7 cells better than artemisinin. In addition, ten artemisinin isomers were found in the feces of antibiotic-treated mice after M7017B transplantation, demonstrating that human intestinal fungi have the potential to participate in the in vivo intestinal transformation of artemisinin.},
}

@article {pmid40398303,
year = {2025},
author = {Xu, Y and Chen, K and Huang, Y and Yan, Y and Zhang, W and Tian, J and Zhang, D and Liu, M and Nie, Q},
title = {Fecal microbiota transplantation improves growth performance of chickens by increasing the intestinal Lactobacillus and glutamine.},
journal = {Poultry science},
volume = {104},
number = {8},
pages = {105243},
doi = {10.1016/j.psj.2025.105243},
pmid = {40398303},
issn = {1525-3171},
abstract = {Chicken meat is an essential source of high-quality animal protein, mainly derived from slow-growth chicken (SC) and fast-growth chicken (FC) breeds. Skeletal muscle is a highly adaptable tissue that is influenced by breed differences and the gut microbiome. Investigation whether remodeling the gut microbiota by fecal microbiota transplantation (FMT) improves chicken growth is an interesting question. We compared the gut microbial composition of eight breeds of SC (Xinghua chicken, Yangshan chicken, Zhongshan Salan chicken, Qingyuan Partridge chicken, Huiyang Bearded chicken and Huaixiang chicken) and FC (Xiaobai chicken and White rock chicken). Fecal microbiota from donor FC (Xiaobai chickens) with superior growth performance were transferred to SC (Xinghua chickens). The effects of FMT on growth performance, metabolic profile and gut microbiome of recipient chickens were evaluated. We found significant differences in gut microbial composition, with a higher abundance of Bacteroidetes in SC and a higher abundance of Firmicutes in FC. Xiaobai chickens with better growth performance and abundant Lactobacillus, and FMT significantly enhanced growth performance, the expression of mRNA (MYOG, MYF5, MYF6 and IGF1) related to breast and leg muscle development and improved the villus/crypt ratio in the jejunum. FMT altered the microbiota in the duodenum, jejunum, and ileum, increased Lactobacillus abundance, decreased the relative mRNA expression of the intestinal inflammatory factors (IL-1β, IL-6 and TNF-α), increased glutamine levels in the host, including in muscle tissues and intestinal contents, and Spearman correlation analysis indicated that the relative abundance of Lactobacillus was positively correlated with glutamine levels. Additionally, antibiotic treatment reduces glutamine levels in the intestines, blood, and muscle tissues of chickens. Glutamine can increase the expression of cyclinD1, cyclinD2, cyclinB2, MYOG, MYF5, MYF6 and IGF1 mRNA to promote chicken myoblasts proliferation and differentiation. This study found that the SC and FC gut microbes were significantly different, and the FC chicken gut microbes were able to reshape the FC gut microbiota through FMT, i.e., higher Lactobacillus, promoted chicken myoblasts proliferation and differentiation and growth performance by increasing glutamine levels.},
}

@article {pmid40395920,
year = {2025},
author = {Ishikawa, D and Zhang, X and Nagahara, A},
title = {Current Applications and Future Prospects of Fecal Microbiota Transplantation.},
journal = {Juntendo medical journal},
volume = {71},
number = {2},
pages = {68-75},
pmid = {40395920},
issn = {2759-7504},
abstract = {In recent years, the impact of gut microbiota on human health has gained increasing recognition, highlighting the potential benefits of regulating gut microbiota for patient care. Consequently, fecal microbiota transplantation (FMT) has emerged as a novel treatment for improving dysbiosis. It is necessary to summarize and discuss the current research and future development possibilities. This advanced microbial therapy restores the gut microbiome by introducing a diverse array of microorganisms from healthy donors, thereby correcting dysbiosis and re-establishing a fully functional ecosystem. Ongoing research on FMT is actively conducted in various fields worldwide. This study provides an overview of the progress of clinical research on the effects of FMT in gastrointestinal diseases, immune checkpoint inhibitors, allergic diseases, and central nervous system diseases, as well as the results of our ongoing clinical study on "FMT combined with antibiotics for ulcerative colitis."},
}

@article {pmid40395507,
year = {2025},
author = {Shabani, M and Ghoshehy, A and Mottaghi, AM and Chegini, Z and Kerami, A and Shariati, A and Taati Moghadam, M},
title = {The relationship between gut microbiome and human diseases: mechanisms, predisposing factors and potential intervention.},
journal = {Frontiers in cellular and infection microbiology},
volume = {15},
number = {},
pages = {1516010},
pmid = {40395507},
issn = {2235-2988},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Dysbiosis/microbiology ; Probiotics ; Prebiotics ; Metabolic Diseases/microbiology ; Fecal Microbiota Transplantation ; Gastrointestinal Diseases/microbiology ; Nervous System Diseases/microbiology ; Disease Susceptibility ; Diet ; Diabetes Mellitus, Type 2/microbiology ; },
abstract = {The complex interrelation of gut microbiota with human health underlines the profound influence this microbial ecosystem has on mechanisms of disease and wellness. The gut microbiome profoundly impacts various human diseases, encompassing gastrointestinal disorders, metabolic disorders, neurological disorders, and immune-related diseases. Gastrointestinal disorders are closely linked to microbial imbalances in the gut. Metabolic disorders, including obesity and type 2 diabetes, are influenced by the gut microbiota's role in energy regulation and glucose metabolism. Furthermore, the gut-brain axis highlights the correlation between gut microbiota and neurological conditions such as Alzheimer's and Parkinson's. Moreover, the gut microbiome assumes a pivotal function in regulating the immune system, whereby dysbiosis is implicated in developing immunological-related ailments, including allergies and autoimmune disorders. Predisposing factors, including diet, medicines, lifestyle, and environmental influences, are described as having an important role in the composition of the gut microbiome. By understanding these factors, we can get valuable insights into how to intervene to reduce the chances of a disease. Current interventions, including probiotics, prebiotics, fecal microbiota transplants, and lifestyle modification, show promise, but there are still challenges and unanswered questions in this evolving field that may lead to improvements. This review interrelates the complicated gut microbiome with various human diseases, mechanisms, predisposing factors, and potential interventions.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Dysbiosis/microbiology
Probiotics
Prebiotics
Metabolic Diseases/microbiology
Fecal Microbiota Transplantation
Gastrointestinal Diseases/microbiology
Nervous System Diseases/microbiology
Disease Susceptibility
Diet
Diabetes Mellitus, Type 2/microbiology

@article {pmid40394204,
year = {2025},
author = {Oliver, PJ and Civitelli, L and Hu, MT},
title = {The gut-brain axis in early Parkinson's disease: from prodrome to prevention.},
journal = {Journal of neurology},
volume = {272},
number = {6},
pages = {413},
pmid = {40394204},
issn = {1432-1459},
mesh = {Humans ; *Parkinson Disease/prevention & control/metabolism/microbiology/physiopathology ; *Gastrointestinal Microbiome/physiology ; alpha-Synuclein/metabolism ; *Prodromal Symptoms ; *Brain-Gut Axis/physiology ; *Brain/metabolism ; Dysbiosis ; Animals ; },
abstract = {Parkinson's disease is the second most common neurodegenerative disorder and fastest growing neurological condition worldwide, yet its etiology and progression remain poorly understood. This disorder is characterized pathologically by the prion-like spread of misfolded neuronal alpha-synuclein proteins in specific brain regions leading to Lewy body formation, neurodegeneration, and progressive neurological impairment. It is unclear what triggers Parkinson's and where α-synuclein protein aggregation begins, although proposed induction sites include the olfactory bulb and dorsal motor nucleus of the vagus nerve. Within the last 20 years, there has been increasing evidence that Parkinson's could be triggered by early microbiome changes and α-synuclein accumulation in the gastrointestinal system. Gut microbiota dysbiosis that alters gastrointestinal motility, permeability, and inflammation could enable prion-like spread of α-synuclein from the gut-to-brain via the enteric nervous system. Individuals with isolated rapid eye movement sleep behavior disorder have a high likelihood of developing Parkinson's and might represent a prodromal 'gut-first' subtype of the condition. The gut-first model of Parkinson's offers novel gut-based therapeutic avenues, such as anti-, pre-, and pro-biotic preparations and fecal microbiota transplants. Crucially, gut-based interventions offer an avenue to treat Parkinson's at early prodromal stages with the aim of mitigating evolution to clinically recognizable Parkinson's disease characterized by motor impairment.},
}

Humans
*Parkinson Disease/prevention & control/metabolism/microbiology/physiopathology
*Gastrointestinal Microbiome/physiology
alpha-Synuclein/metabolism
*Prodromal Symptoms
*Brain-Gut Axis/physiology
*Brain/metabolism
Dysbiosis
Animals

@article {pmid40300608,
year = {2025},
author = {Wirbel, J and Andermann, TM and Brooks, EF and Evans, L and Groth, A and Dvorak, M and Chakraborty, M and Palushaj, B and Reynolds, GZM and Porter, IE and Al Malki, M and Rezvani, A and Gooptu, M and Elmariah, H and Runaas, L and Fei, T and Martens, MJ and Bolaños-Meade, J and Hamadani, M and Holtan, S and Jenq, R and Peled, JU and Horowitz, MM and Poston, KL and Saber, W and Kean, LS and Perales, MA and Bhatt, AS},
title = {Accurate prediction of absolute prokaryotic abundance from DNA concentration.},
journal = {Cell reports methods},
volume = {5},
number = {5},
pages = {101030},
doi = {10.1016/j.crmeth.2025.101030},
pmid = {40300608},
issn = {2667-2375},
mesh = {Humans ; RNA, Ribosomal, 16S/genetics ; Feces/microbiology ; *DNA, Bacterial/genetics/analysis ; Machine Learning ; *Prokaryotic Cells ; Male ; Parkinson Disease/microbiology ; },
abstract = {Quantification of the absolute microbial abundance in a human stool sample is crucial for a comprehensive understanding of the microbial ecosystem, but this information is lost upon metagenomic sequencing. While several methods exist to measure absolute microbial abundance, they are technically challenging and costly, presenting an opportunity for machine learning. Here, we observe a strong correlation between DNA concentration and the absolute number of 16S ribosomal RNA copies as measured by digital droplet PCR in clinical stool samples from individuals undergoing hematopoietic cell transplantation (BMT CTN 1801). Based on this correlation and additional measurements, we trained an accurate yet simple machine learning model for the prediction of absolute prokaryotic load, which showed exceptional prediction accuracy on an external cohort that includes people living with Parkinson's disease and healthy controls. We propose that, with further validation, this model has the potential to enable accurate absolute abundance estimation based on readily available sample measurements.},
}

Humans
RNA, Ribosomal, 16S/genetics
Feces/microbiology
*DNA, Bacterial/genetics/analysis
Machine Learning
*Prokaryotic Cells
Male
Parkinson Disease/microbiology

@article {pmid40393939,
year = {2025},
author = {Zhang, X and He, Q and Zhang, C and Ji, Z and Yang, D and Wang, X and Liu, C and Zhang, C and Yuan, J and Xu, N and Chu, J},
title = {Gegen Qinlian Decoction protects kidney in diabetic rats by improving intestinal barrier and regulating intestinal microbiota.},
journal = {The Journal of pharmacy and pharmacology},
volume = {},
number = {},
pages = {},
doi = {10.1093/jpp/rgaf030},
pmid = {40393939},
issn = {2042-7158},
support = {82204707//National Natural Science Foundation of China/ ; },
abstract = {OBJECTIVES: To investigate the renoprotective effects of Gegen Qinlian Decoction (GQD) in Diabetes mellitus (DM) rats via the intestinal barrier and microbiota.

METHODS: GQD was analyzed by UPLC. STZ-induced DM rat models and antibiotic-induced sterile DM rat models were established, and fecal microbiota transplantation was performed in the latter. Renal function, oxidative stress, serum inflammatory factors, and pathological alterations were assessed. Intestinal cells and tight junction were observed by transmission electron microscopy. Inflammatory factors in the colon and tight junction protein expression were evaluated. The gut microbiota and its abundance were assessed by 16sRNA sequencing.

KEY FINDINGS: Four components were determined in the GQD, including puerarin, baicalin, berberine, and liquiritin. After GQD treatment, Scr and BUN were reduced, renal pathological changes were attenuated, intestinal cell swelling was reduced, intestinal tight junctions were improved, and GQD modulated the intestinal microbiota. Furthermore, a fecal bacterial solution containing GQD reduced renal lesions, improved intestinal tight junctions, and regulated intestinal microbiota in DM rats.

CONCLUSIONS: GQD regulated the intestinal microbiota of DM rats, reduced intestinal inflammation, and repaired the intestinal barrier, thus reducing the burden on the kidneys, and exerting a protective effect on the kidneys of DM rats.},
}

@article {pmid40393246,
year = {2025},
author = {Liu, X and Li, Y and Yuan, C and Zhao, Y and Zhou, L and Yan, Y and Ren, J and Liu, Q},
title = {Sophocarpine suppresses MAPK-mediated inflammation by restoring gut microbiota in colorectal cancer.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {143},
number = {},
pages = {156833},
doi = {10.1016/j.phymed.2025.156833},
pmid = {40393246},
issn = {1618-095X},
abstract = {BACKGROUND: Colorectal cancer (CRC), as one of the most common cancers globally, poses a significant challenge to public health due to its high incidence and mortality rates. This underscores the need for continuous exploration of new therapeutic targets and effective drugs. Sophocarpine (SC), a natural compound derived from traditional Chinese medicine, holds considerable therapeutic potential in the treatment of CRC, however, the relevant mechanisms remains unclear.

PURPOSE: This study aims to explore the anti-tumor effects of SC against CRC by modulating gut microbiota, and uncover potential mechanisms linking SC's therapeutic effects to gut microbiota regulation by analyzing the impact of SC on microbiota composition and CRC progression.

MATERIAL: This study explores the impact of SC on the gut microbiota in CRC by constructing subcutaneous xenograft tumors of CRC and integrating 16S rRNA sequencing and RNA transcriptomic sequencing. The fecal microbiota transplantation (FMT) mouse model was used to validate the biological function of SC in correcting gut microbiota dysbiosis to treat CRC. Subsequently, we conducted in vitro studies on the molecular mechanisms by which SC regulates the gut microbiota as an effective hallmark of CRC treatment, using lipopolysaccharide (LPS) to simulate an inflammatory gut microbiota environment and P38 MAPK knockdown cell line.

RESULTS: SC significantly inhibited CRC cell proliferation with IC50 values of 2.547±0.256 μM for HCT116 and 2.851±0.332 μM for LoVo cells. In vivo experiments demonstrated that SC effectively suppressed tumor growth in xenograft models. 16S rRNA sequencing revealed that SC modulated gut microbiota composition, particularly affecting Bacteroides and Alistipes populations. SC significantly reduced the levels of inflammatory factors and inhibited the MAPK signaling pathway, as evidenced by decreased p-JNK, p-p38 MAPK, and p-NF-κB p65 expression.

CONCLUSIONS: Current clinical practice still lacks effective therapeutic agents targeting CRC through gut microbiota modulation. This study presents the first evidence that SC, a natural compound, exhibits dual-action therapeutic efficacy against CRC progression by simultaneously modulating gut microbial composition and suppressing MAPK pathway-mediated inflammatory responses. These findings highlight SC's novel therapeutic potential as a promising microbiota-regulating candidate for CRC intervention, offering an innovative approach that bridges microbial ecology with cancer signaling pathways.},
}