@article {pmid40615512,
year = {2025},
author = {Ruan, S and Liu, J and Yuan, X and Ye, X and Zhang, Q},
title = {Aerobic exercise alleviates cognitive impairment in T2DM mice through gut microbiota.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {23917},
pmid = {40615512},
issn = {2045-2322},
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; *Cognitive Dysfunction/therapy/etiology/microbiology ; *Physical Conditioning, Animal ; *Diabetes Mellitus, Type 2/complications/microbiology ; Male ; Mice ; Mice, Inbred C57BL ; *Diabetes Mellitus, Experimental/complications/microbiology ; Fecal Microbiota Transplantation ; },
abstract = {The risk of cognitive impairment is markedly elevated in patients with type 2 diabetes mellitus (T2DM). While exercise has been shown to mitigate cognitive deficits associated with diabetes, the underlying mechanisms remain poorly understood. Recent studies suggest that exercise can modulate the composition of the gut microbiota, which, in turn, may influence the central nervous system via the microbiota-gut-brain axis. However, the specific role of gut microbiota in mediating exercise-induced improvements in cognitive function in T2DM remains unclear. In this study, we aimed to investigate whether exercise can alleviate cognitive impairment in T2DM mice by modulating the intestinal microbiota, and to elucidate the mechanisms underlying this effect. This study was conducted using male C57BL/6J mice. Mice fed a normal diet were assigned to the non-diabetic control group (NC), while those fed a high-fat diet were intraperitoneally injected with streptozotocin (STZ) and subsequently divided into the diabetic control group (DM), an exercise group (DM-EXE), and a fecal microbiota transplantation group (DM-FMT). The DM-EXE group underwent treadmill exercise for 8 weeks. During this period, the DM-FMT group received fecal microbiota transplants from the DM-EXE group for 2 consecutive days per week. Following the 8-week intervention, stool samples were collected for 16S rDNA high-throughput sequencing. The fear conditioning test was performed to assess cognitive function. Intestinal mucosa samples were collected to evaluate the expression of intestinal tight junction proteins. Additionally, the expression levels of synaptic proteins, glucose transporters, neurotrophic factors, and inflammatory markers were measured in the hippocampus. Our findings demonstrate that T2DM mice exhibit impaired cognitive function and significant alterations in their gut microbiota compared to non-diabetic controls. Exercise partially reversed these changes in the intestinal microbiota and alleviated cognitive impairment in T2DM mice. Additionally, transplantation of intestinal microbiota from exercised mice improved cognitive function in T2DM mice. Aerobic exercise may mitigate cognitive impairment in T2DM mice by modulating the gut microbiota. The underlying mechanisms appear to involve enhanced neural synaptic plasticity, reduced neuroinflammation, and improved neuronal glucose metabolism.},
}

Animals
*Gastrointestinal Microbiome/physiology
*Cognitive Dysfunction/therapy/etiology/microbiology
*Physical Conditioning, Animal
*Diabetes Mellitus, Type 2/complications/microbiology
Male
Mice
Mice, Inbred C57BL
*Diabetes Mellitus, Experimental/complications/microbiology
Fecal Microbiota Transplantation

@article {pmid40615289,
year = {2025},
author = {Chen, H},
title = {Mapping the clinical trial landscape of gut microbiota modulation in neurodegenerative diseases.},
journal = {European journal of internal medicine},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ejim.2025.06.032},
pmid = {40615289},
issn = {1879-0828},
}

@article {pmid40614920,
year = {2025},
author = {Yadav, S and Raj, RG},
title = {Parkinson's disease and the gut microbiota connection: unveiling dysbiosis and exploring therapeutic horizons.},
journal = {Neuroscience},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.neuroscience.2025.07.003},
pmid = {40614920},
issn = {1873-7544},
abstract = {Parkinson's disease (PD) is a progressive neurodegenerative disorder marked by dopaminergic neuronal loss, α-synuclein aggregation, and sustained neuroinflammation. Emerging evidence supports the gut-brain-microbiota axis as a pivotal player in the disease's pathogenesis. Dysbiosis, disruptions in the gut microbial composition, has been consistently observed in individuals with PD, with notable reductions in beneficial, short-chain fatty acid-producing bacteria and elevations in pro-inflammatory microbial species. These alterations contribute to increased intestinal permeability, systemic inflammation, and heightened neuroinflammatory responses that may drive α-synuclein misfolding and dopaminergic degeneration. In addition, microbial metabolites, including lipopolysaccharides and amyloid proteins such as curli, may promote neurodegeneration via immune and molecular mimicry pathways. Recent advances highlight the bidirectional influence of the microbiota-gut-brain axis on PD symptoms, ranging from motor deficits to non-motor features like constipation, depression, and cognitive decline. Several microbiota-modulating interventions, including probiotics, prebiotics, dietary strategies, antibiotics, and fecal microbiota transplantation, have demonstrated neuroprotective potential in both preclinical and clinical contexts. However, inter-individual variability, methodological heterogeneity, and the absence of longitudinal, multi-omics-integrated studies limit current understanding. The gut microbiome also holds promise as a non-invasive biomarker for early PD detection and prognosis, though standardization remains a challenge. Future research must clarify causal mechanisms, optimize therapeutic delivery, and integrate genetic, metabolic, and environmental data to advance precision medicine approaches. This review consolidates current knowledge on gut microbiota's role in PD pathophysiology and therapeutic innovation, providing a roadmap for future research directions.},
}

@article {pmid40614649,
year = {2025},
author = {Wang, Y and Ma, S and Wu, L and Zhao, R},
title = {Betaine promotes chicken growth through modulating gut microbiota and FXR-mediated activation of IGF genes.},
journal = {Poultry science},
volume = {104},
number = {9},
pages = {105455},
doi = {10.1016/j.psj.2025.105455},
pmid = {40614649},
issn = {1525-3171},
abstract = {Betaine is a growth-promoting additive used in both the animal production and microbial fermentation industries. The primary mechanisms by which betaine promotes animal growth are well known through its direct action on the host cells. However, it remains unclear whether betaine exerts its growth-promoting effects in chickens dependent on the gut microbiota. Here, we found that betaine promotes the growth of broiler chickens while enhancing the richness and diversity of the cecal microbiota and increasing beneficial bacteria, such as Lactobacillus, Limosilactobacillus, and Prevotella (P < 0.05). However, the growth-promoting effects of betaine were abolished in broilers treated with an antibiotic cocktail. Furthermore, fecal microbiota transplantation from betaine-supplemented chickens could recapitulate the promoting effect of betaine on body weight, breast muscle weight, and hepatic insulin-like growth factors (IGFs) synthesis (P < 0.05), indicating that the gut microbiota plays an indispensable role in betaine's growth-promoting action. Mechanistically, betaine promotes (P < 0.05) the synthesis of bile acids, and microbial function predictions suggest that betaine upregulates the biosynthetic pathways of primary and secondary bile acids. Notably, the expression of the bile acid receptor farnesoid X receptor (FXR) was upregulated (P < 0.05) in the liver, promoting FXR binding to the IGFs genes promoter regions and activating the transcription of IGFs gene. Taken together, our findings suggest that betaine promotes broiler growth via microbiota-dependent mechanisms, accompanied by FXR-mediated upregulation of IGFs gene expression in the liver, providing new perspectives and theoretical support for understanding the complexity of animal growth regulation.},
}

@article {pmid40613778,
year = {2025},
author = {Wang, W and He, X and Liang, C and Wang, Y and Yu, Y and Zhang, F},
title = {Washed microbiota transplantation alleviates tyrosine kinase inhibitors associated gastrointestinal adverse effects.},
journal = {International journal of cancer},
volume = {},
number = {},
pages = {},
doi = {10.1002/ijc.70034},
pmid = {40613778},
issn = {1097-0215},
support = {2021YFA0717004//the National Key R&D Program of China/ ; 2023-3HIM//Nanjing Medical University Fan Daiming Research Funds for Holistic Integrative Medicine/ ; },
abstract = {Gut microbiota dysbiosis is implicated in tyrosine kinase inhibitor (TKI)-induced gastrointestinal adverse effects (GAEs), often necessitating medication adjustments or discontinuation in severe or persistent cases. This study aimed to evaluate the efficacy and safety of washed microbiota transplantation (WMT) in managing TKI-induced GAEs. This prospective study involved cancer patients presenting TKI-induced GAEs. The primary outcome was the clinical remission rate at Week 8 post-WMT, which was assessed by the common terminology criteria for adverse events grade. The secondary outcomes included the clinical asymptomatic rate, the onset time of clinical remission, and the variation of C-reactive protein (CRP) levels. Twenty-four patients undergoing 66 WMTs were analyzed. The overall clinical remission and asymptomatic rates were 75.00% (18/24) and 29.17% (7/24), respectively. GAEs, including diarrhea, abdominal pain, and abdominal distention, showed significant improvement post-WMT (all p < .05), while hematochezia exhibited a decreasing trend in severity. Median time to remission was 14.5 days (inter-quartile range, 7-24). Within 8 weeks post-WMT, three initially responsive patients experienced relapse. CRP levels significantly decreased (p < .05), and no severe adverse events were reported. This study proposes WMT as a potential treatment for TKI-induced GAEs, particularly for patients who do not respond adequately to conventional treatments.},
}

@article {pmid40613520,
year = {2025},
author = {Ramos Martínez, A and Gutiérrez-Villanueva, A and González-Haba Ruiz, M and Diego-Yagüe, I and Nieto-Fernández, A and Muñez, E and Fernández Cruz, A and Calderón Parra, J},
title = {Fecal microbiota transplantation for prevention of recurrent acute cholangitis. Review of four published cases.},
journal = {Revista espanola de enfermedades digestivas},
volume = {},
number = {},
pages = {},
doi = {10.17235/reed.2025.11404/2025},
pmid = {40613520},
issn = {1130-0108},
abstract = {INTRODUCTION: Recurrent acute cholangitis (RAC) constitutes a relevant clinical problem that may condition the prognosis of the patient. Chronic suppressive antibiotic therapy can be used for preventive purposes, but it is associated with adverse effects and can select resistant bacterial strains. Fecal microbiota transfer (FMT) has been shown to be effective in preventing recurrent Clostridioides difficile infection and could be a useful strategy in patients with RAC.

OBJECTIVE: To review the experience of the use of FMT in the prevention of episodes of RAC by reviewing published cases.

RESULT: Four cases were identified in which FMT significantly reduced RAC episodes. The patients were characterized by lack of efficacy of conventional treatments, had different predisposing factors for RAC and frequent colonization and infection by multidrug-resistant bacteria.

CONCLUSIONS: The four cases presented provide limited but encouraging evidence of the preventive effect of FMT on successive episodes in patients without biliary tract obstruction. Larger and more adequately designed studies will be necessary to deepen the knowledge of this possible preventive strategy.},
}

@article {pmid40613134,
year = {2025},
author = {Yao, Y and Ye, Y and Zheng, C},
title = {The Impact of Microbiota-Mediated Immune Regulation on Recurrent Pregnancy Loss and Intervention Strategies.},
journal = {American journal of reproductive immunology (New York, N.Y. : 1989)},
volume = {94},
number = {1},
pages = {e70121},
doi = {10.1111/aji.70121},
pmid = {40613134},
issn = {1600-0897},
support = {LHDMZ23H190002//Huadong Medicine Joint Funds of the Zhejiang Provincial Natural Science Foundation of China/ ; },
mesh = {Humans ; Female ; *Abortion, Habitual/immunology/microbiology/therapy ; Pregnancy ; *Gastrointestinal Microbiome/immunology ; *Dysbiosis/immunology ; *Microbiota/immunology ; *Endometrium/microbiology/immunology ; Probiotics/therapeutic use ; Fecal Microbiota Transplantation ; Animals ; Immune Tolerance ; },
abstract = {Recurrent pregnancy loss (RPL) significantly affects reproductive health in couples of childbearing age. Its pathogenesis is complex, with nearly 50% of cases remaining unexplained, and immune regulation plays a key role in its development. This review focuses on the relationship between human microbiota (gut, reproductive tract, and endometrial microbiota), immune regulation, and RPL, systematically summarizing related research progress. RPL patients exhibit characteristic changes in the gut, reproductive tract, and endometrial microbiota, such as reduced gut microbial diversity, decreased beneficial bacteria, increased harmful bacteria in the reproductive tract, and an imbalanced endometrial microbiota structure. Dysbiosis can lead to immune regulation abnormalities, increasing the risk of RPL by disrupting immune tolerance, triggering inflammatory responses, and interfering with metabolism. Although microbiota-based interventions, such as probiotics, prebiotics, and fecal microbiota transplantation, show potential, they face challenges related to strain selection, donor screening, and unclear mechanisms. Current research also faces limitations in detection technology and sample size, and the understanding of the microbiota-immune-RPL relationship requires further deepening. Future studies should clarify causal relationships using advanced technologies, develop more effective detection and intervention methods, and create personalized treatment plans based on individual patient characteristics to improve clinical diagnosis and treatment of RPL and safeguard women's reproductive health.},
}

Humans
Female
*Abortion, Habitual/immunology/microbiology/therapy
Pregnancy
*Gastrointestinal Microbiome/immunology
*Dysbiosis/immunology
*Microbiota/immunology
*Endometrium/microbiology/immunology
Probiotics/therapeutic use
Fecal Microbiota Transplantation
Animals
Immune Tolerance

@article {pmid40612747,
year = {2025},
author = {Wu, J and Jia, B and Gong, S and Li, Y and Wang, J and Huang, Y and Guo, J},
title = {Protective effects of Atractylodes macrocephala polysaccharides on acetaminophen-induced liver injury.},
journal = {Frontiers in pharmacology},
volume = {16},
number = {},
pages = {1583334},
pmid = {40612747},
issn = {1663-9812},
abstract = {BACKGROUND: Drug-induced liver injury (DILI) is a major clinical concern due to its unpredictable nature and lack of effective therapeutic options.

METHODS: This study investigated the hepatoprotective effects of Atractylodes macrocephala polysaccharides (AMPs) in a mouse model of acetaminophen (APAP)-induced liver injury. Mice were pretreated with AMPs for 7 days prior to APAP challenge, and liver injury was evaluated through histopathology, serum biochemistry, molecular assays, and gut microbiota analysis.

RESULTS: AMPs treatment significantly reduced serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels compared to the APAP group (p < 0.05). Hepatic oxidative stress was alleviated, as indicated by increased levels of glutathione (GSH, p < 0.05) and superoxide dismutase (SOD, p < 0.05), and reduced malondialdehyde (MDA, p < 0.05). AMPs also suppressed inflammatory cytokines, including Il-1β, Tnf-α, Il-6, and Nlrp3 (p < 0.05), and modulated apoptosis-related proteins by downregulating Bax and upregulating Bcl-2 and Bcl-xl expression (p < 0.05). Furthermore, AMPs improved gut microbiota diversity and enriched beneficial genera such as Roseburia, as revealed by 16S rDNA sequencing. Fecal microbiota transplantation from AMPs-treated mice replicated these hepatoprotective effects, highlighting the involvement of the gut-liver axis.

CONCLUSION: These findings support the therapeutic potential of AMPs as a multifaceted agent for DILI, exerting protective effects through modulation of oxidative stress, inflammation, apoptosis, and intestinal dysbiosis.},
}

@article {pmid40612440,
year = {2025},
author = {Wenjiao, D and Yurou, W and Jiaqi, X and Yan, H and Hongfang, J and Min, C and Jianjin, G},
title = {Animal studies on the modulation of differential efficacy of polyethylene glycol loxenatide by intestinal flora.},
journal = {Frontiers in endocrinology},
volume = {16},
number = {},
pages = {1508473},
pmid = {40612440},
issn = {1664-2392},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; Male ; Mice ; Mice, Inbred C57BL ; *Fecal Microbiota Transplantation ; *Diabetes Mellitus, Experimental/microbiology/drug therapy/therapy ; *Polyethylene Glycols/pharmacology ; *Diabetes Mellitus, Type 2/microbiology/drug therapy ; *Hypoglycemic Agents/pharmacology/therapeutic use ; Diet, High-Fat/adverse effects ; Blood Glucose ; },
abstract = {BACKGROUND: Gut microbiota has demonstrated an increasingly important role in the onset and development of type 2 diabetes mellitus (T2DM), Further investigations have revealed the interactions between drugs and the gut microbiome. However, there are still gaps in research regarding the potential interactions between the gut microbiota and GLP-1 and their therapeutic response in people with T2DM. In addition, Fecal microbiota transplantation (FMT) has become a promising strategy for patients with T2DM.

50 healthy male C57BL/6 mice were fed a high-fat diet in combination with STZ to establish a T2DM mouse model. 40 mice were divided into the T2DM group (n=10) and the PEX168 group (n=30). the PEX168 group was divided into two subgroups of the IE group (HbA1c ≤6. 5%, n=12) and the SE group (HbA1c >6. 5%, n=12), 12 mice in each group. Using IE mice as fecal donors and SE mice as recipients, fecal microbiota transplantation was performed between the two groups, the FMT group (given fecal bacterial suspension, n=5) and the Sham group (given equal amounts of sterile saline, n=5). The intestinal microorganisms of mice in the IE group (donor) and SE group (recipient) were also analyzed for differences. To assess the protective effect of FMT on drug efficacy and T2DM, and to explore the underlying mechanisms.

RESULTS: After 10 weeks, compared with the control group, the HbA1c of the experimental group was significantly reduced, still, the level of HBA1c of the mice in the unsatisfactory group was significantly higher than that in the ideal group. Compared with the unsatisfactory group, fasting blood glucose, 2h postprandial blood glucose, blood glucose AUC and body weight were significantly reduced in the ideal group. 16srDNA sequencing showed that the levels of Bacteroidota, Akkermansia, Parabacteroides, Bifidobacteria and other bacteria in the ideal efficacy group were significantly higher than those in the non-ideal efficacy group (P<0.05). The levels of Firmicutes, Romboutsia, Clostridium, Turicibacter and other bacteria in the unsatisfactory group were significantly higher than those in the ideal group (P<0.05). The dominant flora of mice in the ideal drug efficacy group was negatively correlated with HbA1c and blood sugar, and the dominant flora of mice in the unsatisfactory drug efficacy group was positively correlated with pro-inflammatory factors such as blood sugar. Moreover, FMT treatment significantly improved the efficacy of PEX168 and liver steatosis in the group with unsatisfactory efficacy.

CONCLUSION: In summary, we used the combined method of 16S rDNA and metabolomics to systematically elucidate the efficacy of microflora on PEX168 and the possible mechanism of FMT in treating T2DM by PEX168. The difference in intestinal flora between individuals can affect the therapeutic effect of drugs. Moreover, FMT therapy can affect multiple metabolic pathways and colonization of beneficial bacteria to maintain the drug's therapeutic effect on T2DM mice.},
}

Animals
*Gastrointestinal Microbiome/drug effects
Male
Mice
Mice, Inbred C57BL
*Fecal Microbiota Transplantation
*Diabetes Mellitus, Experimental/microbiology/drug therapy/therapy
*Polyethylene Glycols/pharmacology
*Diabetes Mellitus, Type 2/microbiology/drug therapy
*Hypoglycemic Agents/pharmacology/therapeutic use
Diet, High-Fat/adverse effects
Blood Glucose

@article {pmid40611525,
year = {2025},
author = {Wang, D and Wang, H and Li, Y and Lu, J and Tang, X and Yang, D and Wang, M and Zhao, D and Liu, F and Zhang, S and Sun, L},
title = {Alistipes senegalensis is Critically Involved in Gut Barrier Repair Mediated by Panax Ginseng Neutral Polysaccharides in Aged Mice.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e16427},
doi = {10.1002/advs.202416427},
pmid = {40611525},
issn = {2198-3844},
support = {U24A20795//National Natural Science Foundation of China/ ; 82204709//National Natural Science Foundation of China/ ; 82004099//National Natural Science Foundation of China/ ; JJKH20230991KJ//Jilin Provincial Department of Education Project/ ; 20240404018ZP//Jilin Provincial Scientific and Technological Development Program/ ; },
abstract = {Ginseng polysaccharides (GPs) are known to have beneficial effects on the gut epithelium and age-related systemic-inflammation through regulation of gut microbiota. However, the underlying pathways and key members of the microbial community involved in this process are poorly understood. In this study, administration of ginseng neutral polysaccharide (GPN) is found to alleviate gut leak and low-grade inflammation, concomitantly with improving the physiological function aged mice. Fecal microbiota transplantation and fecal conditioned medium are used to assess the specific involvement of gut bacterial metabolites in the effects of GPNs. Comprehensive multi-omics analyses showed that GPN significantly enriched the abundance of Alistipes senegalensis, an indole-producing commensal bacterium. Increased expression of tight junction-associated proteins, as well as activation of gut stem cells, are found to be mediated by the AhR pathway, indicating the causal mechanism by which GPN reduced increases in gut permeability. The results are verified in Caco-2/THP-1 cells, Caenorhabditis elegans, and enteroids. To the knowledge, this is the first identification of an integral functional axis through which GPN and functional metabolites of A. senegalensis influence the gut barrier and reduce systemic inflammation, providing clues for the potential development of innovative plant polysaccharide treatment strategies to promote healthy aging.},
}

@article {pmid40611207,
year = {2025},
author = {Wang, Q and Zhang, M and Meng, M and Luo, Z and Pan, Z and Deng, L and Qin, J and Guo, B and Zhu, D and Zhang, Y and Guo, H and Liang, Y and Su, Z},
title = {Integration bile acid metabolomics and gut microbiome to study the anti-liver fibrosis effects of total alkaloids of Corydalis saxicola Bunting.},
journal = {Chinese medicine},
volume = {20},
number = {1},
pages = {106},
pmid = {40611207},
issn = {1749-8546},
support = {82060763//National Natural Science Foundation of China/ ; GXFCDP-PS-2022//Guangxi First-class Discipline Project for Pharmaceutical Sciences/ ; GXQH202409//Guangxi Youth Qihuang Scholars Training Project/ ; },
abstract = {BACKGROUND: Bile acids and gut microbiota participate in the pathogenesis of liver fibrosis (LF). The total alkaloids of Corydalis saxicola Bunting (TACS) is a traditional Chinese medicine extract that has been used to treat LF, but the underlying mechanisms are not clear. This study performed integrated metabolomics and gut microbiome analysis to study the anti-LF mechanism of TACS using a rat model.

METHODS: Ultra-performance liquid chromatography quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF/MS) was used to identify the chemical compounds in TACS. Biochemical and histopathological analysis were performed to determine the efficacy of TACS. Bile acid-targeted metabolomics was used to assess changes in the bile acid (BA) profiles in TACS-treated LF rats. 16S rRNA gene sequencing and metagenomics were used to assess changes in the gut microbiota of the TACS-treated LF rats. Antibiotic cocktail treatment and fecal microbiota transplantation (FMT) were used to determine the relationship between the gut microbiota and the anti-LF effects of TACS. Metagenomics was used to identify significantly enriched gut microbiota after TACS treatment and its correlation with the anti-LF effects was verified by in vivo experiments.

RESULTS: TACS treatment significantly reduced the levels of serum liver enzymes, fibrosis and pro-inflammatory cytokines in the liver. TACS significantly increased the levels of chenodeoxycholic acid (CDCA) and taurochenodeoxycholic acid (TCDCA) in the cecum and decreased the levels of cholic acid (CA) and deoxycholic acid (DCA) in the liver of the LF rats. TACS significantly increased the abundances of Lactobacillus and Akkermansia in the LF rats. Antibiotic cocktail treatment and FMT have shown that the effect of TACS cure liver fibrosis depends on the gut microbiota. The abundance of Lactobacillus reuteri was significantly increased by TACS. Administration of Lactobacillus reuteri via gavage ameliorated LF.

CONCLUSIONS: TACS exerted anti-LF effects in rats by modulating bile acid metabolism and gut microbiome.},
}

@article {pmid40609706,
year = {2025},
author = {Daneri, L and Urbano, A and Escudero-Sánchez, R and Halperin, AV and Moreno-Blanco, A and Corbacho, MD and Suárez-Carantoña, C and Rodríguez-Jiménez, C and Serrano-Villar, S and Campo, RD and Cobo, J},
title = {Lyophilised fecal microbiota transfer in capsules for recurrent Clostridioides difficile infection.},
journal = {International journal of antimicrobial agents},
volume = {},
number = {},
pages = {107561},
doi = {10.1016/j.ijantimicag.2025.107561},
pmid = {40609706},
issn = {1872-7913},
abstract = {BACKGROUND: Recent guidelines recommend fecal microbiota transplantation (FMT) for patients who experience multiple episodes of Clostridioides difficile infection (CDI). The availability of lyophilised and encapsulated FMT in recent years has greatly improved patient comfort and convenience. While the effectiveness of FMT in oral capsules seems comparable to that achieved through other routes, further experience is needed, particularly in Europe, where there is currently limited published experience. The objective of this study was to present our experience with this therapeutic modality.

METHODS: A retrospective cohort study on patients with recurrent CDI treated by lyophilised, encapsulated FMT. All patients were followed for a minimum of 12 weeks. The primary outcome was recurrence at three months.

RESULTS: A total of 36 patients received 38 FMTs. The median age of the cohort was 78.5 years, with a median of four previous episodes. At the three-month follow-up, 27 of the 36 patients (75.0%) were free of CDI. One patient exhibited recurrence before the six-month mark. Two of the ten patients with FMT failure were successfully rescued with a second FMT. Of the nine patients who underwent rescue attempts, seven did not experience recurrence, resulting in a cure rate of 91.7% for the 36 patients. We did not detect severe adverse effects related to the FMT.

CONCLUSION: We confirm an acceptable effectiveness of lyophilised capsulated oral FMT. Interestingly, most patients with FMT failure can be cured with a new treatment, which need not necessarily be a new FMT.},
}

@article {pmid40607920,
year = {2025},
author = {Pan, Y and Shen, L and Wu, Z and Wang, X and Liu, X and Zhang, Y and Luo, Q and Liu, S and Fang, X and Shu, Q and Chen, Q},
title = {Hepcidin sustains Kupffer cell immune defense against bloodstream bacterial infection via gut-derived metabolites in mice.},
journal = {The Journal of clinical investigation},
volume = {},
number = {},
pages = {},
doi = {10.1172/JCI189607},
pmid = {40607920},
issn = {1558-8238},
abstract = {Bloodstream bacterial infections cause one-third of deaths from bacterial infections, and eradication of circulating bacteria is essential to prevent disseminated infections. We here found that hepcidin, the master regulator of systemic iron homeostasis, affected Kupffer cell (KC) immune defense against bloodstream bacterial infections by modulating the gut commensal bacteria-derived tryptophan derivative indole-3-propionic acid (IPA). Hepcidin deficiency impaired bacterial capture by KCs and exacerbated systemic bacterial dissemination through morphological changes in KCs. Gut microbiota depletion and fecal microbiota transplantation revealed that the gut microbiota mediated the alteration of KCs volume. Mechanistically, hepcidin deficiency led to a decreased abundance of the IPA-producing commensal Lactobacillus intestinalis and a concomitant reduction in the gut-to-liver shuttling of its metabolite IPA. IPA supplementation or Lactobacillus intestinalis colonization restored the KC volume and hepatic immune defense against bloodstream bacterial infection in hepcidin-deficient mice. Moreover, hepcidin levels in patients with bacteremia were associated with days of antibiotic usage and hospitalization. Collectively, our findings described a previously unappreciated role of hepcidin in sustaining KC-mediated hepatic defense against bloodstream bacterial infections through the gut commensal Lactobacillus intestinalis and its tryptophan derivative IPA. More importantly, restoring the crosstalk between the gut microbiota and liver through IPA-inspired therapies may offer a promising strategy for enhancing the host defense against bloodstream bacterial infections in those with low hepcidin levels and a high risk for bacterial infections.},
}

@article {pmid40607758,
year = {2025},
author = {Wei, Y and Mao, J and Tang, W and Ma, Y and Li, J and Su, S and Ni, Z and Wu, J and Liu, D and Wang, H},
title = {Targeting Catenibacterium mitsuokai with icariin modulates gut microbiota and improves hepatic lipid metabolism in intrauterine growth restriction.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wraf141},
pmid = {40607758},
issn = {1751-7370},
abstract = {Male offspring with intrauterine growth restriction exhibit more pronounced hepatic lipid metabolism abnormalities than females, necessitating earlier intervention. Icariin has been shown to effectively modulate hepatic lipid metabolism in male piglets with intrauterine growth restriction. However, the role of gut microbiota in this process remains to be elucidated. This study aimed to explore the influence of gut microbiota on icariin-induced enhancement of hepatic lipid metabolism. By examining changes in microbiota composition and hepatic lipid metabolism following icariin intervention, the study demonstrated an association between microbial alterations and hepatic lipid regulation through fecal microbiota transplantation. The impact of Catenibacterium on gut microbiota structure and hepatic lipid metabolism was assessed in vivo, and the direct effect of icariin on Catenibacterium was explored in vitro. Results revealed that icariin intervention modified fecal, ileal, and colonic microbiota in male piglets with intrauterine growth restriction, enhanced gut morphology and barrier function, and normalized the expression of hepatic peroxisome proliferator-activated receptor (PPAR) signaling pathway-related genes. Fecal microbiota transplantation from piglets with intrauterine growth restriction impaired intestinal barrier function and led to hepatic lipid deposition, whereas transplantation from icariin-treated donors showed no pathological changes, an outcome associated with reduced abundance of Catenibacterium. Mechanistically, icariin inhibits adenosine triphosphate synthesis to suppress Catenibacterium, remodels gut microbiota, reduces lipopolysaccharide production and translocation, and activates the hepatic PPARα/CD36 axis. In conclusion, icariin intervention alleviates hepatic lipid metabolic disorders in male offspring with intrauterine growth restriction by suppressing Catenibacterium, restoring gut microbial balance, and enhancing intestinal barrier integrity to limit lipopolysaccharide translocation.},
}

@article {pmid40606926,
year = {2025},
author = {Pandey, H and Goel, P and Srinivasan, VM and Tang, DWT and Wong, SH and Lal, D},
title = {Gut microbiota in non-alcoholic fatty liver disease: Pathophysiology, diagnosis, and therapeutics.},
journal = {World journal of hepatology},
volume = {17},
number = {6},
pages = {106849},
pmid = {40606926},
issn = {1948-5182},
abstract = {Non-alcoholic fatty liver disease (NAFLD), also referred to as metabolic-associated fatty liver disease, is among the most prevalent chronic liver conditions. In some cases, NAFLD may lead to liver inflammation and non-alcoholic steatohepatitis, which can eventually progress to liver cirrhosis and hepatocellular carcinoma. The pathophysiology of NAFLD is complex, involving both genetic and environmental factors. NAFLD is a multisystem disease linked to a higher likelihood of developing metabolic disorders such as type 2 diabetes, obesity, and cardiovascular and chronic kidney diseases. The gut-liver axis represents a key connection between the gut microbiota and the liver, and its disruption has been linked to NAFLD. Growing evidence underscores the significant role of gut microbiota in the onset and progression of NAFLD, with alterations in the gut microbiome and impaired gut barrier function. Studies have identified key microbiota signatures and metabolites linked to NAFLD, implicating oxidative stress, endotoxemia, and inflammatory pathways that further strengthen the connection between gut microbiota and NAFLD. Modulation of gut microbiota through diet and microbiota-centered therapies, such as next-generation probiotics and fecal microbiota transplantation, holds promise for treating NAFLD. In this review, we explore the key link between gut microbiota and the development and progression of NAFLD, as well as its potential applications in the diagnosis and treatment of the disease.},
}

@article {pmid40606817,
year = {2025},
author = {Li, X and Lei, Q and Xie, J and Li, F and Liu, J and Chen, Y and Mao, Q},
title = {Research on functional constipation with anxiety or depression: a bibliometric analysis.},
journal = {Frontiers in psychiatry},
volume = {16},
number = {},
pages = {1607297},
pmid = {40606817},
issn = {1664-0640},
abstract = {BACKGROUND: Although the phenomenon of functional constipation (FC) that accompanies anxiety or depression has been extensively investigated worldwide, no bibliometric studies are available in this regard. This study therefore aimed to analyze the current status and extent of research and areas of interest in the study of FC with anxiety or depression.

METHODS: Data from studies on FC with anxiety or depression, that were performed between 2003 and 2024, were retrieved from the Web of Science Core Collection database. Data regarding the annual number of publications, authors, countries, and references were assessed using CiteSpace v6.3.R1 (64-bit) and Microsoft Excel, and those pertaining to keywords and cited authors were evaluated using VOSviewer 1.6.20. The co-occurrence and clustering functions were then used to generate visual knowledge maps.

RESULTS: The overall annual publication volume demonstrated an upward trend between 2003 and 2024; this was indicative of promising research prospects. The 427 publications identified included 6 types of papers, among which original research articles represented the highest proportion (357 [83.61%] articles published across 200 journals). Neurogastroenterology and Motility had the highest publication volume (30 articles, 7.02%). The United States of America had published most of the papers (135 articles, 31.61%) on the topic. Harvard University was the research institution with the most published papers (21 articles, 4.92%), and Michel Bouchoucha had authored the highest number of articles (13 articles, 3.04%).

CONCLUSION: Future studies in the field of basic medicine need to determine the etiology and pathogenesis of FC with anxiety or depression; in particular, they need to evaluate the role of opioid drugs as a key etiological factor. The role played by the brain-gut axis also warrants investigation. From the clinical perspective, studies need to focus on evidence-based medicine; particular emphasis needs to be placed on randomized double-blind controlled trials with stringent quality control, high-quality meta-analyses, and evaluation of questionnaires and scales. Treatment techniques need to be explored in greater detail; in this context, it is recommended that fecal microbiota transplantation and biofeedback therapy are adopted in the clinic. Furthermore, Patients with FC, especially those with a history of anxiety or depression, tend to have overlapping dyspepsia symptoms.},
}

@article {pmid40606527,
year = {2025},
author = {Paaske, SE and Baunwall, SMD and Rubak, T and Rågård, N and Kelsen, J and Hansen, MM and Lødrup, AB and Erikstrup, LT and Mikkelsen, S and Erikstrup, C and Dahlerup, JF and Hvas, CL},
title = {Clinical management of Clostridioides difficile infection with faecal microbiota transplantation: a real-world cohort study.},
journal = {EClinicalMedicine},
volume = {85},
number = {},
pages = {103302},
pmid = {40606527},
issn = {2589-5370},
abstract = {BACKGROUND: Clostridioides difficile infection (CDI) causes high morbidity and mortality. Faecal microbiota transplantation (FMT) is well-established for CDI, but therapeutic strategies may be optimised. We aimed to evaluate clinical outcomes by analysing therapeutic strategies in a real-life cohort of patients with CDI treated with FMT.

METHODS: We conducted a multi-site cohort study, including 1170 patients with CDI, treated with FMT through capsules, colonoscopy, or nasojejunal tube between May 2016 and December 2023. The primary outcome was cure of C. difficile-associated diarrhea (CDAD) eight weeks after treatment. We investigated antibiotic pretreatment type and length, FMT dosing and administration, and post-FMT prophylactic vancomycin during non-CDI antibiotic use, applying multivariable mixed-effect regression analysis including the patient as a random effect. The study was preregistered at ClinicalTrials.gov, NCT03712722.

FINDINGS: The 1170 patients received 1643 FMT treatments. Patients' median age was 71 years (interquartile range 56-80 years). Following their first FMT treatment, 699 patients (60% (95% confidence interval: 57-63%)) were cured of CDAD. After repeated FMT treatments, 944 patients (81% (78-83%)) were cured. Prolonged antibiotic pretreatment was associated with higher cure rates (65% (59-70%), odds ratio (OR): 1.22 (1.10-1.36), p < 0.001). FMT administration through oral, multi-dose capsules (69% (63-74%), OR: 1.19 (1.11-1.27), p < 0.001) or colonoscopy (69% (61-76%), OR: 1.14 (1.04-1.24), p = 0.01) resulted in the highest cure rates. Neither antibiotic pretreatment type nor prophylactic vancomycin during non-CDI antibiotics affected cure rates. In patients for whom FMT was initially unsuccessful, repeated FMT was more effective than antibiotic treatment alone.

INTERPRETATION: CDI outcomes could be improved by optimising antibiotic pretreatment duration, selecting appropriate FMT delivery methods, and repeating FMT.

FUNDING: Innovation Fund Denmark (j.no. 8056-00006B).},
}

@article {pmid40605266,
year = {2025},
author = {Herman, C and Barker, BM and Bartelli, TF and Chandra, V and Krajmalnik-Brown, R and Jewell, M and Li, L and Liao, C and McAllister, F and Nirmalkar, K and Xavier, JB and Caporaso, JG},
title = {A review of engraftment assessments following fecal microbiota transplant.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2525478},
doi = {10.1080/19490976.2025.2525478},
pmid = {40605266},
issn = {1949-0984},
mesh = {*Fecal Microbiota Transplantation ; Humans ; *Gastrointestinal Microbiome ; *Clostridium Infections/therapy/microbiology ; Clostridioides difficile/physiology ; Animals ; Feces/microbiology ; Bacteria/classification/genetics/isolation & purification ; },
abstract = {Fecal Microbiota Transplant (FMT) is a treatment for recurrent Clostridium difficile infections and is being explored for other clinical applications, from alleviating digestive and neurological disorders, to restoring microbiomes impacted by cancer treatment. Quantifying the extent of engraftment following an FMT is important in understanding a recipient's response to treatment. Engraftment and clinical response need to be investigated independently to evaluate an FMT's role (or lack thereof) in achieving a clinical response. Standardized bioinformatics methodologies for quantifying engraftment extent would not only improve assessment and understanding of FMT outcomes, but also facilitate comparison of FMT results and protocols across studies. Here we review FMT studies, integrating three concepts from microbial ecology as framework to discuss how these studies approached assessing engraftment extent: 1) Community Coalescence investigates microbiome shifts following FMT engraftment, 2) Indicator Features tracks specific microbiome features as a signal of engraftment, and 3) Resilience examines how resistant post-FMT recipients' microbiomes are to reverting back to baseline. These concepts explore subtly different questions about the microbiome following FMT. Taken together, they provide holistic insight into how an FMT alters a recipient's microbiome composition and provide a clear framework for quantifying and communicating about microbiome engraftment.},
}

*Fecal Microbiota Transplantation
Humans
*Gastrointestinal Microbiome
*Clostridium Infections/therapy/microbiology
Clostridioides difficile/physiology
Animals
Feces/microbiology
Bacteria/classification/genetics/isolation & purification

@article {pmid40604869,
year = {2025},
author = {Rychlik, A and Kaczmar, E and Mikulska, I and Makowska, K},
title = {Assessment of the effect of prokinetic drugs on transit time and gastrointestinal cleanliness in capsule endoscopy.},
journal = {BMC veterinary research},
volume = {21},
number = {1},
pages = {417},
pmid = {40604869},
issn = {1746-6148},
mesh = {Animals ; *Metoclopramide/pharmacology ; *Capsule Endoscopy/veterinary/methods ; Dogs ; *Gastrointestinal Transit/drug effects ; *Gastrointestinal Agents/pharmacology ; *Cisapride/pharmacology ; Male ; Female ; *Gastrointestinal Tract/drug effects ; },
abstract = {BACKGROUND: Endoscopic examinations are increasingly used in veterinary medicine. Examination using flexible endoscopes is limited to the anterior gastrointestinal tract (panendoscopy) and colon (colonoscopy), while a significant part of the small intestine remains unexamined. Capsular endoscopy is increasingly used, allowing macroscopic assessment of the entire digestive tract. The current study assessed the effect of prokinetic drugs on transit time and cleanliness of the tested part of the digestive tract in capsule endoscopy.

METHODS: The study aimed to evaluate the usefulness of two prokinetic drugs (metoclopramide and cisapride) in capsule endoscopy studies while assessing the quality of the macroscopic image. Each animal included into the study had endoscopic examination three times - without the administration of prokinetic drugs, after receiving metoclopramide and after receiving cisapride.

RESULTS: The total passage time of the capsule through the gastrointestinal tract was the longest in the group receiving metoclopramide (691.33 min) and the shortest in the group receiving cisapride (584.17 min). The best quality images were observed in the control group.

CONCLUSION: This research has confirmed the hypothesis that administration of prokinetic drugs increases the probability of recording the entire macroscopic image of the gastrointestinal tract during endoscopy in dogs. A negative feature of their administration is significantly reduced recording quality because of the level of cleanliness of the tested gastrointestinal section.},
}

Animals
*Metoclopramide/pharmacology
*Capsule Endoscopy/veterinary/methods
Dogs
*Gastrointestinal Transit/drug effects
*Gastrointestinal Agents/pharmacology
*Cisapride/pharmacology
Male
Female
*Gastrointestinal Tract/drug effects

@article {pmid40602277,
year = {2025},
author = {Wu, H and Li, YL and Wang, Y and Wang, YG and Hong, JH and Pang, MM and Liu, PM and Yang, JJ},
title = {Anemoside B4 alleviates ulcerative colitis by attenuating intestinal oxidative stress and NLRP3 inflammasome via activating aryl hydrocarbon receptor through remodeling the gut microbiome and metabolites.},
journal = {Redox biology},
volume = {85},
number = {},
pages = {103746},
doi = {10.1016/j.redox.2025.103746},
pmid = {40602277},
issn = {2213-2317},
abstract = {Ulcerative colitis (UC) is a chronic, non-specific inflammatory disease of the intestines with a significant increase in global incidence in recent years. Oxidative stress and inflammation are two hallmarks of UC pathogenesis. Anemoside B4 (AB4), a pentacyclic triterpenoid saponin, exhibits significant antioxidant and anti-inflammatory properties and shows potential for preventing UC. Here, an animal model induced by dextran sodium sulfate (DSS) was used to investigate the effect of AB4 on UC. The results demonstrated that AB4 significantly reduces intestinal oxidative stress and inflammation in UC mice, while also protecting intestinal barrier function. Furthermore, AB4 helps restore intestinal microbial balance primarily by modulating the abundance of Lactobacillus, which enhances the metabolism of short-chain fatty acids and upregulates the production of butyric acid (BA). Pseudogerm-free mice and fecal microbiota transplantation (FMT) demonstrated that AB4 significantly mitigated UC in a gut microbe-dependent manner. Both AB4 and BA markedly activate the aromatic hydrocarbon receptor (AhR). The intestinal organoid results suggest BA may activate the AhR to inhibit ROS production and activation of NLRP3 inflammasome, thereby protecting intestinal integrity. Administration of AhR antagonists abolished the protective effects, thus confirming the involvement of AhR in the underlying mechanism. Overall, these results indicate that AB4 is an effective agent against UC mainly by activating the AhR through gut microbial short-chain fatty acid metabolites to inhibit intestinal oxidative stress and inflammation.},
}

@article {pmid40601184,
year = {2025},
author = {Rico-Caballero, V and Romero-Rivera, M and Moreno-Blanco, A and Aira, A and Casals-Pascual, C and Rodríguez-Jiménez, C and Quereda, C and Soriano, A and Del Campo, R},
title = {Fecal microbiota transplant as treatment for recurrent urinary tract infections: a proof-of-concept study.},
journal = {European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology},
volume = {},
number = {},
pages = {},
pmid = {40601184},
issn = {1435-4373},
}

@article {pmid40600295,
year = {2025},
author = {Shao, H and Min, F and Bai, T and Liu, Y and Zheng, S and Wu, Y and Di, C and Lin, M and Li, X and Chen, H},
title = {Bifidobacterium breve M-16V alleviates cow's milk allergy by regulating the gut microbiota and metabolites in human microbiota-associated mice.},
journal = {Food & function},
volume = {},
number = {},
pages = {},
doi = {10.1039/d5fo02012c},
pmid = {40600295},
issn = {2042-650X},
abstract = {Cow's milk allergy (CMA) is one of the most common food allergies, especially in infants and young children. Growing evidence from animal studies has shown that some specific probiotics can alleviate CMA, but clinical evidence remains insufficient due to certain limitations. In the present study, we transplanted fecal material from three CMA children into antibiotic-pretreated mice (hum-CMA mice) to mimic the intestinal microecology of allergic individuals, followed by allergen sensitization and Bifidobacterium breve (B. breve) M-16V intervention. Our results showed that B. breve M-16V effectively ameliorated CMA symptoms and allergy-related indicators in hum-CMA mice. Moreover, B. breve M-16V differentially affected the composition of intestinal microbes, but the abundance of beneficial bacteria, such as short-chain fatty acid-producing bacteria, was consistently elevated in all three groups of hum-CMA mice. Subsequent untargeted metabolomics analyses revealed that B. breve M-16V improved the pattern of serum metabolites, and these differential metabolites were mainly involved in glutathione metabolism, glycerophospholipid metabolism, and tryptophan metabolism. All the findings indicate that B. breve M-16V can alleviate the anaphylactic reaction in hum-CMA mice by regulating the intestinal microbiota and metabolites, providing a valuable scientific basis for the clinical application of probiotics in food allergy.},
}

@article {pmid40600174,
year = {2025},
author = {Ebrahimi, R and Shahrokhi Nejad, S and Fekri, M and Nejadghaderi, SA},
title = {Advancing prostate cancer treatment: the role of fecal microbiota transplantation as an adjuvant therapy.},
journal = {Current research in microbial sciences},
volume = {9},
number = {},
pages = {100420},
pmid = {40600174},
issn = {2666-5174},
abstract = {Prostate cancer (PCa) is a major cause of cancer-related deaths worldwide. While current treatments such as surveillance, surgery, and radiation are effective, they have their limitations. These can include patient incompliance due to side effects or resistance to hormonal changes, highlighting the need for alternative approaches. Human microbiota, a complex and dynamic host, plays a significant role in the homeostasis and is associated with several diseases or cancers in cases of dysregulation and dysbiosis. Research on fecal microbiota profiling and its association with certain cancers has opened new possibilities for preventing and managing tumor progression. One such possibility is fecal microbial transplantation (FMT). Studies show that different composition of urinary microbiota is found in various urinary tract diseases. Gut microbiota can regulate immune response against tumors; therefore, FMT may help modulate gut microbiota in a way that potentially enhances responses to immune checkpoint inhibitors, as suggested by emerging evidence in other cancers, though this needs further validation in PCa. Nevertheless, long-term complications and the safety of FMT are still questioned. We reviewed the roles of gut microbiota in PCa and suggested FMT as a potential tool in the treatment of PCa, which needs further investigations.},
}

@article {pmid40599506,
year = {2025},
author = {Alnahwi, HH and AlGhawi, RJ and Alsahaf, HAA and Ahmed, E},
title = {Recurrent Clostridioides difficile Infection (CDI) in Patients Treated With Vancomycin at Johns Hopkins Aramco Healthcare (JHAH), Dhahran, Saudi Arabia.},
journal = {Cureus},
volume = {17},
number = {5},
pages = {e85116},
pmid = {40599506},
issn = {2168-8184},
abstract = {Introduction Clostridioides difficile infection (CDI) is a leading cause of healthcare-associated diarrhea with a significant risk of recurrence, posing challenges for patient management and infection control. Identifying risk factors for recurrence is essential to improve outcomes and prevent relapses. Methods This retrospective cohort study included 860 adult patients (≥18 years) treated with vancomycin for CDI at Johns Hopkins Aramco Healthcare (JHAH) in Dhahran, Saudi Arabia, between January 2015 and December 2020. Patients with confirmed CDI based on stool polymerase chain reaction (PCR) or toxin assays, complete medical records, and adequate follow-up data were included. The study excluded those not treated with vancomycin, under 18 years of age, with incomplete records, those who received fecal microbiota transplantation or experimental treatments, and those lacking follow-up data. Data on demographics, comorbidities, hospitalization, medication use, and recurrence were analyzed using univariate and multivariate logistic regression models. Results Univariate analysis showed that age 40-65 years (OR = 1.53; 95% CI: 1.024-2.285; p = 0.038), age >65 years (OR = 1.894; 95% CI: 1.282-2.799; p = 0.001), cirrhosis (OR = 9.104; 95% CI: 1.233-67.192; p = 0.03), hospitalization (OR = 1.974; 95% CI: 1.417-2.749; p < 0.0001), and type 2 diabetes mellitus (OR = 1.65; 95% CI: 1.106-2.462; p = 0.014) were significantly associated with CDI recurrence. After adjusting for confounders, only hospitalization remained a statistically significant independent predictor (OR = 1.597; 95% CI: 1.098-2.325; p = 0.014). Conclusion Hospitalization was identified as the most significant independent risk factor for CDI recurrence. These findings highlight the need for enhanced infection control practices and close monitoring of hospitalized patients with CDI. Future prospective and multicenter studies are recommended to validate these results and explore additional modifiable risk factors to reduce recurrence rates.},
}

@article {pmid40599494,
year = {2025},
author = {Boton, N and Patel, PK and Beekmann, SE and Polgreen, PM and Buckel, WR and Mahoney, MV and Mehrotra, P and Lee, MSL},
title = {Clinician Management Preferences for Clostridioides difficile Infection in Adults: A 2024 Emerging Infections Network Survey.},
journal = {Open forum infectious diseases},
volume = {12},
number = {7},
pages = {ofaf335},
pmid = {40599494},
issn = {2328-8957},
abstract = {BACKGROUND: The 2021 Infectious Diseases Society of America (IDSA) and Society for Healthcare Epidemiology of America (SHEA) guidelines for Clostridioides difficile infection (CDI) introduced new recommendations for managing initial and recurrent CDI. Since then, new microbiome-based therapies for preventing recurrent CDI have become available. We surveyed infectious diseases (ID) clinicians to understand their experiences, practices, and challenges in CDI management.

METHODS: An electronic survey was distributed to members of the IDSA Emerging Infections Network in May 2024, targeting ID physicians and healthcare professionals in the United States who manage adult CDI. The survey assessed treatment preferences, clinical practices, and barriers to accessing and prescribing CDI therapies.

RESULTS: Of the 500 respondents who reported treating CDI in the past year, 83% (417/500) indicated that vancomycin was their most frequently prescribed agent for initial, nonfulminant CDI. Additionally, 72% (357/498) reported that their institutional guidelines recommended vancomycin as the first-line agent. The most common barrier to fidaxomicin use was challenges with outpatient insurance coverage (82% [408/496]). Bezlotoxumab was available to 74% (370/500) of respondents, though 33% (165/497) indicated they do not use bezlotoxumab routinely. Most clinicians (87% [437/500]) had previously recommended fecal microbiota transplantation (FMT) for recurrent CDI, though only 48% (239/500) had current access to FMT using donor stool. Fecal microbiota live-jslm was available to 36% (179/500), and fecal microbiota spores live-brpk was available to 30% (150/500).

CONCLUSIONS: Significant barriers, including high costs, insurance challenges, and limited availability of CDI therapies, impact clinical decision-making and adherence to guideline recommendations.},
}

@article {pmid40597484,
year = {2025},
author = {Zhang, C and Zhang, X and Qiu, H and Song, Q and Wang, Y and Zhang, C and Zhang, Q},
title = {Fermented Gastrodia elata Bl. Intervenes gut microbiota and amino acid metabolism in zebrafish to promote 5-HT homeostasis against sleep disturbances.},
journal = {Food research international (Ottawa, Ont.)},
volume = {217},
number = {},
pages = {116757},
doi = {10.1016/j.foodres.2025.116757},
pmid = {40597484},
issn = {1873-7145},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; Zebrafish ; *Amino Acids/metabolism ; *Serotonin/metabolism ; *Gastrodia/chemistry ; Homeostasis/drug effects ; *Fermented Foods ; Fermentation ; *Sleep Wake Disorders/prevention & control ; Sleep Initiation and Maintenance Disorders/chemically induced ; Fecal Microbiota Transplantation ; },
abstract = {Sleep disturbances (SD) is a prevalent health issue in modern society. Consequences involve negative impacts on numerous aspects of physical, psychological, and daily life. This study aimed to elucidate the protective effects of Fermented Gastrodia elata Bl. (FGE) against pentylenetetrazole (PTZ)-induced SD and uncover the underlying molecular mechanisms. Our findings revealed that FGE significantly attenuated PTZ-induced insomnia behavior, circadian rhythm disturbances, and compromised gut barrier functions. Mechanistically, gut microbiota and 5-HT within the microbiota-gut-brain axis are the key regulators in short-term SD. Fecal microbiota transplantation (FMT) experiment identified gut microbiota as a key mediator and potential therapeutic target for FGE. The comprehensive analysis of 16S rRNA sequencing and metabolomic analysis showed that amino acid metabolism-related pathways as key factors of FGE intervention. Notably, omics joint analysis demonstrated a strong association between the variations of the intestinal microbiota among different groups and the notable alterations in the brain metabolomic landscape. Meanwhile, the remodeling of intestinal microbial structure and metabolites drove the homeostasis of 5-HT levels in different tissues. Importantly, exogenous keystone bacteria supplementation to sleep-deprived zebrafish restored insomnia responses and amino acid metabolism. Targeted amino acid metabolism further confirmed amino acid metabolism as the central mechanistic pathway through which FGE exerts its protective function. Collectively, Collectively, these findings suggested that FGE showed a significant preventative action on short-term SD by intervening gut microbiota and amino acid metabolism in zebrafish to promote 5-HT homeostasis, which offers perspectives into new preventive strategies of traditional Chinese medicine dietary supplements for transient insomnia.},
}

Animals
*Gastrointestinal Microbiome/drug effects
Zebrafish
*Amino Acids/metabolism
*Serotonin/metabolism
*Gastrodia/chemistry
Homeostasis/drug effects
*Fermented Foods
Fermentation
*Sleep Wake Disorders/prevention & control
Sleep Initiation and Maintenance Disorders/chemically induced
Fecal Microbiota Transplantation

@article {pmid40596796,
year = {2025},
author = {Liu, K and Wang, Y and Zhou, J and van der Meij, JJ and van der Laan, LJW and Li, P and Pan, Q},
title = {Decoding the role of the intestinal epithelium in hepatitis E virus infection using a human organoid prototype of "gut-liver" axis.},
journal = {Virology},
volume = {610},
number = {},
pages = {110615},
doi = {10.1016/j.virol.2025.110615},
pmid = {40596796},
issn = {1096-0341},
abstract = {Hepatitis E virus (HEV), a leading cause of acute viral hepatitis worldwide, is primarily transmitted via the fecal-oral route. A clinical study has reported that the intestine of a chronic hepatitis E patient is positive for HEV. However, whether the intestinal epithelium acts as a barrier for HEV transmission or whether productive enteric infection enhances transfer of the virus to the liver remains unclear. The advent of organoid technology provides a valuable platform for advancing the study of HEV-host interactions in a more physiologically relevant context. In this study, we demonstrate that primary human intestinal organoids (HIOs) efficiently support HEV replication. The infection was sustained in differentiated HIOs with specific phenotypes of intestinal cell types, namely enterocyte, goblet cell, and enteroendocrine cell lineages. Next, we constructed a gut-liver axis model using a transwell system by co-culturing HIOs with human liver-derived organoids. Importantly, infectious viral particles produced in HIOs were capable of transmission to human liver-derived organoids in this model. Bile acids are essential mediators of gut-liver crosstalk. We found that supplementing human bile or the primary bile acid chenodeoxycholic acid inhibited HEV replication in organoids via the farnesoid X receptor (FXR) signaling pathway. The effects of the secondary bile acid, ursodeoxycholic acid, were opposite and promoted viral replication. In conclusion, this model provides a novel approach to study the gut-liver axis in HEV transmission and the impact of bile acids in modulating HEV infection.},
}

@article {pmid40596758,
year = {2025},
author = {Wang, J and Tan, H and Ye, Z and Weng, S and Shi, Y and Xu, J and Liu, H and Li, J and Huang, L and Zhai, L and Luo, H and Lin, Z and Zhong, C and Tang, J and Wang, Z and Zhang, H and Zhang, B and Huang, C},
title = {Gut microbial Nordihydroguaiaretic acid suppresses macrophage pyroptosis to regulate epithelial homeostasis and inflammation.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2518338},
doi = {10.1080/19490976.2025.2518338},
pmid = {40596758},
issn = {1949-0984},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; Mice ; Fecal Microbiota Transplantation ; *Colitis/microbiology/chemically induced ; Homeostasis/drug effects ; *Macrophages/drug effects ; *Masoprocol/pharmacology/metabolism ; *Pyroptosis/drug effects ; Mice, Inbred C57BL ; Dysbiosis/microbiology ; Male ; Dextran Sulfate ; Disease Models, Animal ; Intestinal Mucosa/drug effects ; Aging ; Inflammatory Bowel Diseases/microbiology ; Bacteria/classification/genetics/isolation & purification/metabolism ; Humans ; },
abstract = {BACKGROUND: Aging is associated with increased severity of inflammatory bowel disease (IBD). Gut senescence and altered environmental factors contribute to changes in the intestinal metabolome, particularly in frail older individuals. However, the role of age-associated dysbiosis, characterized by a decline in beneficial gut microbiota and their metabolites, in exacerbating IBD remains unclear.

METHODS: To investigate the impact of aging-associated dysbiosis on colitis development, we employed fecal microbiota transplantation (FMT) in wild-type and IL-10-deficient mice. Aged mice were treated with gut microbiota from either young or aged mice and then subjected to dextran sulfate sodium (DSS) to induce experimental colitis. 16S rDNA sequencing and metabolomics were used to analyze microbial and metabolite profiles. Single-cell RNA sequencing (scRNA-seq) was performed to characterize lamina propria CD45[+] immune cell composition.

RESULTS: Aged mice receiving microbiota from young mice exhibited less severe colitis than those receiving microbiota from aged mice, as evidenced by reduced disease activity, weight loss, and colonic shortening. Besides, aged mice displayed a significant decrease in the Lactobacillus population, accompanied by a reduction in Nordihydroguaiaretic acid (NDGA) levels. Decreased fecal NDGA levels were also observed in both IBD patients and elderly individuals. Administration of NDGA alleviated experimental colitis by downregulating the GSDMD/NR4A1/NLRP3 axis-mediated macrophage pyroptosis. Deletion of GSDMD in macrophages significantly diminished the protective effect of NDGA on colitis.

CONCLUSIONS: Our findings demonstrate that aging is associated with dysbiosis and reduced NDGA production, which increases susceptibility to intestinal inflammation. Gut microbial NDGA exhibits potential anti-inflammatory activity in colitis, suggesting a promising therapeutic target for aged-related IBD.},
}

Animals
*Gastrointestinal Microbiome/drug effects
Mice
Fecal Microbiota Transplantation
*Colitis/microbiology/chemically induced
Homeostasis/drug effects
*Macrophages/drug effects
*Masoprocol/pharmacology/metabolism
*Pyroptosis/drug effects
Mice, Inbred C57BL
Dysbiosis/microbiology
Male
Dextran Sulfate
Disease Models, Animal
Intestinal Mucosa/drug effects
Aging
Inflammatory Bowel Diseases/microbiology
Bacteria/classification/genetics/isolation & purification/metabolism
Humans

@article {pmid40593111,
year = {2025},
author = {Zhou, X and Wei, C and Liu, J and Xia, X and Wang, L and Li, X},
title = {Cold environment regulates ischemic stroke through modulation of gut microbiota.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {21558},
pmid = {40593111},
issn = {2045-2322},
support = {42275197//National Natural Science Foundation of China/ ; TJYXZDXK-065B//Tianjin Key Medical Discipline (Specialty) Construction Project/ ; TJWJ2023XK007//the Key Projects of Tianjin Municipal Health Commission/ ; },
mesh = {*Gastrointestinal Microbiome/physiology ; *Cold Temperature/adverse effects ; Animals ; Fecal Microbiota Transplantation ; Mice ; Male ; Mice, Inbred C57BL ; Humans ; Dysbiosis/microbiology ; *Ischemic Stroke/microbiology/etiology ; Female ; Middle Aged ; Platelet Aggregation ; Aged ; Methylamines ; },
abstract = {Many diseases are influenced by environmental temperature, and recent studies have confirmed that cold exposure increases the risk of conditions such as ischemic stroke (IS). However, direct evidence supporting this hypothesis is lacking, and the molecular mechanisms through which cold exposure affects IS remain unclear. In this study, we found that chronic cold exposure increased platelet aggregation and the levels of certain inflammatory factors in high-risk stroke patients (HR), thereby increasing the risk of IS. Furthermore, before and after a cold wave, we observed gut microbiota dysbiosis in the HR group, including reduced relative abundance differences in Lachnospiraceae and Ruminococcaceae. The relative abundances of the Prevotella_9 and Catenibacterium genera increased, whereas that of Anaerostipes decreased. Notably, the results of fecal microbiota transplantation (FMT) indicated that cold-adapted microbiota transplantation partially replicated the microbiota characteristics of each donor subject and replicated the effects of cold exposure in C57BL/6J mice. Cold exposure impaired intestinal barrier function and interfered with microbial functions, such as increased lipid metabolism and LPS production, particularly by increasing the levels of TMAO derived from the gut microbiota. Our findings identify the significant role of abnormal gut microbiota-derived metabolites in cold exposure-related IS and highlight the potential opportunity to prevent or treat cold-related IS through the modulation of the gut microbiota.},
}

*Gastrointestinal Microbiome/physiology
*Cold Temperature/adverse effects
Animals
Fecal Microbiota Transplantation
Mice
Male
Mice, Inbred C57BL
Humans
Dysbiosis/microbiology
*Ischemic Stroke/microbiology/etiology
Female
Middle Aged
Platelet Aggregation
Aged
Methylamines

@article {pmid40593020,
year = {2025},
author = {Yue, Y and Yao, B and Liao, F and He, Z and Sangsawad, P and Yang, S},
title = {Fecal microbiota transplantation improves Sansui duck growth performance by balancing the cecal microbiome.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {22403},
pmid = {40593020},
issn = {2045-2322},
support = {31960682//The National Nature Science Foundation of China/ ; 31960682//The National Nature Science Foundation of China/ ; 31960682//The National Nature Science Foundation of China/ ; 31960682//The National Nature Science Foundation of China/ ; 31960682//The National Nature Science Foundation of China/ ; },
abstract = {Improving growth performance is vital in poultry production. Although several studies have established associations between gut microbiota and growth, the direct impacts remain unclear. A total of 120 1-day-old Sansui ducks were randomly assigned to the FMT and CON groups. From the 1st day, ducks in the FMT group were orally administrated with 0.5 mL fecal microbiota suspension for three consecutive days, while sterile PBS solution was used as a substitute in the CON group. The results revealed that FMT improved average daily gain (ADG) (P < 0.001) and body weight (BW) (P < 0.001), with a tendency for a better feed conversion rate (FCR) (P = 0.062). LEfSe analysis indicated a significant increase in the abundance of the Lactobacillus (P < 0.001), Bifidobacterium (P = 0.006), Megamonas (P = 0.008), and Subdoligranulum (P = 0.005) in the FMT group. Similarly, the phyla Firmicutes/Bacteroidetes ratio was higher in the FMT group compared to the CON group. Additionally, the ACE, Chao, and Shannon indices were also significantly higher in the FMT group (P < 0.001). To sum up, FMT enhanced growth performance, which could be associated with reducing proinflammatory pathogen colonization in the duck cecum. This modulating effect likely results from increased microbial diversity and the enrichment of beneficial bacteria.},
}

@article {pmid40592776,
year = {2025},
author = {Zhang, X and Ishikawa, D and Nagahara, A},
title = {Fecal Microbiota Transplantation for Immune Regulation: Improving Ulcerative Colitis and Enhancing Cancer Immunotherapy.},
journal = {International immunology},
volume = {},
number = {},
pages = {},
doi = {10.1093/intimm/dxaf038},
pmid = {40592776},
issn = {1460-2377},
abstract = {The gut microbiota plays an integral role in maintaining health and regulating various host functions, including immune responses. Fecal microbiota transplantation (FMT) has emerged as a promising therapeutic approach to restore gut microbial balance. Although widely recognized for its efficacy in treating ulcerative colitis (UC), FMT is now being investigated as an adjuvant therapy to enhance the efficacy of immune checkpoint inhibitors (ICIs) in cancer treatment. This review summarizes the clinical applications of FMT in UC treatment and its potential role in cancer immunotherapy. FMT exhibits varying degrees of efficacy in the treatment of UC, with differences in outcomes attributed to variations in administration methods and donor selection. In cancer therapy, FMT has demonstrated the potential to improve ICI responses, particularly in patients with melanoma. However, its effects on other cancers remain unclear. Although FMT holds promise for UC and cancer immunotherapy, challenges such as inconsistent clinical outcomes and methodological variations persist. Standardized protocols and mechanistic studies are crucial to optimize FMT-based therapeutic strategies, and further research is required to establish its efficacy under diverse clinical conditions.},
}

@article {pmid40592615,
year = {2025},
author = {Sasaki, K and Takeshima, Y and Fujino, A},
title = {Reproducing in vitro artificial gut microbiota using glycerol stocks of fecal cultures combined with different prebiotic additives.},
journal = {Journal of bioscience and bioengineering},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jbiosc.2025.06.002},
pmid = {40592615},
issn = {1347-4421},
abstract = {Artificial human microbiota can be produced in gut simulators from cryopreserved stocks. They are used for in vitro fermentation models and as alternative material for fecal microbiota transplantation therapy. However, current methods have limited information on microbial structure at the genus level and present challenges during cryopreservation. In this study, we used an edible glycerol stock of fecal batch culture instead of fresh feces to create artificial gut microbiota. Three glycerol stocks, generated through in vitro fecal fermentation with different prebiotic additives (such as fructooligosaccharide, xylan, pectin, and guar gum), were combined. Profiling via 16S rRNA gene amplicon sequencing revealed that the artificial gut microbiota derived from the combined glycerol stocks showed more amplicon sequence variants than those from a single glycerol stock. In the artificial microbiota, relative abundance values of common genera such as Bifidobacterium, Bacteroides, Prevotella, Faecalibacterium, and Escherichia were more than 10 % of those found in the original feces. Other commensal genera such as Collinsella, Anaerobutyricum hallii (formerly Eubacterium hallii) group, Anaerostipes, Blautia, Dorea, Lachnospiraceae UCG-004, and Oscillospiraceae UCG-003 were similarly maintained. Our data indicated that combining glycerol stocks of fecal cultures with different additives in a batch-type gut simulator is a useful option for producing artificial gut microbiota, the taxonomic compositions of which are comparable to those of the original feces.},
}

@article {pmid40592538,
year = {2025},
author = {Cymbal, M and Chatterjee, A and Baggott, B},
title = {Fecal microbiota transplantation: Current evidence and future directions.},
journal = {Cleveland Clinic journal of medicine},
volume = {92},
number = {7},
pages = {421-428},
doi = {10.3949/ccjm.92a.24107},
pmid = {40592538},
issn = {1939-2869},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods/trends ; *Clostridium Infections/therapy ; *Gastrointestinal Microbiome ; Clostridioides difficile ; Dysbiosis/therapy ; },
abstract = {As we advance our understanding of the gut microbiota, the implications of dysbiosis are becoming increasingly apparent. Fecal microbiota transplantation (FMT), a well-established procedure, is recognized for effectively treating recurrent Clostridioides difficile infection, prompting further investigation into its other possible clinical applications. Donor selection and screening are essential to ensure safety and efficacy. Product development and standardization, such as the US Food and Drug Administration-approved live biotherapeutic products Rebyota and Vowst, are helping efforts to evaluate FMT for other gastrointestinal and extraintestinal diseases. However, additional clinical trials are needed to support its use beyond recurrent C difficile infection.},
}

Humans
*Fecal Microbiota Transplantation/methods/trends
*Clostridium Infections/therapy
*Gastrointestinal Microbiome
Clostridioides difficile
Dysbiosis/therapy

@article {pmid40591032,
year = {2025},
author = {Abebaw, D and Akelew, Y and Adugna, A and Tegegne, BA and Teffera, ZH and Belayneh, M and Fenta, A and Selabat, B and Kindie, Y and Baylie, T and Mekuriaw, MG and Jemal, M and Atnaf, A},
title = {Immunomodulatory properties of the gut microbiome: diagnostic and therapeutic potential for rheumatoid arthritis.},
journal = {Clinical and experimental medicine},
volume = {25},
number = {1},
pages = {226},
pmid = {40591032},
issn = {1591-9528},
mesh = {Humans ; *Arthritis, Rheumatoid/therapy/diagnosis/immunology/microbiology ; *Gastrointestinal Microbiome/immunology ; Dysbiosis/immunology ; Probiotics/therapeutic use ; *Immunomodulation ; Fecal Microbiota Transplantation ; Biomarkers ; Animals ; },
abstract = {Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by persistent joint inflammation, synovial hyperplasia, and progressive joint destruction. Despite advancements in biologic disease-modifying antirheumatic drugs (bDMARDs) and TNF-α blockers, many RA patients still require more effective treatment options. Although genetic and environmental factors play a role in RA development, recent studies have emphasized the influence of the gut microbiota on disease onset and progression. Dysbiosis, or an imbalance in the gut microbial composition, has been linked to immune dysregulation, increased intestinal permeability, and systemic inflammation, all contributing to RA development. Research has revealed changes in the gut microbiome of RA patients, including an increased prevalence of Prevotella copri and a decreased presence of beneficial microbes such as Bifidobacterium, Bacteroides, and Lactobacillus. RA patients exhibit altered metabolite profiles, with reduced levels of short-chain fatty acids (SCFAs), such as acetate, propionate, and butyrate, which are linked to immune regulation and intestinal barrier function. Specific metabolites, such as L-arginine, phosphorylcholine, and arachidonic acid, have potential as RA biomarkers, with predictive value for diagnosis. Therapeutic approaches focusing on the microbiome, including probiotics, fecal microbiota transplantation, and traditional medicines, show promise in alleviating RA symptoms and regulating immune function. This review provides an updated overview of the immunomodulatory effects of the gut microbiome and explores its potential applications in the diagnosis and treatment of RA.},
}

Humans
*Arthritis, Rheumatoid/therapy/diagnosis/immunology/microbiology
*Gastrointestinal Microbiome/immunology
Dysbiosis/immunology
Probiotics/therapeutic use
*Immunomodulation
Fecal Microbiota Transplantation
Biomarkers
Animals

@article {pmid40589476,
year = {2025},
author = {Olajide, TS and Ijomone, OM},
title = {Targeting gut microbiota as a therapeutic approach for neurodegenerative diseases.},
journal = {Neuroprotection},
volume = {3},
number = {2},
pages = {120-130},
pmid = {40589476},
issn = {2770-730X},
abstract = {Recent evidence suggests a more important role of the gut microbiota in neurodegenerative diseases (NDDs) given its relationship through the microbiota-gut-brain as an active communication system aiding in maintaining homeostasis between the brain and the gut. This review focuses on how modulation of gut microbiota can serves as a therapeutic strategy for NDDs, emphasizing the neuroprotective effects of probiotics. Probiotics are live microorganisms that confer health benefits, and their interaction with gut-microbiota influences neurogenesis, neurotransmitter regulation, and neuroinflammation. Recent advancements, including germ-free animal models, fecal microbiota transplantation (FMT), and diverse probiotic strains, have revealed the underlying mechanisms linking gut health to brain function. Notably, several Lactobacillus and Bifidobacterium species have been shown to exert neuroprotective effects via the upregulation of neurotrophic factors such as brain-derived neurotrophic factor and enhancing mitochondrial function through reducing the impacts of oxidative stress. Interestingly, FMT has exhibited a degree of success in overcoming cognitive impairment and motor deficits in preclinical studies and clinical trials. However, further research is warranted to explore its therapeutic potential in humans. Overall, this review highlights the significant role of gut microbiota in NDDs and advocates for gut-targeted interventions as innovative approaches to mitigate these diseases.},
}

@article {pmid40589142,
year = {2025},
author = {Tiwari, R and Paswan, A and Tiwari, G and Reddy, VJS and Posa, MK},
title = {Perspectives on Fecal Microbiota Transplantation: Uses and Modes of Administration.},
journal = {Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology},
volume = {41},
number = {},
pages = {e20250014},
doi = {10.62958/j.cjap.2025.014},
pmid = {40589142},
issn = {1000-6834},
mesh = {*Fecal Microbiota Transplantation/methods ; Humans ; *Gastrointestinal Microbiome ; Feces/microbiology ; *Nervous System Diseases/therapy ; },
abstract = {Fecal microbiota Transplantation (FMT), often referred to as stool transplantation, fecal transfusion, and fecal bacteria therapy, is considered one of the most medical innovations of the 20th century. Fecal microbiota Transplantation entails filtering and dilution of a healthy donor's feces before injecting it into the recipient's digestive system. In China, it was first administered orally in the fourth century for diarrhea and food poisoning under the name "Yellow Soup." It has recently been widely employed in a variety of clinical settings, including cases of Clostridium difficile infection that are recurring and resistant. By replacing the unhealthy intestinal microbiota with a healthy bacterial community, the FMT treatment aims to enhance the intestinal flora. It also looks at neurological conditions where alterations in gut microbiota are prevalent. We have discussed FMT in the context of its use in conditions affecting the nerve system, such as neurological and other conditions (multiple sclerosis, Parkinson's disease, Alzheimer's disease, stroke, epilepsy, Amyotrophic lateral sclerosis, Tourette syndrome, neuropathic pain, Huntington's diseases, etc.), as well as the role of gut microbiota in many neurological disorders.},
}

*Fecal Microbiota Transplantation/methods
Humans
*Gastrointestinal Microbiome
Feces/microbiology
*Nervous System Diseases/therapy

@article {pmid40589086,
year = {2025},
author = {Yadav, M and Gupta, A and Mathew, B and Tripathi, G and Dalal, N and Sharma, N and Yadav, P and Yadav, G and Singh, R and Bindal, V and Saif, R and Yadav, S and Sharma, N and Pandey, S and Bhat, SH and Singh, R and Kumar, J and Kushwaha, M and Khan, T and Sharma, NK and Bhaskar, A and Dwivedi, VP and Kumar, A and Kumar, N and Tripathi, DM and Trehanpati, N and Anupama Kumara, and Sharma, S and Sarin, SK and Maras, JS},
title = {Circulating urobilinogen contributes to Inflammation, Intestinal Permeability and corticosteroid non-response in Severe Alcohol-associated Hepatitis.},
journal = {Molecular therapy : the journal of the American Society of Gene Therapy},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ymthe.2025.06.041},
pmid = {40589086},
issn = {1525-0024},
abstract = {Severe alcohol-associated hepatitis (SAH) is a life-threatening condition with high mortality rates and poor response to prednisolone therapy. Identifying reliable early predictors of therapy response and survival is critical. Plasma metabolomics was conducted on 70 SAH patients (50 responders, 20 non-responders) to identify biomarkers for non-response and early mortality. These findings were validated in a cohort of 153 patients and an independent cohort of 245 using high resolution mass spectrometry, machine learning, and severity indices. Temporal metabolic changes indicated interactions between the host and microbiome, with a focus on inflammation and intestinal permeability. Plasma metabolomics revealed that non-responders had significantly higher urobilinogen levels (3.6-fold change). Additionally, a decrease in alpha/beta diversity and temporal metabolic inactivity characterized non-responders. Plasma urobilinogen levels predicted non-response (AUC>0.97) and identified non-survivors (AUC=0.94) with a threshold of >0.07 mg/ml. Urobilinogen levels correlated with bacterial peptides belonging to Firmicutes and Proteobacteria, neutrophil activation, oxidative stress, and pro-inflammatory cytokine production. These changes contributed to non-response by increasing glucocorticoid receptor β expression and compromising intestinal permeability. Fecal microbiota transplantation decreased urobilinogen levels by reducing bilirubin reductase gene-containing microbiota. Plasma urobilinogen >0.07 mg/ml could predict early mortality, and modulation of the gut microbiome may improve outcomes in SAH patients.},
}

@article {pmid40588803,
year = {2025},
author = {Hu, J and Feng, T and Zhang, L and Zhou, Q and Zhu, L},
title = {Leveraging gut microbiota for enhanced immune checkpoint blockade in solid tumor therapy.},
journal = {Chinese medical journal},
volume = {},
number = {},
pages = {},
pmid = {40588803},
issn = {2542-5641},
abstract = {Gut microbiota can modulate antitumor immunity and influence immune checkpoint blockade (ICB) therapy efficacy and treatment-associated toxicity. Variations in the therapeutic effect of ICB among individuals are partially attributed to microbiota. This review summarizes current knowledge on how specific bacterial species enhance or hinder ICB outcomes by regulating immune cell activation, antigen presentation, and systemic inflammation. The review further outlines translational strategies to optimize ICB, including microbiota-targeted interventions (e.g., prebiotics, fecal microbiota transplantation, and metabolite therapies) to overcome resistance and mitigate treatment-related toxicities, focusing on immune-related colitis. Additionally, emerging microbial biomarkers in melanoma, lung cancer, and hepatobiliary cancers that predict ICB response are discussed, highlighting the gut microbiome as a potential target for personalized cancer immunotherapy. By integrating mechanistic insights with clinical evidence, this review underscores the potential of microbiota-centered approaches to improve patient outcomes in ICB-based treatments, emphasizing the pivotal role of the gut microbiota in modulating both therapeutic efficacy and immune-related adverse events.},
}

@article {pmid40586386,
year = {2025},
author = {Li, K and Arbab, S and Du, Q and Zhou, J and Chen, Y and Tian, Y and Qijie, L and Ullah, H and Zhang, B},
title = {Regulatory and Influencing Factors of Digestive Function in Elderly People: Roles of the Gut Microbiota and Nutritional Interventions.},
journal = {Aging and disease},
volume = {},
number = {},
pages = {},
doi = {10.14336/AD.2025.0565},
pmid = {40586386},
issn = {2152-5250},
abstract = {Aging is a natural and gradual biological process through which living organisms undergo physical, physiological, and sometimes psychological changes over time. Aging is commonly associated with a decline in gastrointestinal function, leading to various digestive disorders that impact the quality of life of older adults. The gut microbiota is a highly complex ecosystem that plays crucial roles in digestion, metabolic processes, immune functions, and overall health. However, emerging evidence indicates that many elderly individuals maintain relatively stable digestive health, suggesting the influence of modifiable regulatory factors. In this review, we describe the key physiological, microbial, and nutritional factors that regulate and influence digestive function in an aging population. Additionally, we explored the impact of age-associated alterations in the gut microbiota on digestive health challenges in older adults and emphasized the therapeutic potential of targeted nutritional intervention approaches, such as dietary modifications, prebiotics, probiotics, and symbiotic and fecal microbiota transplantation, which have shown promise in rebalancing the gut microbiome and reducing inflammation.},
}

@article {pmid40585700,
year = {2025},
author = {Hamza Saeed, M and Qamar, S and Ishtiaq, A and Umaira Khan, Q and Atta, A and Atta, M and Ishtiaq, H and Khan, M and Saeed, MR and Iqbal, A},
title = {Fecal Microbiota Transplantation (FMT) in Clostridium difficile Infection: A Paradigm Shift in Gastrointestinal Microbiome Modulation.},
journal = {Cureus},
volume = {17},
number = {5},
pages = {e85054},
doi = {10.7759/cureus.85054},
pmid = {40585700},
issn = {2168-8184},
abstract = {Clostridium difficile (C. difficile) infection (CDI) poses a tremendous clinical challenge, especially in patients with recurrent disease and antibiotic resistance. Fecal microbiota transplantation (FMT) has become a new therapeutic strategy for restoring gut microbiota and decreasing CDI recurrence. The study aims to assess the clinical effectiveness of FMT in adult subjects with recurrent or refractory CDI, determine its effect on gut microbiome diversity, and track safety outcomes and rates of recurrence post-treatment. FMT was compared against standard antibiotic treatments to establish its efficacy in decreasing infection persistence and improving patients' quality of life. This study examines the efficacy, safety, and modulation of microbiota by FMT in an ensemble of 250 patients diagnosed with CDI, with equal gender distribution and a mean age of 55.61. Among the study participants, 131 (52.4%) underwent FMT by various routes of administration, including 66 (25.2%) through colonoscopy, 73 (29.2%) via a nasogastric tube, 60 (24.0%) via enema, and 54 (21.6%) through oral capsule administration. The success rate for FMT was reported as 88 (35.2%), partial success at 74 (29.6%), and treatment failure at 88 (35.2%). CDI recurrence was reported in 130 (52.0%) of patients after FMT. The gut microbiome enhanced diversity, measured in terms of the Shannon Diversity Index, increased significantly from 3.96 before FMT to 5.88 after FMT, thus indicating a favorable impact on gut microbial composition. Furthermore, 132 (52.8%) converted from C. difficile polymerase chain reaction (PCR) toxin positive to negative, corroborating successful pathogen clearance. On secondary outcomes, the quality of life in patients improved in 90 (36%), antibiotic dependence was reduced in 88 (35.2%), and hospitalization was lessened in 72 (28.8%). Inflammatory markers, such as white blood cell (WBC) counts and C-reactive protein (CRP), went downward but did not reach statistical significance. Logistic regression analysis identified age, severity of CDI, and prior exposure to antibiotics as the main predictors for the efficacy of FMT (p < 0.05). It is concluded that FMT is a promising alternative treatment for recurrent CDI through modulation of gut microbiota and decreasing the severity of infection. Future work is, however, required to establish treatment protocols with optimized results for long-term effectiveness and minimized recurrence risks.},
}

@article {pmid40585508,
year = {2025},
author = {Zhu, B and Wu, H and Zhang, H and Song, Q and Xiao, Y and Yu, B},
title = {Gut microbiota from voluntary exercised mice protects the intestinal barrier by inhibiting neutrophil extracellular trap formation.},
journal = {iScience},
volume = {28},
number = {6},
pages = {112763},
doi = {10.1016/j.isci.2025.112763},
pmid = {40585508},
issn = {2589-0042},
abstract = {Ulcerative colitis is an inflammatory bowel disease characterized by impaired intestinal barrier function, dysregulated immune responses, and alterations in the gut microbiota. Excessive formation of neutrophil extracellular traps (NETs), driven by peptidyl arginine deiminase 4 (PAD4) activity, contributes to inflammation modulated by the gut microbiota. In this study, we used a mouse model of dextran sulfate sodium-induced colitis to investigate the effects of voluntary exercise and its underlying mechanisms. Exercise preconditioning attenuated colitis severity, maintained intestinal barrier integrity, normalized gut microbiota composition, and suppressed NET formation. PAD4 inhibition further enhanced these effects. By contrast, the depletion of the gut microbiota by antibiotics largely abolished the benefits of exercise. Additionally, fecal microbiota transplantation from exercised mice recapitulated these protective effects. These findings elucidate the interplay among exercise, gut microbiota, and PAD4-mediated NET formation. Targeting these pathways may offer promising therapeutic strategies for colitis.},
}

@article {pmid40584885,
year = {2025},
author = {Guo, M and Gao, H and Wang, Y and Xiang, Y},
title = {Exploring the role of gut microbiota in Parkinson's disease: insights from fecal microbiota transplantation.},
journal = {Frontiers in neuroscience},
volume = {19},
number = {},
pages = {1574512},
doi = {10.3389/fnins.2025.1574512},
pmid = {40584885},
issn = {1662-4548},
abstract = {As a common neurodegenerative disease, Parkinson's disease (PD) is typified by α-synuclein (α-syn) aggregation and progressive degeneration of dopaminergic neurons within the substantia nigra. Clinical manifestations encompass motor symptoms and non-motor aspects that severely impair quality of life. Existing treatments mainly address symptoms, with no effective disease-modifying therapies available. The gut microbiota refers to the community of microorganisms that colonize the intestinal tract. The gut microbiota, gut, and brain are all connected via a complicated, mutual communication pathway known as the "gut microbiota-gut-brain axis." Gut microbiota dysbiosis is strongly linked to the onset and course of PD, according to growing data. In individuals with PD, gut dysbiosis correlates with clinical phenotype, disease duration, severity, and progression rates. Mechanistically, gut dysbiosis contributes to PD through enhanced intestinal permeability, increased intestinal inflammation and neuroinflammation, abnormal α-syn aggregation, oxidative stress, and reduced neurotransmitter synthesis. Therefore, focusing on the gut microbiota is regarded as a potentially effective treatment strategy. Fecal microbiota transplantation (FMT) is an emerging approach to modulate gut microbiota, with the goal of recovering microbiota diversity and function by transferring functional intestinal flora from healthy individuals into patients' gastrointestinal tracts. FMT is expected to become a promising therapy of PD and has a broad research and application prospect. Evidence suggests that FMT may restore gut microbiota, ease clinical symptoms, and provide potential neuroprotective benefits. However, the precise therapeutic mechanisms of FMT in PD remain uncertain, necessitating further research to clarify its effectiveness. This review examines alterations in gut microbiota linked to PD, mechanisms through which gut dysbiosis influences the disease, and the latest advancements in FMT research for treating PD, setting the stage for its clinical application.},
}

@article {pmid40583967,
year = {2025},
author = {Wang, H and Tian, J and Mi, J},
title = {Clinical effectiveness of fecal microbial transplantation for metabolic syndrome: Advances in clinical efficacy and multi-omics research.},
journal = {Current research in microbial sciences},
volume = {9},
number = {},
pages = {100415},
doi = {10.1016/j.crmicr.2025.100415},
pmid = {40583967},
issn = {2666-5174},
abstract = {Even though metabolic syndrome (MetS) poses a serious risk to human health and life, existing treatment approaches are not very effective. The impact of gut bacteria on host metabolism has been the subject of numerous research, and fecal microbial transplantation (FMT) has demonstrated great promise in reducing insulin resistance and abdominal obesity in individuals with metabolic syndrome. These FMT investigations have connected alterations in the gut microbiota to clinical indicators of insulin resistance and obesity, in addition to using high-throughput methods to analyze the gut microbiome, metabolome, and epigenome of peripheral blood mononuclear cells in patients with MetS. It is still necessary to clarify and assess the clinical effectiveness and mode of action of FMT in the management of MetS. This review examines the connection between gut bacteria and MetS, the effectiveness of FMT as a treatment, and the changes in the gut microbiome, metabolome, epigenome, and other histones following the intervention. We also discuss the safety of FMT and suggest areas for further investigation.},
}

@article {pmid40582671,
year = {2025},
author = {Bi, R and Abbas, W and Li, J and Huang, J and Hu, J and Guo, F and Wang, Z},
title = {Yeast β-glucan ameliorated Salmonella-induced gut impairment in broiler chickens by modulating gut microbiome.},
journal = {International journal of biological macromolecules},
volume = {},
number = {},
pages = {145630},
doi = {10.1016/j.ijbiomac.2025.145630},
pmid = {40582671},
issn = {1879-0003},
abstract = {Yeast β-glucan (YG) was reported to control Salmonella infection in poultry. Gut microbiota plays an important role in regulating immune functions and intestinal health. However, it is still unclear whether YG protects chickens from Salmonella infection by regulating gut microbiota. The impacts of YG on gut health of chickens infected with Salmonella enteritidis (SE) was investigated through histochemical and immunological methods, along with microbiomics. The role of gut microbiome induced by YG treatment in combating Salmonella infection was explored through FMT. Our findings showed that YG administration significantly ameliorated SE-induced gut impairment by decreasing gut permeability, enhancing intestinal barrier function, inhibiting intestinal inflammation, reducing Salmonella colonization, lowering g_Streptococcus and g_Ligilactobacillus but increasing g_Blautia, g_Bacillus and g_Faecalibacterium relative abundance. Transplantation fecal microbiota from YG-treated healthy donor chickens to antibiotic-treated recipient chicks significantly attenuated gut injury caused by SE infection through decreasing Salmonella colonization and invasion along with intestinal permeability, improving gut morphology, upregulating intestinal tight junction genes and proteins expression, downregulating pro-inflammatory cytokines expression. Additionally, FMT remarkably increased g_Bacteroides and g_Faecalibacterium relative abundances and butyric acid level, decreased g_Ruminococcus-torque-group relative abundance in the cecum.Collectively, we assume that yeast β-glucan alleviated Salmonella-induced gut impairment, a mechanism that is dependent on the gut commensal Bacteroides and Faecalibacterium.},
}

@article {pmid40581627,
year = {2025},
author = {Nørgaard, JC and Marandi, RZ and Ilett, EE and Gulay, A and Paredes, R and Lundgren, JD and Jørgensen, M and Sengeløv, H},
title = {The gut microbiome and its resistome as predictors of clinical infections and phenotypic antibiotic resistance in hematopoietic stem cell transplant recipients.},
journal = {The Journal of infectious diseases},
volume = {},
number = {},
pages = {},
doi = {10.1093/infdis/jiaf330},
pmid = {40581627},
issn = {1537-6613},
abstract = {A relationship between the gut microbiome composition, its resistome, and risk of clinical infections may exist and was explored here using 663 shotgun-sequenced fecal samples from 276 stem cell transplant patients. E. faecium, E. coli, and E. faecalis were the three most prevalent causes of clinical infection, with vancomycin resistance in E. faecium as the most common antibiotic resistance feature. Associations between the gut microbiome, resistome, and clinical infections were tested, with significant findings (FDR<0.05) evaluated in multivariable analysis. A 10% increase in gut abundance of E. faecium was positively associated with subsequent clinical infection with E. faecium (OR=1.14, p=0.02). Additionally, a 1% increase in vanA gene abundance was positively associated with vancomycin-resistant E. faecium infection (OR=1.27, p<0.01). Here we used metagenomics to enhance the understanding of infectious sources and to identify patients at risk of clinical infection with antibiotic-resistant bacterial strains.},
}

@article {pmid40580532,
year = {2025},
author = {Urbonas, T and Petrauskas, D and Kiudelis, V and Jonaitis, L and Skieceviciene, J and Gedgaudas, R and Kiudeliene, E and Valantiene, I and Zykus, R and Varkalaite, G and Inciuraite, R and Trapenske, E and Kulokiene, U and Jonaitis, P and Ramonaite, R and Velickiene, J and Zvirbliene, A and Morkunas, E and Kuliaviene, I and Sumskiene, J and Adamonis, K and Macas, A and Kupcinskiene, K and Lukosiene, L and Janciauskas, D and Poskiene, L and Vitkauskiene, A and Ianiro, G and Gasbarrini, A and Kiudelis, G and Kupcinskas, J},
title = {Fecal Microbiome Transplantation for Recurrent CDI: Treatment Efficacy and Safety with Oral Capsules.},
journal = {Journal of gastrointestinal and liver diseases : JGLD},
volume = {34},
number = {2},
pages = {199-204},
doi = {10.15403/jgld-5990},
pmid = {40580532},
issn = {1842-1121},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods/adverse effects ; Male ; Female ; Retrospective Studies ; Middle Aged ; Treatment Outcome ; Administration, Oral ; *Clostridium Infections/therapy/microbiology/diagnosis ; Aged ; Capsules ; Recurrence ; *Clostridioides difficile ; Adult ; Anti-Bacterial Agents/administration & dosage ; Time Factors ; Feces/microbiology ; },
abstract = {BACKGROUND AND AIMS: Fecal microbiota transplantation is an effective treatment method for recurrent Clostridioides difficile infection. Widely used enteric tube and colonoscopy methods demonstrate excellent efficacy and safety results. Recent data suggest that new fecal microbiota transplantation methods using oral capsules may provide a less invasive approach. In this study, we aimed to compare primary fecal microbiota transplantation efficacy as well as short- and long-term safety of two different administration routes: oral capsules and enteric tube.

METHODS: This retrospective study included 60 consecutive patients who underwent fecal microbiota transplantation for recurrent Clostridioides difficile infection. Thirty participants received 50 oral capsules containing frozen material for a single day and 30 patients received fecal microbiota transplantation via nasoenteric tube. All patients received standard treatment with oral vancomycin 500 mg q.i.d. for at least five days before the procedure. After intervention, patients were followed up for at least six months. Data on Clostridioides difficile infection recurrences and health status were collected and analyzed.

RESULTS: The oral capsules group consisted of 30 patients. Among them, 22 (73.3%) participants experienced resolution of symptoms after a single fecal microbiota transplantation, while eight (26.7%) patients developed recurrent diarrhea within eight weeks. The other 30 patients received treatment via nasoenteric tube. Among them, 24 (80%) patients were cured after a single fecal microbiota transplantation, while six (20%) experienced recurrent disease within eight weeks. The primary efficacy did not show significant differences between the two groups (p=0.85). Throughout the follow-up period, no serious adverse events or fecal microbiota transplantation related deaths were reported in both groups.

CONCLUSIONS: Fecal microbiota transplantation with frozen oral capsules is a safe, less invasive method with comparable efficacy to nasoenteric administration route.},
}

Humans
*Fecal Microbiota Transplantation/methods/adverse effects
Male
Female
Retrospective Studies
Middle Aged
Treatment Outcome
Administration, Oral
*Clostridium Infections/therapy/microbiology/diagnosis
Aged
Capsules
Recurrence
*Clostridioides difficile
Adult
Anti-Bacterial Agents/administration & dosage
Time Factors
Feces/microbiology

@article {pmid40579140,
year = {2025},
author = {Zhu, Y and Zhu, Z and Wu, P},
title = {[Pentosan polysulfate alleviates cyclophosphamide-induced interstitial cystitis/bladder pain syndrome in mice by modulating gut microbiota and bile acid metabolism].},
journal = {Nan fang yi ke da xue xue bao = Journal of Southern Medical University},
volume = {45},
number = {6},
pages = {1270-1279},
pmid = {40579140},
issn = {1673-4254},
support = {82370782//National Natural Science Foundation of China/ ; },
mesh = {Animals ; *Cystitis, Interstitial/chemically induced/drug therapy ; *Gastrointestinal Microbiome/drug effects ; *Pentosan Sulfuric Polyester/pharmacology/therapeutic use ; Cyclophosphamide/adverse effects ; Mice, Inbred C57BL ; Female ; Mice ; *Bile Acids and Salts/metabolism ; Urinary Bladder ; Fecal Microbiota Transplantation ; Humans ; },
abstract = {OBJECTIVES: To investigate the therapeutic efficacy and mechanism of pentosan polysulfate (PPS) for cyclophosphamide (CYP)-induced interstitial cystitis/bladder pain syndrome (IC/BPS) in mice.

METHODS: Female C57BL/6 mice (6-8 weeks old) were randomized into control group, PPS treatment (25 mg/kg via gavage for 3 weeks) group, CYP treatment (3 separate intraperitoneal injections at 50 mg/kg in week 4), and CYP+PPS treatment group. Gut microbiota alterations of the mice were analyzed using 16S rDNA sequencing and non-targeted metabolomics. Fecal microbiota transplantation (FMT) was performed in CYP-treated recipient mice and those treated with both CYP and PPS. In the in vitro experiment, LPS-stimulated human bladder epithelial cells (SV-HUC-1) were used to assess the effects of deoxycholic acid (DCA) and TGR5 signaling inhibitor SBI-115 on barrier functions of bladder epithelial cells.

RESULTS: PPS treatment significantly improved the mechanical pain thresholds, restored the urodynamic parameters, and attenuated bladder inflammation and barrier dysfunction in CYP-treated mice. Mechanistically, PPS enriched the abundance of Eubacterium xylanophilum and increased DCA levels in the intestines of CYP-treated mice. FMT experiments confirmed microbiota-dependent therapeutic effects of PPS, shown by reduced bladder pathology in the recipient mice treated with both CYP and PPS. In SV-HUC-1 cells, DCA obviously alleviated LPS-induced inflammation and barrier disruption, and treatment with SBI-115 abolished these protective effects of DCA.

CONCLUSIONS: PPS ameliorates IC/BPS in mice by remodeling gut microbiota to enhance DCA production and activate TGR5 signaling, suggesting a novel microbiota-bile acid-TGR5 axis that mediates the therapeutic effect of PPS and a therapeutic strategy for IC/BPS by targeting gut-bladder crosstalk.},
}

Animals
*Cystitis, Interstitial/chemically induced/drug therapy
*Gastrointestinal Microbiome/drug effects
*Pentosan Sulfuric Polyester/pharmacology/therapeutic use
Cyclophosphamide/adverse effects
Mice, Inbred C57BL
Female
Mice
*Bile Acids and Salts/metabolism
Urinary Bladder
Fecal Microbiota Transplantation
Humans

@article {pmid40578039,
year = {2025},
author = {Wen, Y and Li, M and Hao, Y and Peng, J and Wei, X and Zhang, Z and Liu, B and Wang, Y and Peng, T and Ma, Y},
title = {HDAC/NF-κB signaling pathway mediates gut microbiota dysbiosis in rheumatoid arthritis: Intervention mechanisms of Fengshining decoction.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {145},
number = {},
pages = {156976},
doi = {10.1016/j.phymed.2025.156976},
pmid = {40578039},
issn = {1618-095X},
abstract = {BACKGROUND: Gut microbiota dysbiosis has been associated with the development of rheumatoid arthritis (RA). Fengshining (FSN) is a traditional Chinese medicine decoction that can effectively alleviate RA. However, how FSN modulates the gut microbiota to mitigate RA has not been comprehensively studied. This study evaluated the gut microecological mechanisms underlying FSN's effects on RA, focusing on the impact of gut-derived short-chain fatty acids (SCFAs), specifically butyrate, in RA treatment.

METHODS: The pharmacological effects of FSN on type II collagen-induced arthritis (CIA) in mice were assessed via pathological indicators, metagenomics, and metabolomics analyses. Furthermore, the impact of FSN on gut microbiota and metabolic profiles was also evaluated. Moreover, a pseudo-germ-free CIA model was established to validate whether exogenous butyrate alleviates RA. This study also elucidated whether fecal microbiota transplantation (FMT) from FSN-treated mice could mitigate RA symptoms.

RESULTS: The data showed that FSN markedly alleviated CIA symptoms and reduced serum inflammatory cytokine levels. Metagenomic and metabolomic analyses revealed that FSN-enriched SCFA-producing bacteria, including Butyrivibrio, Faecalicatena, and Lacrimispora. Furthermore, FSN increased the activity of carbohydrate metabolism-related enzymes and upregulated the expression patterns of homologous protein families. Moreover, exogenous butyrate supplementation suppressed pro-inflammatory factors, modulating immune responses, and enhanced intestinal barrier function. Further, Western blot analysis validated that FSN inhibited the HDAC/NF-κB pathway.

CONCLUSION: This study indicated that the gut microecological mechanism of FSN might be associated with its herbal components, which regulate gut microbiota diversity, restore the intestinal barrier, and boost microbial metabolite production. Furthermore, butyrate was observed to modulate intestinal mucosa, inhibit inflammatory responses, repair the intestinal barrier, and mitigate joint damage, thus alleviating RA symptoms.},
}

@article {pmid40576702,
year = {2025},
author = {Shtrozberg, S and Bazzichi, L and Sarzi-Puttini, P and Aloush, V and Ablin, JN},
title = {Is the gut microbiome of importance in fibromyalgia? A critical review of emerging evidence.},
journal = {Clinical and experimental rheumatology},
volume = {43},
number = {6},
pages = {990-998},
doi = {10.55563/clinexprheumatol/pmajsv},
pmid = {40576702},
issn = {0392-856X},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Fibromyalgia/microbiology/physiopathology/therapy/diagnosis ; Animals ; Probiotics/therapeutic use ; Nutritional Status ; Dysbiosis ; Prebiotics ; Fecal Microbiota Transplantation ; },
abstract = {Fibromyalgia (FM) is a multifaceted chronic pain syndrome, predominantly affecting women, and characterised by a constellation of symptoms including diffuse musculoskeletal pain, fatigue, cognitive impairment and poor sleep quality. Its complex pathophysiology likely involves genetic, environmental and psychosocial factors. Recent studies have raised the possibility that the gut microbiome may influence FM symptoms via the gut-brain axis, although this hypothesis remains unconfirmed. This review aims to explore potential associations between gut microbiome alterations, nutrition, and FM, with particular attention to the limitations of current evidence. While certain studies have reported differences in the gut microbiota composition of patients with FM, these findings are preliminary and often derive from small, heterogeneous cohorts. Likewise, faecal microbiota transplantation studies in animals and limited human trials suggest a possible link to pain sensitivity, but further validation is needed.Nutritional interventions, including prebiotics, probiotics and specific dietary strategies, have shown early promise in modulating gut microbiota and alleviating FM symptoms. Nutrients such as magnesium, selenium and omega-3 fatty acids, as well as antioxidant compounds, may influence pain and inflammation pathways, but definitive clinical recommendations are lacking. Given the emerging nature of this field, larger and better-controlled studies are required to clarify the role of the gut microbiome and nutrition in FM. A multidisciplinary management strategy, integrating nutritional approaches cautiously and based on individual profiles, may offer benefits, although no standard therapeutic guidelines currently exist.},
}

Humans
*Gastrointestinal Microbiome
*Fibromyalgia/microbiology/physiopathology/therapy/diagnosis
Animals
Probiotics/therapeutic use
Nutritional Status
Dysbiosis
Prebiotics
Fecal Microbiota Transplantation

@article {pmid40576662,
year = {2025},
author = {Goldschmidt, I and Kramer, M and Junge, N and Ouro-Djobo, N and Poets, A and Rathert, M and Geffers, R and Baumann, U and Hartleben, B and Schulze, KD and Woltemate, S and Vital, M},
title = {Short- and long-term development of gut microbiota in children after liver transplantation - a prospective observational trial.},
journal = {Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society},
volume = {},
number = {},
pages = {},
doi = {10.1097/LVT.0000000000000659},
pmid = {40576662},
issn = {1527-6473},
abstract = {In children, little is known on gut microbiota (GM) in end-stage liver disease and its association with graft function after pediatric liver transplantation (pLT). We analyzed GM composition and function in children before pLT, longitudinally post-pLT and in long-term survivors (LT-pLT) in order to assess the impact of disease severity, treatment and pLT on GM and delineate associations with graft and patient health. Fecal samples (FS) of 29 children (17f, age 2.6 [0.2-15.7] years) awaiting pLT were included with longitudinal follow-ups until 12M post-transplant in 18, and compared with 38 LT-pLT (21f, age 11 [2.7-17.7] years, 7.8 [1.0-17.0] years post-pLT) and 94 healthy controls (HC). Samples were analyzed using quantitative 16S rRNA gene analyses combined with shotgun metagenomics (subset of samples). Pre-pLT patients showed reduced alpha-diversities and altered GM composition compared with LT-pLT and HC, associated with disease severity and anti-pruritic treatment with Rifampicin. Dysbiosis increased after pLT and started to recover after 3M. Although bacterial concentrations, alpha diversity and gene richness increased post-pLT, levels remained below those of HC. Abundances of key functions, e.g. the capacity to synthesize butyrate, also remained reduced. Quantitative analyses revealed true extent of differences between patients and HC that were underestimated using relative abundance data. GM diversity and functional capacities correlated negatively with transaminase levels mid- and long-term after pLT. Random Forest analyses based on GM were able to predict hepatocellular damage at high accuracy (AUC: 0.89). We provide comprehensive, quantitative insights into GM composition and function before and after pLT. A link between GM alterations with (long-term) graft health was uncovered providing possible targets to modulate GM function in order to increase graft and patient health.},
}

@article {pmid40575995,
year = {2025},
author = {Zhang, D and Dong, B and Chen, J and Zhang, Z and Zeng, W and Liao, L and Xiong, X and Qin, X and Fan, X},
title = {Fecal Microbiota Transplantation Modulates Th17/Treg Balance via JAK/STAT Pathway in ARDS Rats.},
journal = {Advanced biology},
volume = {},
number = {},
pages = {e00028},
doi = {10.1002/adbi.202500028},
pmid = {40575995},
issn = {2701-0198},
support = {2022NSFSC0046//Natural Science Foundation of Sichuan Province of China/ ; 2022QN074//Southwest Medical University School-Level Project/ ; 2023JYJ049//Luzhou City Science and Technology Program Project/ ; LRYGCC202120//Guangxi Key Specialty Construction Project Funding, Liuzhou City People's Hospital High-Level Talent Research Startup Fund/ ; lry202408//Liuzhou People's Hospital In-house Project Funding/ ; lry202409//Liuzhou People's Hospital In-house Project Funding/ ; lry202411//Liuzhou People's Hospital In-house Project Funding/ ; GXZYB20240601//Guangxi Autonomous Region Traditional Chinese Medicine Self-Funded Project/ ; 2024YB0103B003//Liuzhou City Science and Technology Program Project/ ; },
abstract = {This study evaluated the therapeutic effects of fecal microbiota transplantation (FMT) on lipopolysaccharide (LPS)-induced acute respiratory distress syndrome (ARDS) in rats. The study focused on the balance of T-helper 17 (Th17) and regulatory T (Treg) cells, as well as the modulation of the JAK/STAT pathway. This study established a rat ARDS model using intranasal LPS instillation, administering interventions such as FMT, Treg cell depletion, and JAK inhibitors. Assessments included histopathological examination of lung and intestinal tissues, flow cytometry for Th17 and Treg cell proportions, qPCR and Western blot for gene and protein expression, ELISA for inflammatory cytokines, and correlation analysis using Spearman's method for cytokine-immune cell interactions. Results indicated that FMT and JAK inhibitors significantly reduce lung damage induced by LPS, reduced alveolar destruction and inflammation, restored Th17/Treg balance, and inhibited JAK/STAT pathway activity. Notably, FMT decreased pro-inflammatory cytokines (IL-2, IL-6, IL-8, IL-17A, IL-23, TGF-β1) and increased anti-inflammatory cytokines (IL-10, IL-35) in serum. Spearman correlation analysis indicated that FMT restored immune balance by modulating the interactions between cytokines and immune cells. In conclusion, FMT effectively alleviates lung and intestinal injury in LPS-induced ARDS rat models by modulating Th17/Treg balance and inhibiting JAK/STAT pathway activity, demonstrating promising therapeutic potential for ARDS treatment.},
}

@article {pmid40575647,
year = {2025},
author = {Tüsüz Önata, E and Özdemir, Ö},
title = {Microbiome, dysbiosis and use of probiotics in various diseases.},
journal = {World journal of virology},
volume = {14},
number = {2},
pages = {99574},
pmid = {40575647},
issn = {2220-3249},
abstract = {The community of microorganisms that colonize certain areas of the human body is called microbiota. Microorganisms such as bacteria, fungi and viruses make up the microbiota. The sum of the genomes of these microorganisms and microorganisms refers to the microbiome. It has been shown that microbiota has important effects such as protecting the organ from pathogens, contributing to metabolic functions (such as vitamin synthesis, carbohydrate digestion) and providing immunoregulation. Dysbiosis refers to compositional and functional changes in the microbiota. At the beginning of the 21[st] century, numerous studies have investigated the human microbiota and its imbalance in relation to various diseases and found that dysbiosis is associated with many diseases. The aim of this mini-review article is to provide brief information about dysbiosis and its care and to raise awareness.},
}

@article {pmid40575364,
year = {2025},
author = {Bangolo, A and Amoozgar, B and Habibi, M and Simms, E and Nagesh, VK and Wadhwani, S and Wadhwani, N and Auda, A and Elias, D and Mansour, C and Abbott, R and Jebara, N and Zhang, L and Gill, S and Ahmed, K and Ip, A and Goy, A and Cho, C},
title = {Exploring the gut microbiome's influence on cancer-associated anemia: Mechanisms, clinical challenges, and innovative therapies.},
journal = {World journal of gastrointestinal pharmacology and therapeutics},
volume = {16},
number = {2},
pages = {105375},
pmid = {40575364},
issn = {2150-5349},
abstract = {BACKGROUND: Anemia is a prevalent and challenging complication in patients with hematologic and solid malignancies, which stems from the direct effects of malignancy, treatment-induced toxicities, and systemic inflammation. It affects patients' survival, functional status, and quality of life profoundly. Recent literature has highlighted the emerging role of the gut microbiome in the pathogenesis of cancer-associated anemia. The gut microbiota, through its intricate interplay with iron metabolism, inflammatory pathways, and immune modulation, may either exacerbate or ameliorate anemia depending on its composition, and functional integrity. Dysbiosis, characterized by disruption in the gut microbial ecosystem, is very common in cancer patients. This microbial imbalance is implicated in anemia causation through diminished iron absorption, persistent low-grade inflammation, and suppression of erythropoiesis.

AIM: To consolidate current evidence regarding the interplay between gut microbiome and anemia in the setting of malignancies. It aims to provide a detailed exploration of the mechanistic links between dysbiosis and anemia, identifies unique challenges associated with various cancer types, and evaluates the efficacy of microbiome-focused therapies. Through this integrative approach, the review seeks to establish a foundation for innovative clinical strategies aimed at mitigating anemia and improving patient outcomes in oncology.

METHODS: A literature search was performed using multiple databases, including Google Scholar, PubMed, Scopus, and Web of Science, using a combination of keywords and Boolean operators to refine results. Keywords included "cancer-associated anemia", "gut microbiome", "intestinal microbiota", "iron metabolism", "gut dysbiosis", "short-chain fatty acids", "hematopoiesis", "probiotics", "prebiotics", and "fecal microbiota transplantation". Articles published in English between 2000 and December 2024 were included, with a focus on contemporary and relevant findings.

RESULTS: Therapeutic strategies aimed at restoration of gut microbial homeostasis, such as probiotics, prebiotics, dietary interventions, and fecal microbiota transplantation (FMT), can inhibit anemia-causing pathways by enhancing microbial diversity, suppressing detrimental flora, reducing systemic inflammation and optimizing nutrient absorption.

CONCLUSION: Gut dysbiosis causes anemia and impairs response to chemotherapy in cancer patients. Microbiome-centered interventions, such as probiotics, prebiotics, dietary modifications, and FMT, have shown efficacy in restoring microbial balance, reducing inflammation, and enhancing nutrient bioavailability. Emerging approaches, including engineered probiotics and bacteriophage therapies, are promising precision-based, customizable solutions for various microbiome compositions and imbalances. Future research should focus on integrating microbiome-targeted strategies with established anemia therapies.},
}

@article {pmid40574876,
year = {2025},
author = {Odenwald, MA and Ramaswamy, R and Lin, H and Lehmann, C and Moran, A and Mullowney, MW and Sidebottom, AM and Hernandez, A and McMillin, M and Rose, A and Moran, D and Little, J and Sulakhe, D and D'Souza, M and Woodson, C and Tanveer, T and de Porto, A and Dylla, N and Sundararajan, A and Burgo, V and Cantoral, J and Jadczak, C and Adler, E and Aronsohn, A and Pamer, EG and Rinella, ME},
title = {Fecal Butyrate and Deoxycholic Acid Concentrations Correlate With Mortality in Patients With Liver Disease.},
journal = {Gastro hep advances},
volume = {4},
number = {8},
pages = {100695},
pmid = {40574876},
issn = {2772-5723},
abstract = {BACKGROUND AND AIMS: The intestinal microbiome produces metabolites, including short chain fatty acids (SCFAs) and secondary bile acids (BAs), that impact host physiology. Loss of intestinal microbiome diversity is associated with cirrhosis progression, but the impact of microbiome-associated metabolites on liver disease remains largely undefined. We aimed to correlate fecal metabolite concentrations with the severity and progression of liver disease.

METHODS: In this cross-sectional study, fecal samples from patients hospitalized with liver disease were analyzed by shotgun metagenomic sequencing to determine microbiome compositions and targeted mass spectrometry to quantify SCFAs and BAs. Random survival forest and logistic regression models identified clinical, metagenomic, and metabolomic features associated with rehospitalization and survival.

RESULTS: This cross-sectional study included 24 chronic liver disease, 18 compensated cirrhosis, 225 decompensated cirrhosis and 40 acute-on-chronic liver failure patients and 27 control fecal donors. Microbiome sequencing and metabolite profiling correlated microbial diversity and SCFA and BA concentrations with liver disease severity. Butyrate and deoxycholic acid (DCA) were more important features than individual microbial species in random survival forest models predicting 30-day transplant-free survival, and low butyrate and DCA were associated with 30-day mortality (P < .0001). After controlling for model for end stage liver disease (MELD)-sodium score, disease stage, age and gender, low fecal concentrations of butyrate and DCA remained significant risk factors for death (Cox 1.38, P = .027). Bacterial species associated with butyrate and DCA concentrations included Bifidobacterium spp. and F. prausnitzii.

CONCLUSION: Mass spectrometry rapidly identifies patients with low fecal butyrate and DCA concentrations who are at increased risk of 30-day mortality. These findings set the stage for clinical trials of microbiome reconstitution with butyrate and DCA-producing bacterial species.},
}

@article {pmid40574831,
year = {2025},
author = {Guo, X and Wang, K and Liu, Q and Baran, N and Ma, W},
title = {The gut-immune axis in primary immune thrombocytopenia (ITP): a paradigm shifts in treatment approaches.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1595977},
pmid = {40574831},
issn = {1664-3224},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; *Purpura, Thrombocytopenic, Idiopathic/therapy/immunology/microbiology ; Dysbiosis/immunology ; Fecal Microbiota Transplantation ; Animals ; Blood Platelets/immunology ; Probiotics/therapeutic use ; },
abstract = {Primary immune thrombocytopenia (ITP) is an autoimmune disorder characterized by platelet destruction and impaired production, leading to bleeding risk. While immunosuppressive therapies are standard, many patients experience relapses or refractory disease, highlighting the need for novel approaches. Emerging evidence suggests the gut microbiota plays a role in immune regulation, yet its impact on ITP remains unclear. Dysbiosis has been linked to immune dysfunction in other autoimmune diseases, but whether it drives or results from immune dysregulation in ITP is debated. This review explores the gut-immune axis in ITP, focusing on microbiota-driven immune modulation, cytokine signaling, and platelet homeostasis. We assess microbiota-targeted interventions, including fecal microbiota transplantation (FMT), probiotics, and dietary modifications, while addressing key controversies and knowledge gaps. Advances in microbiome sequencing and artificial intelligence may facilitate personalized interventions. Standardizing microbiota-based diagnostics and validating their efficacy in clinical trials are crucial for their integration into ITP management. Bridging these gaps may lead to microbiota-driven strategies that enhance immune regulation and improve patient outcomes.},
}

Humans
*Gastrointestinal Microbiome/immunology
*Purpura, Thrombocytopenic, Idiopathic/therapy/immunology/microbiology
Dysbiosis/immunology
Fecal Microbiota Transplantation
Animals
Blood Platelets/immunology
Probiotics/therapeutic use

@article {pmid40574570,
year = {2025},
author = {Yang, D and Yang, X and Zhou, Y and Wang, H and Wang, R},
title = {Fecal Microbiota Transplantation from Noni Fruit Phenolic-Rich Extract Intervention Mouse Donors Ameliorates Lipid Metabolism Disorder by Regulating the FXR-FGF15 Pathway in a Gut Microbiota-Dependent Manner.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c05184},
pmid = {40574570},
issn = {1520-5118},
abstract = {Noni fruit phenolic-rich extract (NFE) has been confirmed to alleviate lipid metabolism disturbance, with emerging evidence implicating bile acids (BAs) metabolism in a gut microbiota-dependent manner in mediating the effect. The effect and potential mechanism of fecal microbiota transplantation from NFE intervention mouse donors (FMT-NFE) on lipid metabolism disorder were investigated. The results reveal FMT-NFE intervention regulated the body weight, lipid profile levels, and liver damage. FMT-NFE intervention upgraded the abundance of bile salt hydrolase (BSH)-expressing bacteria and short-chain fatty acid (SCFA)-producing bacteria in feces, which is accompanied by changes of BSH activity and BAs profile as well as elevation of the SCFA level. Moreover, western blotting and immunofluorescence results confirmed the intestinal FXR-FGF15 pathway was activated by FMT-NFE intervention, which was accompanied by activation of the liver FXR and inhibition of CYP7A1 expression to control cholesterol-to-BAs conversion. These findings underscore the mechanisms behind maintaining BAs and lipid metabolism homeostasis of NFE.},
}

@article {pmid40573435,
year = {2025},
author = {Ajileye, TG and Akinleye, TE and Faleye, TOC and De Coninck, L and George, UE and Onoja, AB and Agbaje, ST and Ifeorah, IM and Olayinka, OA and Oni, EI and Oragwa, AO and Popoola, BO and Olayinka, OT and Osasona, OG and George, OA and Ajayi, PG and Suleiman, AA and Muhammad, AI and Komolafe, I and Adeniji, AJ and Matthijnssens, J and Adewumi, MO},
title = {Ten Previously Unassigned Human Cosavirus Genotypes Detected in Feces of Children with Non-Polio Acute Flaccid Paralysis in Nigeria in 2020.},
journal = {Viruses},
volume = {17},
number = {6},
pages = {},
doi = {10.3390/v17060844},
pmid = {40573435},
issn = {1999-4915},
mesh = {Humans ; *Feces/virology ; Nigeria/epidemiology ; Phylogeny ; *Genotype ; Child ; Child, Preschool ; *Picornaviridae/genetics/classification/isolation & purification ; Genome, Viral ; Infant ; *Picornaviridae Infections/virology/epidemiology ; Genetic Variation ; Adolescent ; Female ; Male ; Metagenomics ; *Paralysis/virology ; },
abstract = {Since its discovery via metagenomics in 2008, human cosavirus (HCoSV) has been detected in the cerebrospinal fluid (CSF) and feces of humans with meningitis, acute flaccid paralysis (AFP), and acute gastroenteritis. To date, 34 HCoSV genotypes have been documented by the Picornaviridae study group. However, the documented genetic diversity of HCoSV in Nigeria is limited. Here we describe the genetic diversity of HCoSV in Nigeria using a metagenomics approach. Archived and anonymized fecal specimens from children (under 15 years old) diagnosed with non-polio AFP from five states in Nigeria were analyzed. Virus-like particles were purified from 55 pools (made from 254 samples) using the NetoVIR protocol. Pools were subjected to nucleic acid extraction and metagenomic sequencing. Reads were trimmed and assembled, and contigs classified as HCoSV were subjected to phylogenetic, pairwise identity, recombination analysis, and, when necessary, immuno-informatics and capsid structure prediction. Fifteen pools yielded 23 genomes of HCoSV. Phylogenetic and pairwise identity analysis showed that all belonged to four species (eleven, three, three, and six members of Cosavirus asiani, Cosavirus bepakis, Cosavirus depakis, and Cosavirus eaustrali, respectively) and seventeen genotypes. Ten genomes belong to seven (HCoSV-A3/A10, A15, A17, A19, A24, D3, and E1) previously assigned genotypes, while the remaining thirteen genomes belonged to ten newly proposed genotypes across the four HCoSV species, based on the near-complete VP1 region (VP1*) of the cosavirus genome. Our analysis suggests the existence of at least seven and eight Cosavirus bepakis and Cosavirus eaustrali genotypes, respectively (including those described here). We report the first near-complete genomes of Cosavirus bepakis and Cosavirus depakis from Nigeria, which contributes to the increasing knowledge of the diversity of HCoSV, raising the number of tentative genotypes from 34 to over 40. Our findings suggest that the genetic diversity of HCoSV might be broader than is currently documented, highlighting the need for enhanced surveillance.},
}

Humans
*Feces/virology
Nigeria/epidemiology
Phylogeny
*Genotype
Child
Child, Preschool
*Picornaviridae/genetics/classification/isolation & purification
Genome, Viral
Infant
*Picornaviridae Infections/virology/epidemiology
Genetic Variation
Adolescent
Female
Male
Metagenomics
*Paralysis/virology

@article {pmid40573341,
year = {2025},
author = {Hu, J and Zhang, Q and Liu, D and Cui, X and Wang, Q and Gong, W and Wang, X},
title = {Inhibition of Bovine Enterovirus Infection by Magnolol via Modulating the Gut Microbiota in Mice.},
journal = {Viruses},
volume = {17},
number = {6},
pages = {},
doi = {10.3390/v17060750},
pmid = {40573341},
issn = {1999-4915},
support = {2016YFD0500904 and 2017YFD0500104//National Key Research & Development Program/ ; },
mesh = {Animals ; *Lignans/pharmacology/therapeutic use ; *Gastrointestinal Microbiome/drug effects ; Mice ; *Biphenyl Compounds/pharmacology/therapeutic use ; *Enterovirus Infections/drug therapy/virology/veterinary/microbiology ; Cattle ; Disease Models, Animal ; Feces/microbiology ; Fecal Microbiota Transplantation ; *Antiviral Agents/pharmacology ; Viral Load/drug effects ; Enterovirus/drug effects ; },
abstract = {Bovine enterovirus (BEV) infection is one of the important infectious diseases that cause digestive and respiratory symptoms in cattle, posing a significant threat to the cattle industry. Currently, no vaccines or therapeutic drugs are available for this disease. In our study, we utilized a mouse model to investigate the effects of BEV infection on the gut microbiota and examine the therapeutic potential of magnolol (Mag), a polyphenolic bioactive substance, in terms of BEV infection. BEV infection significantly altered the microbiota composition, where the abundance of some beneficial bacteria, such as Lactobacillaceae and Lactobacillus, was markedly reduced. Mag effectively inhibited BEV infection in vivo. Upon BEV infection, Mag treatment reduced the α-diversity of the microbiota, with statistically significant differences on day 3 post-infection compared to the Mag-untreated group. More interestingly, Mag treatment significantly reversed the effect of BEV infection on the Lactobacillaceae and Lactobacillus abundance, indicating that Mag positively regulates beneficial bacteria. The fecal microbiota transplantation (FMT) experiment demonstrated that feces from Mag-treated mice significantly decreased the virus loads in the small intestine samples of BEV-infected mice. These findings demonstrate the interaction between BEV infection and the gut microbiota and highlight the important regulatory role of the gut microbiota in Mag's anti-BEV effects, opening up a new avenue for preventing and controlling BEV infection via targeted modulation of the gut microbiota.},
}

Animals
*Lignans/pharmacology/therapeutic use
*Gastrointestinal Microbiome/drug effects
Mice
*Biphenyl Compounds/pharmacology/therapeutic use
*Enterovirus Infections/drug therapy/virology/veterinary/microbiology
Cattle
Disease Models, Animal
Feces/microbiology
Fecal Microbiota Transplantation
*Antiviral Agents/pharmacology
Viral Load/drug effects
Enterovirus/drug effects

@article {pmid40573072,
year = {2025},
author = {Wakino, S and Hasegawa, K and Tamaki, M and Minato, M and Inagaki, T},
title = {Kidney-Gut Axis in Chronic Kidney Disease: Therapeutic Perspectives from Microbiota Modulation and Nutrition.},
journal = {Nutrients},
volume = {17},
number = {12},
pages = {},
doi = {10.3390/nu17121961},
pmid = {40573072},
issn = {2072-6643},
mesh = {Humans ; *Renal Insufficiency, Chronic/microbiology/therapy/physiopathology ; *Gastrointestinal Microbiome/physiology ; *Dysbiosis/therapy/microbiology ; Probiotics/therapeutic use ; Prebiotics/administration & dosage ; *Kidney/physiopathology ; Synbiotics/administration & dosage ; Fecal Microbiota Transplantation ; Uremia/microbiology ; *Nutrition Therapy/methods ; },
abstract = {Chronic kidney disease (CKD) has a high prevalence worldwide, with an increasing incidence. One of the mechanisms of CKD progression involves a disordered inter-organ relationship between the kidneys and the intestine, known as the kidney-gut axis. In CKD, two pathological gut conditions-disturbed gut microbiota composition called uremic dysbiosis and leaky gut-contribute to the progression of CKD. Dysbiosis is associated with the increased production of gut-derived uremic toxins, leaky gut, and chronic systemic inflammation, leading to worsening uremia, which in turn aggravates the gut condition. This vicious cycle should be a target of the therapeutic strategy against CKD. The modulation of uremic dysbiosis, including prebiotics, probiotics, and synbiotics, has been a typical treatment approach, although clinical evidence for their efficacy has been insufficient. Some non-antibiotic drugs have an impact on human gut bacteria that are believed to play a role in their clinical efficacy on kidney function. Nutrition therapies, including a low-protein diet, dietary fiber, a Mediterranean diet, and whole grains, positively influence gut microbiota composition and have been linked to a decreased risk of CKD. Novel strategies are currently being explored, involving the use of postbiotics, microbiome sequencing techniques, and fecal microbiota transplantation, although clinical application remains to be tested. Human trials investigating the above-mentioned interventions remain inconclusive due to several limitations, including dietary variability and genetic factors. Future research should focus on the development of more effective probiotics, prebiotics, and microbial metabolism-modifying drugs, not only for CKD but for other systemic diseases as well.},
}

Humans
*Renal Insufficiency, Chronic/microbiology/therapy/physiopathology
*Gastrointestinal Microbiome/physiology
*Dysbiosis/therapy/microbiology
Probiotics/therapeutic use
Prebiotics/administration & dosage
*Kidney/physiopathology
Synbiotics/administration & dosage
Fecal Microbiota Transplantation
Uremia/microbiology
*Nutrition Therapy/methods

@article {pmid40572299,
year = {2025},
author = {Cintoni, M and Palombaro, M and Zoli, E and D'Agostino, G and Pulcini, G and Leonardi, E and Raoul, P and Rinninella, E and De Maio, F and Capristo, E and Gasbarrini, A and Mele, MC},
title = {The Interplay Between the Gut Microbiota and Colorectal Cancer: A Review of the Literature.},
journal = {Microorganisms},
volume = {13},
number = {6},
pages = {},
pmid = {40572299},
issn = {2076-2607},
abstract = {Lifestyle, diet, and genetics are established risk factors for developing colorectal cancer (CRC). In recent years, the role of the gut microbiota (GM) has been increasingly highlighted in several studies, suggesting an effect on both the disease's pathogenesis and the efficacy and tolerability of treatments. We conducted a search on Medline, aiming to identify published studies exploring the role of the GM in the development and treatment of CRC. Dysbiosis, an imbalance in GM, is common in CRC patients and is associated with precancerous lesions, aggressive tumors, and varied therapy outcomes. Restoring GM balance can reduce treatment complications and may improve prognosis. The review details how GM influences CRC through metabolite production, inflammation modulation, and immune response alteration. Diet significantly impacts GM composition, with processed meats and high-fat diets increasing CRC risk, while fiber-rich diets are protective. The role of the GM in CRC treatments like surgery, chemotherapy, radiotherapy, and immunotherapy is also explored, noting its influence on complications, chemoresistance, and treatment efficacy. Future strategies involving GM modulation through diet, probiotics, and fecal microbiota transplantation (FMT) show promise for CRC prevention and treatment, warranting further research.},
}

@article {pmid40572244,
year = {2025},
author = {Roy, S and Alizadeh Bahmani, AH and Davids, M and Herrema, H and Nieuwdorp, M},
title = {Modulating the Gut-Muscle Axis: Increasing SCFA-Producing Gut Microbiota Commensals and Decreasing Endotoxin Production to Mitigate Cancer Cachexia.},
journal = {Microorganisms},
volume = {13},
number = {6},
pages = {},
pmid = {40572244},
issn = {2076-2607},
abstract = {Cancer cachexia is a multi-organ and multifactorial syndrome characterized by muscle wasting (with or without adipose tissue loss) and systemic inflammation in patients with advanced malignancies. Gut microbiota dysbiosis, particularly the depletion of short-chain fatty acid (SCFA)-producing bacteria, may contribute to the progression of cancer cachexia. Studies in both murine models and humans consistently associate cachexia with a decline in SCFA-producing gut microbiota commensals and an overgrowth of pro-inflammatory pathobionts. These microbial imbalances may lead to reduced levels of SCFAs and branched-chain amino acids (BCAAs) and alter the normal bile acid profile. BCAAs and the maintenance of a normal bile acid profile are associated with muscle synthesis and decreased breakdown. While SCFAs (acetate, propionate, and butyrate), contribute to intestinal barrier integrity and immune regulation. SCFA depletion may increase gut permeability, allowing bacterial endotoxins, such as lipopolysaccharide (LPS), to enter the bloodstream. This may lead to chronic inflammation, muscle catabolism, and impairment of anabolic pathways. Interventions targeting gut microbiota in preclinical models have mitigated inflammation and muscle loss. While clinical data are limited, it suggests an improvement in immune functions and better tolerance to anticancer therapies. Current evidence is predominantly derived from cross-sectional studies suggesting associations without causality. Thus, future longitudinal studies are needed to identify biomarkers and optimize personalized therapy.},
}

@article {pmid40572178,
year = {2025},
author = {Maniscalco, I and Bartochowski, P and Priori, V and Iancau, SP and De Francesco, M and Innamorati, M and Jagodzinska, N and Giupponi, G and Masucci, L and Conca, A and Mroczek, M},
title = {The Effects of Fecal Microbial Transplantation on the Symptoms in Autism Spectrum Disorder, Gut Microbiota and Metabolites: A Scoping Review.},
journal = {Microorganisms},
volume = {13},
number = {6},
pages = {},
pmid = {40572178},
issn = {2076-2607},
abstract = {The bilateral interaction between the brain and the gut has recently been on the spectrum of researchers' interests, including complex neural, endocrinological, and immunological signaling pathways. The first case reports and clinical studies have already reported that delivering microbes through fecal microbial transplantation (FMT) may alleviate symptoms of psychiatric disorders. Therefore, modifying the gut microbiota through FMT holds promise as a potential treatment for psychiatric diseases. This scoping review assessed studies from PubMed related to FMT in autism spectrum disorder and attention deficit hyperactivity disorder. The evaluation included nine clinical studies and case reports. The beneficial and persistent effect on the autism spectrum disorder (ASD) symptoms has been reported. Also, an increased microflora diversity and altered levels of neurometabolites in serum were identified, albeit with a tendency to return to baseline over time. The microbiome-gut-brain axis could provide new targets for preventing and treating psychiatric disorders. However, a recent large randomized clinical trial has shed light on the previously collected data and suggested a possible contribution of the placebo effect. This highlights the necessity of large randomized double-blind studies to reliably assess the effect of FMT in ASD.},
}

@article {pmid40571138,
year = {2025},
author = {Chen, QZ and Shang, JM and Jiang, YQ and Yang, Y and Zang, CX and Ma, JW and Dong, YR and Wang, JR and Zhou, N and Yang, X and Li, FF and Bao, XQ and Zhang, D},
title = {Gut microbial dysbiosis aggravated Parkinson-like pathology induced by MPTP/probenecid.},
journal = {Physiology & behavior},
volume = {},
number = {},
pages = {115008},
doi = {10.1016/j.physbeh.2025.115008},
pmid = {40571138},
issn = {1873-507X},
abstract = {Parkinson's disease (PD) is a common neurodegenerative disorder, characterized by resting tremor, bradykinesia, rigidity and postural instability. Recent studies have proved that gut microbiota (GM) dysbiosis exists in PD patients. However, the causal relationship between gut microbial dysbiosis and pathogenesis of PD remains unexplored. Here, using MPTP/probenecid-induced PD mouse model and an antibiotic cocktail (ABX)-induced pseudo-germ-free status, we observed that GM diversity and abundance significantly decreased in feces of ABX-treated PD mice by 16S rRNA sequencing. Remarkably, gut microbial dysbiosis induced by ABX aggravated GI dysfunction and motor deficits in PD mice. Moreover, ABX treatment caused more severe inflammation, and dopaminergic (DAergic) neuronal loss in both the gut and brain. Further study showed that fecal microbiota transplantation (FMT) corrected gut microbial dysbiosis, along with increased short-chain fatty acids (SCFAs). Additionally, GI and motor dysfunctions were improved, peripheral and central inflammation were also attenuated when PD mice were treated with FMT. These findings revealed that gut microbial dysbiosis could aggravate PD pathological damages, and highlighted that gut microbial dysbiosis might be an important factor that impacts PD pathogenesis through the microbiota-gut-brain axis.},
}

@article {pmid40570572,
year = {2025},
author = {Ordóñez, C and Zurita, S and Ramírez, G and Cordeiro, F and Garcia-Matamoros, K and Huaman-Garaicoa, F and Orellana-Manzano, A and Sandoya-Onofre, L and Pogo, J and Carvajal-Aldaz, D},
title = {Are we there yet? Gut microbiota for cancer diagnosis, prognosis and treatment.},
journal = {Seminars in oncology},
volume = {52},
number = {4},
pages = {152376},
doi = {10.1016/j.seminoncol.2025.152376},
pmid = {40570572},
issn = {1532-8708},
abstract = {Cancer remains as one of the leading causes of death worldwide, emphasizing the need for innovative diagnostic and therapeutic tools. The gut microbiota has emerged as a factor that influences cancer progression, prognosis, and treatment outcomes. This review analyzes observational and interventional studies conducted with human subjects over the past 5 years, highlighting significant advancements in gut microbiota research for cancer management. Observational studies consistently demonstrated differences in gut microbial composition between cancer patients and healthy controls. Moreover, microbial diversity, particularly at the species and strain level, correlated significantly with clinical outcomes. Interventional studies showed the potential of probiotics and fecal microbiota transplantation (FMT) as adjuncts in cancer therapy by restoring microbial diversity, reducing inflammation, and alleviating chemotherapy-induced complications. Collectively, these findings suggest the gut microbiota's potential as a tool for cancer care. Future research should focus on standardizing taxonomic-level analyses, optimizing probiotic formulations, and validating FMT/AFMT clinical protocols to fully harness the gut microbiota's diagnostic and therapeutic capabilities in oncology.},
}

@article {pmid40570072,
year = {2025},
author = {Shatova, OP and Shestopalov, AV and Zlatnik, EY and Novikova, IA and Goncharova, AS and Maksimov, AY},
title = {The effect of fecal microbiota transplantation on levels of tryptophan metabolites in intestine and serum of gnotobiotic mice.},
journal = {Biomeditsinskaia khimiia},
volume = {71},
number = {3},
pages = {209-216},
doi = {10.18097/PBMCR1554},
pmid = {40570072},
issn = {2310-6972},
mesh = {Animals ; *Tryptophan/metabolism/blood ; Mice ; *Fecal Microbiota Transplantation ; *Gastrointestinal Microbiome ; Germ-Free Life ; Indoles/metabolism/blood ; *Intestines/microbiology ; Feces/microbiology ; Male ; Kynurenine/blood/metabolism ; Quinolinic Acid/metabolism/blood ; },
abstract = {Gut microbiota is one of the key suppliers of tryptophan metabolites, which perform various functions in the host organism, including their role as signaling molecules. Fecal microbiota transplantation (FMT) is widely used as a method for determining the contribution of microorganisms to the content of various metabolites in the holoorganism. In this regard, the aim of our study was to investigate the effect of FMT on the level of tryptophan metabolites in feces and blood in gnotobiotic mice. It was found that both before and after FMT, indole-3-lactate, and quinolinic acid were the dominant tryptophan metabolites in the intestine. FMT increased the content of both indoles (indole-3-acetate, indole-3-acrylate, indole-3-butyrate, indole-3-lactate) and kynurenines (anthranilic and xanthurenic acids) in the intestine. In serum of mice after FMT, indole metabolites (indole-3-butyrate, indole-3-carboxaldehyde, indole-3-lactate, indole-3-propionate) predominantly increased; however, tryptamine and xanthurenic acid also demonstrated a clear increase. The use of FMT demonstrates that the intestinal microbiota is a source of not only indole derivatives of tryptophan, but also metabolites of the kynurenine pathway.},
}

Animals
*Tryptophan/metabolism/blood
Mice
*Fecal Microbiota Transplantation
*Gastrointestinal Microbiome
Germ-Free Life
Indoles/metabolism/blood
*Intestines/microbiology
Feces/microbiology
Male
Kynurenine/blood/metabolism
Quinolinic Acid/metabolism/blood

@article {pmid40569502,
year = {2025},
author = {Mortezaee, K},
title = {Microbiota interaction with Tregs: a target for colitis.},
journal = {Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico},
volume = {},
number = {},
pages = {},
pmid = {40569502},
issn = {1699-3055},
abstract = {Gut-resident microbiota associate with host immune system to promote homeostasis, and regulatory T cells (Tregs) are critical in the maintenance of immune balance. Tregs have immunosuppressive activity, and their presence hampers the development of inflammatory diseases. This review aims to unravel microbiome impact on Tregs in bowel inflammation and harnessing such interaction to combat colitis as a separate disease or a consequence of immune checkpoint inhibitor (ICI) therapy of cancer. Short-chain fatty acids (SCFAs) are microbial-derived metabolites associated positively with Treg generation and maintenance and being effective for hampering bowel inflammation. Treg induction shapes gut microbiota profile and support microorganism colonization in their niche and protect the host from inflammation, while suppression of Treg differentiation and activity directs microbiota-induced Th17 expansion and inducing inflammation. Thus, balancing Treg representation with Th17 cells and Treg reprogramming through manipulation of gut microbiota can offer therapy. Microbiota epithelial attachment/detachment and interaction with antigen-presenting cells (APCs) are important for the final fate of T cell signature. Fecal microbial transplantation (FMT) is a strategy for promoting normobiosis and represents a navel approach to targeting colitis. FMT with appropriate microbiota from healthy donors can reinforce microbial diversity, density and persistence to enrich their environment with transforming growth factor (TGF)-β, induce IL-10 producing APCs and reinforce gut barrier, with all these being effective for recovering Tregs, restoring intestinal homeostasis and hampering colitis. ICI therapy of cancer may predispose subjects to colitis due to the impact on microbiome and reducing Treg population. FMT promotes local Treg reorchestration, being advantageous in cancer patients.},
}

@article {pmid40568731,
year = {2025},
author = {Masetti, R and Barbara, G and Muratore, E and Marasco, G and Cremon, C and Marangoni, A and Brigidi, P and Putignani, L and Angelino, G and Quagliarella, F and Galaverna, F and Leardini, D and Lazzarotto, T and Gabelli, M and Savarino, E and Zecca, M and Faraci, M and Prete, A and Biffi, A and Locatelli, F and Merli, P},
title = {Fecal microbiota transplantation for decolonization from multidrug-resistant bacteria in pediatric allogeneic hematopoietic stem cell transplantation recipients: a retrospective real-word data study.},
journal = {Haematologica},
volume = {},
number = {},
pages = {},
doi = {10.3324/haematol.2025.288067},
pmid = {40568731},
issn = {1592-8721},
abstract = {Not available.},
}

@article {pmid40568683,
year = {2025},
author = {Wang, C and Fan, Y and Zhang, L and Zhao, Z and Luo, F and Sun, K and Zeng, M and Tian, H and Peng, M and Luo, Y and Zhao, H and He, S and Sun, H},
title = {Deciphering the contributions of fecal microbiota from patients with high-grade glioma to tumor development in a humanized microbiome mouse model of glioma.},
journal = {Neuro-oncology advances},
volume = {7},
number = {1},
pages = {vdaf085},
pmid = {40568683},
issn = {2632-2498},
abstract = {BACKGROUND: Recent studies have revealed associations between gut microbiota and glioma. However, the underlying mechanisms remain poorly understood. This study primarily aims to elucidate the impact of altered gut microbiota on tumor progression in glioma-bearing mice.

METHODS: Fecal samples were collected from glioma patients and healthy controls to compare the effects of human-derived gut microbiota on glioma development in mice. We also analyzed the associations between these microbiota profiles and plasma metabolites.

RESULTS: Significant differences were observed in both the composition and diversity of the gut microbiota between glioma patients and healthy controls. Mice transplanted with gut microbiota from high-grade glioma patients (HGG-FMT) exhibited accelerated glioma progression compared to those transplanted with microbiota from healthy individuals (HC-FMT). Specifically, Eisenbergiella, Mailhella, and Merdimonas were significantly enriched in HGG-FMT mice, while Limosilactobacillus and Anaerospora increased in HC-FMT mice. Furthermore, Merdimonas showed a positive correlation with sphingosine, sphingosine 1-phosphate, and D-sphingosine in HGG-FMT mice. Conversely, Limosilactobacillus was positively correlated with stearidonic acid and eicosapentaenoic acid in HC-FMT mice.

CONCLUSIONS: Our findings demonstrate that gut microbiota from high-grade glioma patients can promote glioma progression in mice, potentially through mechanisms involving sphingosine 1-phosphate. This metabolite may enter the bloodstream and accelerate glioma growth, offering novel insights into glioma pathogenesis and potential treatment options.},
}

@article {pmid40564914,
year = {2025},
author = {Wong, JKC and Patel, BK and Tai, YK and Tan, TZ and Khine, WWT and Chen, WC and Kukumberg, M and Ching, J and Lee, LS and Chua, KV and Tan, TY and Wu, KY and Bai, X and Iversen, JN and Purnamawati, K and Abdul Jalil, R and Kumar, AP and Lee, YK and Moochhala, SM and Franco-Obregón, A},
title = {Fecal Microbiota Transplantation from Mice Receiving Magnetic Mitohormesis Treatment Reverses High-Fat Diet-Induced Metabolic and Osteogenic Dysfunction.},
journal = {International journal of molecular sciences},
volume = {26},
number = {12},
pages = {},
doi = {10.3390/ijms26125450},
pmid = {40564914},
issn = {1422-0067},
support = {A-0001177-01-00//iHealthtech Microbiome in Health, Disease and Aging 2018 Joint Research Grant/ ; MOE-T2EP30120-0016//Ministry of Education/ ; NUHSRO/2023/039/RO5+6/Seed-Mar/04//National University Health System/ ; },
mesh = {Animals ; *Diet, High-Fat/adverse effects ; Mice ; *Fecal Microbiota Transplantation/methods ; Male ; *Osteogenesis ; Mice, Inbred C57BL ; Ceramides/metabolism ; Gastrointestinal Microbiome ; *Magnetic Field Therapy/methods ; Liver/metabolism ; *Metabolic Diseases/therapy/etiology/metabolism ; Bone Density ; },
abstract = {This study compared the metabolic consequences of fecal microbiota transplantation (FMT) from donor mice that had been either administered pulsed electromagnetic field (PEMF) therapy or exercised to recipient mice fed a high-fat diet (HFD). Eight weeks of PEMF treatment (10 min/week) enhanced PGC-1α-associated mitochondrial and metabolic gene expression in white and brown adipose to a greater degree than eight weeks of exercise (30-40 min/week). FMT from PEMF-treated donor mice recapitulated these adipogenic adaptations in HFD-fed recipient mice more faithfully than FMT from exercised donors. Direct PEMF treatment altered hepatic phospholipid composition, reducing long-chain ceramides (C16:0) and increasing very long-chain ceramides (C24:0), which could be transferred to PEMF-FMT recipient mice. FMT from PEMF-treated mice was also more effective at recovering glucose tolerance than FMT from exercised mice. PEMF treatment also enhanced bone density in both donor and HFD recipient mice. The gut Firmicutes/Bacteroidetes (F/B) ratio was lowest in both the directly PEMF-exposed and PEMF-FMT recipient mouse groups, consistent with a leaner phenotype. PEMF treatment, either directly applied or via FMT, enhanced adipose thermogenesis, ceramide levels, bone density, hepatic lipids, F/B ratio, and inflammatory blood biomarkers more than exercise. PEMF therapy may represent a non-invasive and non-strenuous method to ameliorate metabolic disorders.},
}

Animals
*Diet, High-Fat/adverse effects
Mice
*Fecal Microbiota Transplantation/methods
Male
*Osteogenesis
Mice, Inbred C57BL
Ceramides/metabolism
Gastrointestinal Microbiome
*Magnetic Field Therapy/methods
Liver/metabolism
*Metabolic Diseases/therapy/etiology/metabolism
Bone Density

@article {pmid40564903,
year = {2025},
author = {Chung, BS and Yang, K and Park, C and Ryu, T},
title = {Prolonged Intestinal Ethanol Absorption and Oxidative Stress: Revisiting the Gut-Liver Axis in Alcohol-Associated Disease.},
journal = {International journal of molecular sciences},
volume = {26},
number = {12},
pages = {},
doi = {10.3390/ijms26125442},
pmid = {40564903},
issn = {1422-0067},
support = {RS-2023-00238039//National Research Foundation of Korea/ ; },
mesh = {Humans ; *Oxidative Stress/drug effects ; *Ethanol/pharmacokinetics/metabolism ; *Intestinal Absorption ; Animals ; *Liver/metabolism/drug effects ; Gastrointestinal Microbiome ; *Liver Diseases, Alcoholic/metabolism ; Intestinal Mucosa/metabolism ; *Alcoholism/metabolism ; Dysbiosis ; },
abstract = {Chronic alcohol consumption induces oxidative stress not only in the liver but also in the gastrointestinal tract, where prolonged intestinal ethanol absorption plays a pivotal and underrecognized role. This review reframes ethanol pharmacokinetics to emphasize sustained jejunal and ileal uptake, which maintains elevated blood alcohol levels and perpetuates redox imbalance across the gut-liver axis. We integrate recent findings on ethanol-induced barrier dysfunction, CYP2E1-mediated ROS production, microbial dysbiosis, and mitochondrial disruption, proposing that the intestine is an active site of injury and a driver of systemic inflammation. Key mechanistic insights reveal that gut-derived endotoxins, compromised epithelial integrity, and microbiome-mitochondria interactions converge to exacerbate hepatic and extrahepatic damage. We further explore emerging therapeutic strategies-ranging from NAD[+] repletion and probiotics to fecal microbiota transplantation-that target this upstream pathology. Recognizing prolonged intestinal ethanol absorption as a clinically meaningful phase offers new directions for early intervention and redox-based treatment in alcohol-associated disease.},
}

Humans
*Oxidative Stress/drug effects
*Ethanol/pharmacokinetics/metabolism
*Intestinal Absorption
Animals
*Liver/metabolism/drug effects
Gastrointestinal Microbiome
*Liver Diseases, Alcoholic/metabolism
Intestinal Mucosa/metabolism
*Alcoholism/metabolism
Dysbiosis

@article {pmid40564111,
year = {2025},
author = {Bieganska, EA and Kosinski, P and Wolski, M},
title = {Possible Applications of Fecal Microbiota Transplantation in the Pediatric Population: A Systematic Review.},
journal = {Biomedicines},
volume = {13},
number = {6},
pages = {},
doi = {10.3390/biomedicines13061393},
pmid = {40564111},
issn = {2227-9059},
abstract = {Background: The potential therapeutic role of fecal microbiota transplantation (FMT) in various diseases has been thoroughly studied over the last few decades. However, the majority of studies focus on the adult population, therefore, conclusions regarding the application of FMT in the pediatric population are much less clear. This systematic review aims to summarize the research conducted so far on the efficacy and safety of FMT in the pediatric population, assess the quality of the evidence of its effectiveness, and outline the most promising areas for future research. Methods: We performed a systematic literature search from the index date to 8 June 2024 on the Embase, PubMed, and Web of Science databases. One author screened the resulting 121 articles. Eventually, 35 eligible studies that reported FMT use in seven different diseases were identified. Results: All of the studies assessed FMT as a safe procedure without many serious adverse effects. The best-documented application, which is the only one recommended in official guidelines, is recurrent Clostridioides difficile infection. Other disease entities in which the use of FMT has been studied with good clinical effects are inflammatory bowel disease, allergic colitis, autism, Tourette syndrome, and colonization with multi-drug-resistant organisms. However, it should be noted that the majority of studies are cohort and case-control studies, without randomization, which translates into low evidence quality. In one randomized, controlled trial focusing on the effect of FMT on weight loss in obese individuals, a lack of effect was found. Conclusions: While FMT and subsequent iterations of gut microbiota-targeted interventions hold promising therapeutic potential for various disease entities in the pediatric population, the current evidence behind this conclusion is of low quality. Based on current studies, these methods appear to be both effective and safe. However, further randomized clinical trials are necessary, especially within the pediatric population, for which such studies remain scarce.},
}

@article {pmid40564097,
year = {2025},
author = {Severino, A and Porcari, S and Rondinella, D and Capuano, E and Rozera, T and Kaitsas, F and Gasbarrini, A and Cammarota, G and Ianiro, G},
title = {The Multi-Faceted Role of Gut Microbiota in Alopecia Areata.},
journal = {Biomedicines},
volume = {13},
number = {6},
pages = {},
doi = {10.3390/biomedicines13061379},
pmid = {40564097},
issn = {2227-9059},
abstract = {Alopecia areata (AA) is a complex autoimmune disorder with multifactorial pathogenesis. Recent research highlights the gut microbiota as a possible key player in AA pathogenesis through the gut-skin axis: gut dysbiosis may disrupt intestinal barrier integrity and immune tolerance by affecting T regulatory cells, potentially contributing to disease onset and progression. The purpose of this review is to analyze the current evidence on the correlation between gut microbiota and AA, dissecting both the pathogenetic role of its alterations in the onset and progression of disease and its potential role as a therapeutic target.},
}

@article {pmid40563141,
year = {2025},
author = {Zhang, Y and Qing, J and Saed, YA and Li, Y},
title = {Gut microbiota implication in diabetic kidney disease: mechanisms and novel therapeutic strategies.},
journal = {Renal failure},
volume = {47},
number = {1},
pages = {2517402},
doi = {10.1080/0886022X.2025.2517402},
pmid = {40563141},
issn = {1525-6049},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Dysbiosis/complications/microbiology/therapy ; *Diabetic Nephropathies/microbiology/therapy/etiology ; Probiotics/therapeutic use ; Fecal Microbiota Transplantation ; Prebiotics/administration & dosage ; *Diabetes Mellitus, Type 2/complications ; Synbiotics/administration & dosage ; Disease Progression ; },
abstract = {Diabetic kidney disease (DKD) is one of the leading causes of chronic kidney disease and end-stage renal disease worldwide, predominantly driven by the rise in type 2 diabetes mellitus. Recent evidence highlights the crucial role of gut microbiota dysbiosis in the development and progression of DKD. Dysbiosis, characterized by a reduction in beneficial short-chain fatty acid-producing bacteria and an increase in pathogenic species such as Proteobacteria and Bacteroides, exacerbates systemic inflammation, insulin resistance, and kidney damage through mechanisms like increased intestinal permeability and the production of pro-inflammatory metabolites like lipopolysaccharides. This review explores the impact of specific bacterial taxa on DKD risk and progression, such as Alistipes, Subdoligranulum, and their interactions with metabolic pathways. Furthermore, we discuss novel therapeutic strategies targeting gut microbiota, including probiotics, prebiotics, synbiotics, and fecal microbiota transplantation, which have shown promise in ameliorating DKD symptoms. However, the heterogeneity of gut microbiota across individuals and the challenges in treatment standardization call for personalized approaches and further research into the gut-kidney axis.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Dysbiosis/complications/microbiology/therapy
*Diabetic Nephropathies/microbiology/therapy/etiology
Probiotics/therapeutic use
Fecal Microbiota Transplantation
Prebiotics/administration & dosage
*Diabetes Mellitus, Type 2/complications
Synbiotics/administration & dosage
Disease Progression

@article {pmid40563092,
year = {2025},
author = {Amimo, JO and Kunyanga, CN and Raev, SA and Kick, M and Micheal, H and Saif, LJ and Vlasova, AN},
title = {Stunting is associated with persistent and transferable alterations in the gut microbiome.},
journal = {Gut pathogens},
volume = {17},
number = {1},
pages = {49},
pmid = {40563092},
issn = {1757-4749},
support = {OPP1117467//Bill and Melinda Gates Foundation/ ; R01A1099451//National Institute of Allergy and Infectious Diseases/ ; },
abstract = {As robust animal models to study the pathophysiology of stunting are absent, we have comparatively characterized the gut microbiota of malnourished/stunted vs. clinically healthy/normal Kenyan toddlers (12-24 months old) and established a gnotobiotic (Gn) pig fecal transplant model to gain understanding of microbial community structure associated with stunting. As expected, the bacterial composition between the two toddler groups was distinct: Actinobacteria was most prevalent in healthy toddlers, whereas Proteobacteria dominated in stunted toddlers. Although the diversity indices showed no significant differences, unique bacterial genera were found in each toddler group: three genera unique to stunted toddlers and ten unique to healthy toddlers, with eight genera shared between the groups. We observed a higher number of enriched bacterial virulence genes in healthy vs. stunted toddlers suggesting that the microbiome plasticity and functional characteristics of the healthy toddlers allow for the pathogen/pathobiont control. In contrast, we noted the presence of more genes associated with antimicrobial-resistance (AMR) bacteria in stunted toddlers, possibly due to early-life antibiotic treatments. Of interest, functional analysis showed that CAZymes associated with carbohydrate biosynthesis, and a few metabolic pathways related to protein/amino acid, carbohydrate and fat catabolism were enriched in stunted toddlers. In contrast carbohydrate degradation CAZymes and numerous anabolic pathways were prevalent in healthy toddlers. These patterns were also evident in the Gn pigs transplanted with stunted/healthy human fecal microbiota (HFM). Overall, our findings suggest that the microbiota transplanted Gn pigs represent a valuable model for studying the infant microbial community structure and the impacts of stunting on the child gut microbiota. Additionally, this is the first study to demonstrate that the healthy vs. stunted microbiota composition and function remained different in the Gn pigs throughout the study. This information and the Gn pig model are vital for developing and testing targeted interventions for malnourished/stunted populations, consequently advancing microbiome-based diagnosis and personalized medicine.},
}

@article {pmid40561430,
year = {2025},
author = {Ung, W and Bonavida, B},
title = {Review Article: Fecal Microbiota Transplantation in Melanoma: Mechanisms-Mediated Enhancement of Anti-Tumor Immunotherapy.},
journal = {Critical reviews in oncogenesis},
volume = {30},
number = {2},
pages = {23-35},
doi = {10.1615/CritRevOncog.2025058249},
pmid = {40561430},
issn = {0893-9675},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; *Melanoma/therapy/immunology/microbiology/etiology ; *Immunotherapy/methods ; *Gastrointestinal Microbiome/immunology ; Immune Checkpoint Inhibitors/therapeutic use ; Animals ; *Skin Neoplasms/therapy/immunology/microbiology ; },
abstract = {The gut microbiota is integral to human health, influencing nutrition, metabolism, and immunity. Dysbiosis has been implicated in cancer development and resistance to therapies, highlighting the potential of microbiota modulation as a therapeutic strategy. Melanoma, while comprising only 1% of skin cancer diagnoses, accounts for over 80% of skin cancer related deaths, emphasizing the need for innovative approaches to enhance treatment efficacy. Although immune checkpoint inhibitors (ICIs) such as anti-programmed cell death protein (PD-1) and cytotoxic T-lymphocyte associated protein 4 (CTLA-4) blockade therapies have significantly improved survival for some melanoma patients, the majority fails to achieve durable responses and often develops long-term resistance to these treatments. Fecal microbiota transplantation (FMT) is emerging as a promising intervention to restore microbial balance and enhance treatment efficacy. This review explores the historical evolution and current applications of FMT in oncology, with a focus on its ability to modulate the gut microbiome, augment antitumor immunity, and overcome resistance to checkpoint blockade therapy in melanoma. Despite its promise, significant challenges remain, including ensuring the safety of the procedure, selecting suitable donors, and addressing regulatory hurdles. Future research aimed at optimizing FMT protocols, identifying key microbial strains, and understanding the mechanisms underlying microbiota-immune interactions will be essential to fully harness the potential of FMT as a transformative adjunct in cancer treatment.},
}

Humans
*Fecal Microbiota Transplantation/methods
*Melanoma/therapy/immunology/microbiology/etiology
*Immunotherapy/methods
*Gastrointestinal Microbiome/immunology
Immune Checkpoint Inhibitors/therapeutic use
Animals
*Skin Neoplasms/therapy/immunology/microbiology

@article {pmid40559778,
year = {2025},
author = {Nishigaki, A and Marchesi, JR and Previdelli, RL},
title = {Faecal Microbiota Transplantation as an Adjuvant Treatment for Extraintestinal Disorders: Translating Insights from Human Medicine to Veterinary Practice.},
journal = {Veterinary sciences},
volume = {12},
number = {6},
pages = {},
doi = {10.3390/vetsci12060541},
pmid = {40559778},
issn = {2306-7381},
abstract = {Faecal microbiota transplantation (FMT) has emerged as a transformative therapy in human medicine, particularly for managing recurrent Clostridioides difficile infections and other gastrointestinal (GI) disorders. Beyond the GI tract, FMT has shown potential in addressing extraintestinal conditions in people, including metabolic, immune-mediated, dermatological, neurological, and infectious diseases. Research in people has highlighted its efficacy in decolonising multidrug-resistant organisms in infection, mitigating autoimmune diseases, and improving outcomes in metabolic disorders such as obesity and diabetes. Furthermore, FMT has also been linked to enhanced responses to immunotherapy in cancer and improved management of hepatic and renal conditions. These findings underscore the intricate connections between the gut microbiome and systemic health, opening novel therapeutic avenues. In veterinary medicine, while FMT has demonstrated benefits for GI disorders, its application in extraintestinal diseases remains largely unexplored. Emerging evidence suggests that conditions such as atopic dermatitis, chronic kidney disease, immune-mediated diseases, and behavioural disorders in companion animals could benefit from microbiome-targeted therapies. However, significant gaps in knowledge persist, particularly regarding the long-term safety and efficacy for veterinary applications. This review synthesises findings from human medicine to assess their relevance for veterinary applications and future research.},
}

@article {pmid40559592,
year = {2025},
author = {Egrek, S and Knapp, J and Sacheli, R and El Moussaoui, K and Léonard, P and Larranaga Lapique, E and Millon, L and Engelskirchen, S and Detry, O and Linden, A and Hayette, MP},
title = {EmsB Microsatellite Analysis of Echinococcus multilocularis Specimens Isolated from Belgian Patients with Alveolar Echinococcosis and from Animal Hosts.},
journal = {Pathogens (Basel, Switzerland)},
volume = {14},
number = {6},
pages = {},
doi = {10.3390/pathogens14060584},
pmid = {40559592},
issn = {2076-0817},
mesh = {Animals ; *Echinococcus multilocularis/genetics/isolation & purification/classification ; Humans ; Foxes/parasitology ; *Microsatellite Repeats ; Belgium/epidemiology ; *Echinococcosis/parasitology ; Retrospective Studies ; Zoonoses/parasitology ; *Echinococcosis, Hepatic/parasitology ; Genotype ; Rodentia/parasitology ; Feces/parasitology ; },
abstract = {Alveolar echinococcosis (AE), caused by Echinococcus multilocularis (E. multilocularis), is a severe parasitic zoonosis that is potentially fatal for humans. The parasite is primarily transmitted by wildlife, with red foxes acting as definitive hosts and rodents as intermediate hosts, while humans can become accidental but dead-end hosts. The aim of this study is to use EmsB typing on E. multilocularis isolates from human AE cases and local animals such as foxes and rodents. In this study, retrospective EmsB typing was performed on 39 samples, including 11 tissue samples from 10 patients, 18 fecal swabs from foxes, and 10 tissue samples from rodents. A dendrogram was created to determine the EmsB profiles present. The results showed that all the rodent samples were associated with the EmsB P1 profile (10/10), while the human and fox samples shared the EmsB profile P1 (5/11 humans and 8/18 foxes), a profile near P4 (2/11 humans and 3 foxes), and a profile near P8 (1/11 humans and 1/18 foxes). The study demonstrates that the same EmsB profiles circulate among humans and animals, confirming that wildlife reservoirs play a key role in transmission.},
}

Animals
*Echinococcus multilocularis/genetics/isolation & purification/classification
Humans
Foxes/parasitology
*Microsatellite Repeats
Belgium/epidemiology
*Echinococcosis/parasitology
Retrospective Studies
Zoonoses/parasitology
*Echinococcosis, Hepatic/parasitology
Genotype
Rodentia/parasitology
Feces/parasitology

@article {pmid40559436,
year = {2025},
author = {Domilescu, I and Miutescu, B and Horhat, FG and Popescu, A and Nica, C and Ghiuchici, AM and Gadour, E and Sîrbu, I and Hutanu, D},
title = {Gut-Microbiome Signatures Predicting Response to Neoadjuvant Chemoradiotherapy in Locally Advanced Rectal Cancer: A Systematic Review.},
journal = {Metabolites},
volume = {15},
number = {6},
pages = {},
doi = {10.3390/metabo15060412},
pmid = {40559436},
issn = {2218-1989},
abstract = {BACKGROUND AND OBJECTIVES: Rectal cancer management increasingly relies on watch-and-wait strategies after neoadjuvant chemoradiotherapy (nCRT). Accurate, non-invasive prediction of pathological complete response (pCR) remains elusive. Emerging evidence suggests that gut-microbiome composition modulates radio-chemosensitivity. We systematically reviewed primary studies that correlated baseline or on-treatment gut-microbiome features with nCRT response in locally advanced rectal cancer (LARC).

METHODS: MEDLINE, Embase and PubMed were searched from inception to 30 April 2025. Eligibility required (i) prospective or retrospective human studies of LARC, (ii) faecal or mucosal microbiome profiling by 16S, metagenomics, or metatranscriptomics, and (iii) response assessment using tumour-regression grade or pCR. Narrative synthesis and random-effects proportion meta-analysis were performed where data were homogeneous.

RESULTS: Twelve studies (n = 1354 unique patients, median sample = 73, range 22-735) met inclusion. Four independent machine-learning models achieved an Area Under the Receiver Operating Characteristic curve AUROC ≥ 0.85 for pCR prediction. Consistently enriched taxa in responders included Lachnospiraceae bacterium, Blautia wexlerae, Roseburia spp., and Intestinimonas butyriciproducens. Non-responders showed over-representation of Fusobacterium nucleatum, Bacteroides fragilis, and Prevotella spp. Two studies linked butyrate-producing modules to radiosensitivity, whereas nucleotide-biosynthesis pathways conferred resistance. Pooled pCR rate in patients with a "butyrate-rich" baseline profile was 44% (95% CI 35-54) versus 21% (95% CI 15-29) in controls (I[2] = 18%).

CONCLUSIONS: Despite heterogeneity, convergent functional and taxonomic signals underpin a microbiome-based radiosensitivity axis in LARC. Multi-centre validation cohorts and intervention trials manipulating these taxa, such as prebiotics or live-biotherapeutics, are warranted before clinical deployment.},
}

@article {pmid40558164,
year = {2025},
author = {Han, X and Qin, Y and Guo, J and Huang, W and You, Y and Zhan, J and Yin, Y},
title = {IgA Dysfunction Induced by Early-Lifetime Low-Dose Antibiotics Exposure Aggravates Diet-Induced Metabolic Syndrome.},
journal = {Antibiotics (Basel, Switzerland)},
volume = {14},
number = {6},
pages = {},
doi = {10.3390/antibiotics14060574},
pmid = {40558164},
issn = {2079-6382},
support = {82330017 and 82270610//National Natural Science Foundation/ ; },
abstract = {Background: Low-dose antibiotic contamination in animal feed is a persistent global food safety challenge. Transient early-life exposure to low-dose penicillin (LDP) is known to induce metabolic syndrome (MetS) in adult mice, but the underlying mechanisms are unclear. Introduction: This study investigated the role of gut microbiota (GM) and intestinal immunity in mediating the long-term metabolic effects of early-life LDP exposure. Methods: Mice were exposed to LDP transiently during early life. GM composition was analyzed. Intestinal IgA responses were quantified. Bacterial encroachment, systemic and adipose tissue inflammation, and diet-induced MetS were assessed. Germ-free (GF) mice received GM transplants from LDP-exposed or control mice to test causality and persistence. Results: Early-life LDP exposure significantly disrupted GM composition, particularly in the ileum, in 30-day-old mice. These GM alterations caused persistent suppression of intestinal IgA responses, evidenced by reduced IgA-producing cells and sIgA levels. This suppression was constrained to early-life exposure: transferring LDP-modified GM to GF mice produced only a transient reduction in fecal sIgA. The LDP-induced sIgA reduction decreased IgA binding of bacteria, leading to increased bacterial encroachment and systemic and adipose tissue inflammation. These pathological changes exacerbated diet-induced MetS. Discussion: Our findings demonstrate that early-life LDP exposure induces persistent intestinal IgA deficiency through lasting GM alterations initiated in early development. This deficiency drives bacterial encroachment, inflammation, and ultimately exacerbates MetS. Conclusions: The exacerbation of diet-induced metabolic syndrome by early-life LDP exposure occurs through an intestinal sIgA-dependent pathway triggered by persistent GM disruption. This highlights a critical mechanism linking early-life antibiotic exposure, gut immune dysfunction, and long-term metabolic health, with significant implications for food safety.},
}

@article {pmid40554893,
year = {2025},
author = {You, L and Peng, H and Liu, J and Sai, N and Zhao, W and Li, X and Yang, C and Guo, P and Ni, J},
title = {Xiaoer Huanglong pellets remodels the periphery microenvironment to improve attention deficit hyperactivity disorder based on the microbiota-gut-brain axis.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {145},
number = {},
pages = {157007},
doi = {10.1016/j.phymed.2025.157007},
pmid = {40554893},
issn = {1618-095X},
abstract = {BACKGROUND: Recently, research interest in attention deficit hyperactivity disorder (ADHD) has grown significantly, driven by its increasing incidence and substantial societal impact. Among the various pathogenic mechanisms under investigation, the microbiota-gut-brain axis has emerged as a crucial area of focus. In the context of ADHD treatment, Xiaoer Huanglong Pellets (XRHLP), a traditional Chinese herbal formulation, have demonstrated therapeutic efficacy, although the underlying mechanisms remain partially understood.

PURPOSE: This study aimed to analyze and compare the therapeutic effects and underlying mechanisms of XRHLP, including gastric release (WR_HL), enteric release (CR_HL), and colon release (JCR_HL) pellets, for ADHD treatment.

METHODS: This study employed a multi-modal approach to investigate the effects of XRHLP on ADHD. Behavioral assessments combined with Enzyme-linked immunosorbent assay and Western-blot analyses were conducted to evaluate the therapeutic outcomes in model rats with ADHD. Comprehensive profiling of the gut-brain axis was performed using 16S ribosomal RNA sequencing and untargeted and targeted metabolomic analyses. The causal role of the gut microbiota was further validated using fecal microbiota transplantation (FMT).

RESULTS: WR_HL, CR_HL, and JCR_HL improved ADHD-like behaviors and neurotransmission dysfunction, with JCR_HL exhibiting superior intervention effects compared to WR_HL and CR_HL. These therapeutic effects are mediated through multiple pathways, including the restoration of gut microbial homeostasis, attenuation of inflammatory cascades, and repair of compromised intestinal and blood-brain barrier. The intervention also corrected systemic metabolic imbalances by specifically addressing the abnormalities in amino acid metabolism, neurotransmitter regulation, and short-chain fatty acid production. FMT experiments further confirmed the critical role of microbial modulation in mediating the behavioral and microbial regulatory effects of XRHLP.

CONCLUSION: In summary, XRHLP exerts anti-ADHD effects by improving the microbiota-gut-brain axis and correcting amino acid metabolic disorders, providing new insights into the molecular mechanisms by which traditional Chinese medicine influences ADHD and offers potential avenues for drug development.},
}

@article {pmid40554061,
year = {2025},
author = {Yang, W and Zou, P and He, S and Cui, H and Yang, Z and An, H and Chen, Q and Huang, W and Guo, H and Liu, J and Ling, X and Cao, J and Ao, L},
title = {Perfluorooctane sulfonic acid impairs spermatogenesis via the liver-gut microbiota-testis axis: a central role of chenodeoxycholic acid metabolism.},
journal = {Journal of advanced research},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jare.2025.06.037},
pmid = {40554061},
issn = {2090-1224},
abstract = {INTRODUCTION: Perfluorooctane sulfonic acid (PFOS) as a global contaminant is ubiquitously presented in the environmental media and human body. The association between PFOS exposure and reduced male fertility has been recently discovered. However, the relevant mechanism remains unexplored.

OBJECTIVES: Our study aimed to investigate the effect and mechanism of PFOS exposure on male reproductive function.

METHODS: In a murine PFOS exposure model, single-nucleus transcriptome sequencing was performed to delineate the transcriptomic landscape of mouse testes at the single-cell resolution. We examined the serum metabolomic profile and conducted in-depth analysis of hepatic transcriptome datasets to explore the metabolic connections between liver and testis under PFOS exposure. Through integrating chenodeoxycholic acid intervention, fecal microbiota transplantation (FMT), metagenomic sequencing, testicular metabolome, Ligilactobacillus murinus (L. murinus) metabolome, and administration of L. murinus, we confirmed the role of the liver-gut microbiota-testis axis and screened the critical gut microbiota involved in PFOS-mediated spermatogenic disorders.

RESULTS: The results showed that PFOS exposure led to spermatogenic arrest and abnormal spermatogenic microenvironment in the mouse testis. The PFOS-repressed hepatic chenodeoxycholic acid (CDCA) synthesis contributed to the reduced serum/testicular levels of essential fatty acid (linoleic acid) and lipid-soluble vitamins (retinol, vitamin D3), which was responsible for the spermatogenic arrest. Beyond this, PFOS-mediated impaired CDCA production decreased the abundance of gut L. murinus, which affected spermatogenesis through the potential involvement of aspartic acid metabolism. For the first time to our knowledge, we comprehensively assessed the effects of PFOS exposure on the spermatogenic process and elucidated the unrecognized role of liver-gut microbiota-testis axis in PFOS-induced abnormal spermatogenesis.

CONCLUSIONS: The unveiled organ crosstalks provide new insights into the metabolism-disrupting properties, hepatotoxicity, and reproductive toxicity of PFOS, which may facilitate the development of molecule-, metabolite-, and microbe-based strategies for PFOS-induced metabolic diseases and reproductive disorders.},
}

@article {pmid40553742,
year = {2025},
author = {Frutkoff, YA and Plotkin, L and Pollak, D and Livovsky, J and Focht, G and Lev-Tzion, R and Ledder, O and Assa, A and Yogev, D and Orlanski-Meyer, E and Broide, E and Kierkuś, J and Kang, B and Weiss, B and Aloi, M and Schwerd, T and Shouval, DS and Bramuzzo, M and Griffiths, AM and Yassour, M and Turner, D},
title = {Whole food diet induces remission in children and young adults with mild-moderate Crohn's disease and is more tolerable than exclusive enteral nutrition: a randomized controlled trial.},
journal = {Gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.1053/j.gastro.2025.06.011},
pmid = {40553742},
issn = {1528-0012},
abstract = {BACKGROUND: Tasty&Healthy (T&H) is a whole-food diet for Crohn's disease (CD), which excludes processed food, gluten, red meat, and dairy, without requiring formula or mandatory ingredients. TASTI-MM was a clinician-blinded, randomized-controlled trial comparing tolerability and effectiveness of T&H vs. exclusive enteral nutrition (EEN).

METHODS: Patients with biologic-naive mild-moderate CD aged 6-25 years were randomized to either T&H or EEN for 8 weeks, receiving weekly dietary support. Tolerability was evaluated by weekly interviews, questionnaires and intake diaries. Other outcomes included symptomatic remission, Mucosal-Inflammation Non-Invasive (MINI) index, calprotectin, C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). Fecal microbiome was analyzed by metagenomics at baseline, week-4 and week-8. Data were analyzed by the intention-to-treat approach unless specified otherwise.

RESULTS: Among 83 included patients (41 T&H, 42 EEN; mean age 14.5±3.7 years), 88% tolerated T&H vs. 52% for EEN (aOR 7.7 [95%CI 2.4-25]; p<0.001). Calprotectin, CRP and ESR decreased significantly in both groups, with no between-group differences. Symptomatic remission was achieved in 56% of T&H group vs. 38% of the EEN group (aOR 2.5 [0.98-6.3], p=0.1; per-protocol: 67% vs. 76%; p=0.47). Calprotectin <250μg/g was achieved in 34% vs. 33% (aOR 0.97 [0.37-2.6], p=0.84) and MINI<8 in 44% vs. 31% (aOR 1.8 [0.7-4.5]; p=0.33). Microbiome α-diversity improved in the T&H arm and declined in the EEN arm, showing superior species richness at both week-4 and week-8. Species associated with bowel inflammation, such as Ruminococcus gnavus, decreased in T&H and increased in EEN (q<0.001).

CONCLUSIONS: T&H demonstrated better tolerability than EEN for inducing remission in mild-to-moderate CD, while positively affecting the microbiome (TASTI-MM, NCT#04239248).},
}

@article {pmid40552988,
year = {2025},
author = {Park, JM and Beckman, I and Delaney, CL},
title = {Narrative review of the association between gut microbiota and peripheral artery disease.},
journal = {Vascular medicine (London, England)},
volume = {},
number = {},
pages = {1358863X251346062},
doi = {10.1177/1358863X251346062},
pmid = {40552988},
issn = {1477-0377},
abstract = {It has been posited that the inflammatory process seen in atherosclerosis is underpinned by gut dysbiosis. Dysbiosis refers to alterations in the function, composition, and diversity of the human gut microbiota, all of which are influenced by endogenous and exogenous stimuli. Currently there is limited literature describing the association between gut microbiota and peripheral artery disease (PAD). This review summarizes the evidence surrounding the role of gut microbiota in the initiation of atherosclerosis (through direct infection of atherosclerotic plaque or systemic immune response to bacterial products and metabolites) and how dysbiosis may influence the various treatment modalities for PAD, including medical therapy (pharmacotherapy, lifestyle changes, and supervised exercise training) and surgery (endovascular and open revascularization). In particular, the role of short chain fatty acids (SCFAs), the effects of exercise on SCFA-producing and lactic acid bacteria (LAB) and, consequently, the lack of targeted research into dietary interventions and supplementation are highlighted in this review. This review highlights the potential for gut microbiota as not only a therapeutic target in patients with PAD, but also as a diagnostic and screening tool. It is imperative that the focus of future research is on the potential for personalized treatment which targets the gut microbiota (such as synbiotics, postbiotics, nicotinamide adenine dinucleotide (NAD) supplementation, selective antibiotics, resistance exercise, senolytics, and fecal microbial transplantation [FMT]) to be utilized as adjuncts to already existing treatment options for PAD. This review also highlights the potential role of biobanks and analysis of atherosclerotic plaques in further advancing knowledge and research in this area.},
}

@article {pmid40552775,
year = {2025},
author = {Yang, T and Shao, Y and Wang, Z and Liu, C and Gu, M},
title = {Epigallocatechin-3-Gallate Attenuates Benign Prostatic Hyperplasia Development via Regulating Firmicutes to Inhibit Gastric Secretion of Insulin-Like Growth Factor-1.},
journal = {Cell biology international},
volume = {},
number = {},
pages = {},
doi = {10.1002/cbin.70032},
pmid = {40552775},
issn = {1095-8355},
support = {//The work was sponsored by the Interdisciplinary Program of Shanghai Jiao Tong University (Project Number YG2024QNB17) and the National Natural Science Foundation of China (Grant Nos. 82170788 and 81900687)./ ; },
abstract = {Benign prostatic hyperplasia (BPH), a prevalent age-related condition in men, is increasingly linked to metabolic syndrome (MetS) and gut microbiota dysbiosis. This study reveals how Firmicutes-dominant microbial imbalance drives BPH progression via IGF-1 signaling and identifies the green tea polyphenol epigallocatechin-3-gallate (EGCG) as a dual-action therapeutic. Using MetS-BPH mouse models and human prostate cell lines, we demonstrated that BPH-associated gut microbiota-particularly elevated Firmicutes and an increased Firmicutes/Bacteroidetes ratio-promotes prostate hyperplasia by upregulating IGF-1. Both BPH mice and recipient mice transplanted with BPH microbiota showed elevated serum and prostate IGF-1 levels, mirroring findings in human BPH patients. Mechanistically, IGF-1 stimulated prostate cell proliferation (RWPE-1/WPMY-1) and suppressed apoptosis via PI3K/AKT/mTOR activation, while the IGF-1 antagonist Linsitinib reversed these effects. EGCG emerged as a potent modulator of this gut-prostate axis: it selectively reduced Firmicutes overgrowth in BPH mice, normalized IGF-1 levels, and inhibited downstream PI3K/AKT/mTOR signaling. In fecal microbiota transplantation experiments, EGCG counteracted IGF-1-driven prostate enlargement and microbial dysbiosis, underscoring its dual role in rebalancing gut flora and blocking growth factor pathways. Our findings position EGCG as a promising intervention for MetS-associated BPH, simultaneously targeting microbial dysbiosis and IGF-1 signaling. This study not only elucidates the Firmicutes-IGF-1 axis in BPH pathogenesis but also highlights the therapeutic potential of dietary polyphenols in metabolic urological disorders.},
}

@article {pmid40552763,
year = {2025},
author = {Claypool, J and Lindved, G and Myers, PN and Ward, T and Nielsen, HB and Blount, KF},
title = {Microbiome compositional changes and clonal engraftment in a phase 3 trial of fecal microbiota, live-jslm for recurrent Clostridioides difficile infection.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2520412},
doi = {10.1080/19490976.2025.2520412},
pmid = {40552763},
issn = {1949-0984},
mesh = {Humans ; *Clostridium Infections/therapy/microbiology ; *Fecal Microbiota Transplantation ; *Gastrointestinal Microbiome ; *Feces/microbiology ; Male ; *Clostridioides difficile/physiology ; Female ; Middle Aged ; *Bacteria/classification/genetics/isolation & purification ; Adult ; Recurrence ; Aged ; },
abstract = {Live microbiota therapies have shown promise in many gastrointestinal diseases, including in the prevention of recurrent Clostridioides difficile infections (rCDI); however, frameworks for their pharmacokinetic and pharmacodynamic analysis are not fully established. Fecal microbiota, live-jslm (RBL) is the first microbiota-based product approved by the US Food and Drug Administration for the prevention of rCDI and was superior to placebo in the PUNCH™ CD3 phase 3 clinical trial (NCT03244644). In this analysis, deep shotgun metagenomic sequencing was used to assess changes in gut microbiome compositions of participants and engraftment of bacterial clonal populations (i.e. strains) from RBL to recipients. Among RBL responders, gut microbiota shifted toward compositions that resembled healthy donors as early as 1 week after RBL administration; the resulting microbiota compositions included clonal populations that engrafted from RBL to recipients. Engraftment was higher in RBL responders compared with non-responders, and many clonally engrafted populations persisted for ≥ 6 months. Bacteroidia species were among the most effectively engrafted species from RBL. This study utilizes data from a large clinical trial to establish a method with high specificity for exploring clonal engraftment from microbiota-based treatments to facilitate future pharmacokinetic and pharmacodynamic analyses.Clinicaltrials Registration: NCT03244644.},
}

Humans
*Clostridium Infections/therapy/microbiology
*Fecal Microbiota Transplantation
*Gastrointestinal Microbiome
*Feces/microbiology
Male
*Clostridioides difficile/physiology
Female
Middle Aged
*Bacteria/classification/genetics/isolation & purification
Adult
Recurrence
Aged

@article {pmid40552153,
year = {2025},
author = {Sun, L and Shang, B and Lv, S and Liu, G and Wu, Q and Geng, Y},
title = {Effects of semaglutide on metabolism and gut microbiota in high-fat diet-induced obese mice.},
journal = {Frontiers in pharmacology},
volume = {16},
number = {},
pages = {1562896},
pmid = {40552153},
issn = {1663-9812},
abstract = {BACKGROUND: The purpose of this study was to explore how semaglutide, a GLP-1RA, regulates serum metabolism and gut microbiota to improve obesity in mice and whether fecal microbiota transplantation (FMT) can transmit the beneficial effects of semaglutide to recipient mice.

METHODS: Male C57BL/6J mice were given standard diet (ND), high-fat diet (HFD), or high-fat diet with semaglutide (SHF, 100 μg/kg). Fecal microbiota transplantation was used to transplant the fecal suspension supernatant (MT) and bacteria (FMT) from SHF group mice to antibiotic-induced pseudo-germ-free mice.

RESULTS: Results showed that semaglutide significantly reduced the body weight, body fat, FBG, and insulin levels induced by high-fat diet, and improved insulin resistance and sensitivity damage (p < 0.05). This was achieved by regulating the expression of genes related to lipid metabolism such as Pparα, Pparγ, Cpt1a, and Pgc1α in the liver and adipose tissue, as well as the appetite-related genes Leptin, Agrp, Npy, and Pomc in the hypothalamus. After stopping semaglutide intervention 4 weeks, the body weight of the mice rebounded significantly. Fecal microbiota transplantation could transmit the beneficial effects of semaglutide to recipient mice. Semaglutide and fecal microbiota transplantation affected metabolic pathways such as serum amino acid metabolism and pyrimidine metabolism in obese mice, and reshaped the composition and proportion of fecal gut microbiota in obese mice.

CONCLUSION: In summary, semaglutide could inhibit food intake and improve obesity, regulate serum metabolism and the composition of gut microbiota in mice. Bacterial transplantation is key to transmitting the improvement brought about by fecal microbiota transplantation of semaglutide to recipient mice.},
}

@article {pmid40550813,
year = {2025},
author = {Song, B and Azad, MAK and Zhu, Q and Cheng, Y and Ding, S and Yao, K and Kong, X},
title = {Lactobacillus regulate muscle fiber type conversion in Chinese native pigs via tryptophan metabolism.},
journal = {NPJ biofilms and microbiomes},
volume = {11},
number = {1},
pages = {114},
pmid = {40550813},
issn = {2055-5008},
support = {32350410424//National Natural Science Foundation of China/ ; 2022JJ30643//Hunan Province Natural Science Foundation/ ; 092GJHZ2022044FN//Future Partner Special Network Fund of Chinese Academy of Sciences/ ; 2023YFD1301305//National Key Research and Development Project/ ; },
mesh = {Animals ; *Tryptophan/metabolism ; Swine/microbiology ; *Lactobacillus/metabolism/physiology ; Mice ; Gastrointestinal Microbiome ; Kynurenic Acid/metabolism ; *Muscle Fibers, Slow-Twitch/metabolism ; Feces/microbiology ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism/genetics ; AMP-Activated Protein Kinases/metabolism ; *Muscle Fibers, Skeletal/metabolism ; Metabolome ; },
abstract = {Identifying potential gut microbes and metabolites that can influence muscle fiber type is gaining interest in meat quality research. In this study, muscle fiber characteristics, muscle metabolite profiles, and gut microbiota and metabolome were compared among three pig breeds (Taoyuan black, TB; Xiangcun black, XB; and Duroc pigs). The results showed that the slow-twitch fiber percentage was higher (P < 0.05) in native pigs (TB and XB pigs) compared to Duroc pigs. The differences were mainly regulated by Lactobacillus abundance and tryptophan metabolism. Further, fecal microbiota transplantation from XB pigs transferred a higher slow-twitch fiber percentage, Lactobacillus abundance, kynurenic acid level, and AMPK/PGC-1α expression to mice. These findings suggest that Lactobacillus in the colon of TB and XB pigs, through kynurenic acid production, may promote slow-twitch fiber formation via the AMPK/PGC-1α signaling pathway.},
}

Animals
*Tryptophan/metabolism
Swine/microbiology
*Lactobacillus/metabolism/physiology
Mice
Gastrointestinal Microbiome
Kynurenic Acid/metabolism
*Muscle Fibers, Slow-Twitch/metabolism
Feces/microbiology
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism/genetics
AMP-Activated Protein Kinases/metabolism
*Muscle Fibers, Skeletal/metabolism
Metabolome

@article {pmid40550671,
year = {2025},
author = {Zhang, S and Liu, X and Zhong, Y and Fu, Y},
title = {[Association between gut microbiota and hyperuricemia: insights into innovative therapeutic strategies].},
journal = {Sheng wu gong cheng xue bao = Chinese journal of biotechnology},
volume = {41},
number = {6},
pages = {2290-2309},
doi = {10.13345/j.cjb.250060},
pmid = {40550671},
issn = {1872-2075},
mesh = {*Hyperuricemia/therapy/microbiology ; Humans ; *Gastrointestinal Microbiome/physiology ; Probiotics/therapeutic use ; Uric Acid/metabolism/blood ; Fecal Microbiota Transplantation ; Prebiotics ; Medicine, Chinese Traditional ; },
abstract = {Uric acid (UA) is the final metabolite of purines in the human body. An imbalance in UA production and excretion that disrupts homeostasis leads to elevated blood UA levels and the development of hyperuricemia (HUA). Approximately one-third of UA is excreted through the intestinal tract. As a crucial component of the intestinal microenvironment, the gut microbiota plays a pivotal role in regulating blood UA levels. Alterations or imbalances in gut microbiota composition are linked to the onset of HUA, which implies the potential of gut microbiota as a novel target for the prevention and treatment of HUA. This review introduces the occurrence mechanism and damage of hyperuricemia, examines the association between HUA and the gut microbiota and their metabolites, and explores the molecular mechanisms underlying gut microbiota-targeted therapies for HUA. Furthermore, it discusses the potential applications of probiotics, prebiotics, and traditional Chinese medicine (including both single herbs and compound formulas) with UA-lowering effects, along with cutting-edge technologies such as fecal microbiota transplantation and machine learning in HUA treatment. This review provides valuable perspectives and strategies for improving the prevention and treatment of HUA.},
}

*Hyperuricemia/therapy/microbiology
Humans
*Gastrointestinal Microbiome/physiology
Probiotics/therapeutic use
Uric Acid/metabolism/blood
Fecal Microbiota Transplantation
Prebiotics
Medicine, Chinese Traditional

@article {pmid40550654,
year = {2025},
author = {Zhang, ZW and Ye, YJ and Shen, ZL},
title = {[Pathogenesis and progress in diagnosis and treatment of diversion colitis after colorectal cancer surgery].},
journal = {Zhonghua wei chang wai ke za zhi = Chinese journal of gastrointestinal surgery},
volume = {28},
number = {6},
pages = {627-632},
doi = {10.3760/cma.j.cn441530-20250326-00125},
pmid = {40550654},
issn = {1671-0274},
support = {82272841//National Natural Science Foundation of China/ ; },
mesh = {Humans ; *Colorectal Neoplasms/surgery ; *Colitis/diagnosis/therapy/etiology ; *Postoperative Complications/therapy/diagnosis/etiology ; Fecal Microbiota Transplantation ; },
abstract = {Diversion colitis (DC) is a non-specific inflammation caused by the lack of fecal flow stimulation in the distal intestine after intestinal diversion surgery. It is mainly related to factors such as intestinal flora imbalance, deficiency of short-chain fatty acid (SCFA) and immune abnormalities. The clinical manifestations of diversion colitis include abdominal pain, mucus and bloody stools, diarrhea and other symptoms, but most patients may have no obvious symptoms. Diagnosis mainly relies on endoscopic examination and pathological characteristics. Common endoscopic findings include mucosal congestion, edema, and increased fragility, and the histological manifestation is mainly lymphoid follicle hyperplasia. Other intestinal inflammatory diseases need to be excluded. The treatment options include surgical and conservative medical therapies, among which stoma reversal is the most effective treatment to restore intestinal continuity. Conservative treatments such as SCFA, 5-aminosalicylic acid (5-ASA), steroid or cellulose solution enema, leukocyte removal therapy and fecal microbiota transplantation (FMT) can be used for those who cannot undergo surgery, combined with diet and lifestyle support to improve symptoms. This article summarized the pathogenesis, status, clinical features, diagnostic strategy and treatment progress of DC, hoping to provide reference for the diagnosis and treatment of DC.},
}

Humans
*Colorectal Neoplasms/surgery
*Colitis/diagnosis/therapy/etiology
*Postoperative Complications/therapy/diagnosis/etiology
Fecal Microbiota Transplantation

@article {pmid40550557,
year = {2025},
author = {Huang, CT and Wang, YC and Lin, SC and Lai, YC and Chen, SH and Feng, ST and Tsai, YJ},
title = {Impact of Gut Microbiota Alterations on Mitochondrial Bioenergetics in Cortical Astrocytes and Sensorimotor Impairment in a Rat Model of Lipopolysaccharide-Associated Encephalopathy.},
journal = {Shock (Augusta, Ga.)},
volume = {},
number = {},
pages = {},
doi = {10.1097/SHK.0000000000002637},
pmid = {40550557},
issn = {1540-0514},
abstract = {PURPOSE: Brain dysfunction is a significant complication of sepsis, commonly referred to as sepsis-associated encephalopathy (SAE). Alterations in gut microbiota during sepsis may contribute to development of SAE through the gut-brain axis. This study investigated effects of fecal transplantation from healthy or endotoxemic individuals on gut microbiota and brain function in a rat model of lipopolysaccharide (LPS)-associated encephalopathy.

METHODS: Following LPS induction, rats received daily oral gavage of fecal microbiota transplants for three days. Sensory and motor functions were assessed daily throughout the seven-day study period after LPS exposure. On day seven post-LPS, the study examined gut microbiota structure and composition, serum and fecal short-chain fatty acids (SCFAs) levels, ileal villus length, intestinal permeability, neuronal and glial ultrastructure, cytokine concentrations (pro-inflammatory and anti-inflammatory), and mitochondrial bioenergetics.

RESULTS: Administration of healthy donor feces preserved gut microbial structure and composition, maintained ileal villus length, and improved intestinal permeability following LPS treatment. Additionally, it increased SCFA levels, reduced pro-inflammatory cytokines, enhanced anti-inflammatory cytokine release, and restored sensitivity to mechanical and thermal stimuli, as well as motor function. Rats treated with healthy donor feces also exhibited reduced neuronal necrosis and a decreased density of mitochondria in cortical astrocytes. Notably, mitochondrial metabolism in LPS-treated rats returned to near-normal levels following treatment with healthy donor feces. In contrast, administration of endotoxemic donor feces exacerbated these effects in LPS-treated rats.

CONCLUSION: Ameliorating gut dysbiosis prevents mitochondrial dysfunction in astrocytes by promoting SCFA production and enhancing anti-inflammatory cytokine release. This process preserves neuronal integrity and mitigates the severity of encephalopathy.},
}

@article {pmid40550284,
year = {2025},
author = {Biggs, GAY},
title = {Fecal microbiota transplant (FMT) is associated with the resolution of recurrent urinary tract infections (UTIs).},
journal = {Urology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.urology.2025.06.040},
pmid = {40550284},
issn = {1527-9995},
}

@article {pmid40549339,
year = {2025},
author = {Bulut, SD and Döndaş, HA and Celebioglu, HU and Sansano, JM and Döndaş, NY},
title = {Recent Insights About Probiotics Related Pharmabiotics in Pharmacology: Prevention and Management of Diseases.},
journal = {Probiotics and antimicrobial proteins},
volume = {},
number = {},
pages = {},
pmid = {40549339},
issn = {1867-1314},
abstract = {The science of pharmacology investigates the effects of drugs on living organisms and vice versa. The frequency of side effects of some drugs used in traditional pharmacological treatment approaches and/or their inability to provide adequate treatment has led to the importance of new drug research and development (R&D) studies. Recently, due to the discovery that some diseases are associated with an imbalanced microbiota (dysbiosis), there has been a surge of interest in therapeutic approaches that can restore balance (biosis) to the microbiota. This review discusses the current status of the pharmabiotic potential of probiotics, prebiotics, synbiotics, paraprobiotics, postbiotics, metabiotics, next-generation probiotics, and fecal microbiota transplantation; describes their pharmacological functions from gastrointestinal disorders to neurodegenerative diseases; and also discusses the developments in pharmaceutical applications of probiotics and their derivatives.},
}

@article {pmid40548224,
year = {2025},
author = {Tüsüz Önata, E and Özdemir, Ö},
title = {Fecal microbiota transplantation in allergic diseases.},
journal = {World journal of methodology},
volume = {15},
number = {2},
pages = {101430},
pmid = {40548224},
issn = {2222-0682},
abstract = {Microorganisms such as bacteria, fungi, viruses, parasites living in the human intestine constitute the human intestinal microbiota. Dysbiosis refers to compositional and quantitative changes that negatively affect healthy gut microbiota. In recent years, with the demonstration that many diseases are associated with dysbiosis, treatment strategies targeting the correction of dysbiosis in the treatment of these diseases have begun to be investigated. Faecal microbiota transplantation (FMT) is the process of transferring faeces from a healthy donor to another recipient in order to restore the gut microbiota and provide a therapeutic benefit. FMT studies have gained popularity after probiotic, prebiotic, symbiotic studies in the treatment of dysbiosis and related diseases. FMT has emerged as a potential new therapy in the treatment of allergic diseases as it is associated with the maintenance of intestinal microbiota and immunological balance (T helper 1/T helper 2 cells) and thus suppression of allergic responses. In this article, the definition, application, safety and use of FMT in allergic diseases will be discussed with current data.},
}

@article {pmid40548146,
year = {2025},
author = {Vermeulen, A and Bootsma, E and Proost, S and Vieira-Silva, S and Kathagen, G and Vázquez-Castellanos, JF and Tito, RY and Sabino, J and Vermeire, S and Matthys, C and Raes, J and Falony, G},
title = {Dietary convergence induces individual responses in faecal microbiome composition.},
journal = {eGastroenterology},
volume = {3},
number = {2},
pages = {e100161},
pmid = {40548146},
issn = {2976-7296},
abstract = {BACKGROUND: Dietary variation has been identified as a key contributor to microbiome diversification. However, assessing its true impact in a cross-sectional setting is complicated by biological confounders and methodological hurdles. We aimed to estimate the impact of a reduction of dietary variation (dietary convergence) on faecal microbiota composition among individuals consuming a Western-type diet.

METHODS: 18 healthy volunteers recruited in the region of Flanders (Belgium) were followed up for 21 days. Participants were allowed to consume their habitual diet during a baseline and follow-up period (7 and 8 days, respectively), intersected by a 6-day intervention during which dietary options were restricted to oat flakes, whole milk and still water. Faecal samples were collected on a daily basis. Quantitative microbiome profiles were constructed, combining 16S rRNA gene amplicon sequencing with flow cytometry cell counting. Blood samples were taken at the beginning and end of each study week.

RESULTS: While the intervention did not affect transit time (as assessed through the analysis of stool moisture), consumption of the restricted diet resulted in an increased prevalence of the Bacteroides2 microbiome community type. Microbial load and Faecalibacterium abundance decreased markedly. Despite dietary restrictions, no convergence of microbial communities (reduction of interindividual and intraindividual variation) was observed. The effect size (ES) of the intervention on genus-level microbiome community differentiation was estimated as 3.4%, but substantial interindividual variation was observed (1.67%-16.42%).

CONCLUSION: The impact of dietary variation on microbiome composition in a Western population is significant but limited in ES, with notable individual exceptions. Dietary convergence does not invariably translate into interindividual convergence of faecal microbial communities.},
}

@article {pmid40546666,
year = {2025},
author = {Jeyaraman, N and Jeyaraman, M and Dhanpal, P and Ramasubramanian, S and Nallakumarasamy, A and Muthu, S and Santos, GS and da Fonseca, LF and Lana, JF},
title = {Integrative review of the gut microbiome's role in pain management for orthopaedic conditions.},
journal = {World journal of experimental medicine},
volume = {15},
number = {2},
pages = {102969},
pmid = {40546666},
issn = {2220-315X},
abstract = {The gut microbiome, a complex ecosystem of microorganisms, has a significant role in modulating pain, particularly within orthopaedic conditions. Its impact on immune and neurological functions is underscored by the gut-brain axis, which influences inflammation, pain perception, and systemic immune responses. This integrative review examines current research on how gut dysbiosis is associated with various pain pathways, notably nociceptive and neuroinflammatory mechanisms linked to central sensitization. We highlight advancements in meta-omics technologies, such as metagenomics and metaproteomics, which deepen our understanding of microbiome-host interactions and their implications in pain. Recent studies emphasize that gut-derived short-chain fatty acids and microbial metabolites play roles in modulating neuroinflammation and nociception, contributing to pain management. Probiotics, prebiotics, synbiotics, and faecal microbiome transplants are explored as potential therapeutic strategies to alleviate pain through gut microbiome modulation, offering an adjunct or alternative to opioids. However, variability in individual microbiomes poses challenges to standardizing these treatments, necessitating further rigorous clinical trials. A multidisciplinary approach combining microbiology, immunology, neurology, and orthopaedics is essential to develop innovative, personalized pain management strategies rooted in gut health, with potential to transform orthopaedic pain care.},
}

@article {pmid40546462,
year = {2025},
author = {Inayat, N and Zahir, A and Hashmat, AJ and Khan, A and Ahmad, A and Sikander, M and Zakir, S and Ahmad, S and Awan, SK and Raza, SS and Varrassi, G},
title = {Gut Microbiota as a Key Modulator of Chronic Disease: Implications for Diabetes, Autoimmunity, and Cancer.},
journal = {Cureus},
volume = {17},
number = {5},
pages = {e84687},
doi = {10.7759/cureus.84687},
pmid = {40546462},
issn = {2168-8184},
abstract = {The gut microbiota (GM) represents an intricate, dynamic, and complex ecosystem. It plays a key role in health and disease. The GM interacts with the host and modulates various physiological functions, including metabolism, immune regulation, and neurological function. This narrative review comprehensively analyses the role of the GM in the development and progression of three major chronic conditions, namely diabetes, autoimmune disorders, and cancer. Using a structured literature search strategy across databases such as Google Scholar, PubMed, Scopus, and Web of Science, relevant studies published between 2000 and 2025 were identified and analysed. This review highlights that dysbiosis contributes significantly to the pathogenesis of these chronic conditions. In type 2 diabetes mellitus (T2DM), alterations in the GM are associated with systemic inflammation, insulin resistance, and decreased microbial diversity. Similarly, in autoimmune disorders such as rheumatoid arthritis (RA), multiple sclerosis (MS), and inflammatory bowel disease (IBD), dysbiosis disrupts immune homeostasis, which in turn causes sustained inflammation and aberrant immune responses. Lastly, dysbiosis has been linked to the onset and progression of various gastrointestinal cancers through mechanisms including chronic inflammation and the production of carcinogenic metabolites. Fecal microbiota transplantation (FMT), probiotics, prebiotics, and dietary modifications are being explored for their potential to restore microbial balance and improve clinical outcomes. In conclusion, this review highlights the GM's pivotal role in the pathogenesis of chronic diseases and its potential as a therapeutic target.},
}

@article {pmid40546285,
year = {2025},
author = {Pei, X and Liu, M and Yu, S},
title = {How is the human microbiome linked to kidney stones?.},
journal = {Frontiers in cellular and infection microbiology},
volume = {15},
number = {},
pages = {1602413},
doi = {10.3389/fcimb.2025.1602413},
pmid = {40546285},
issn = {2235-2988},
abstract = {In recent years, the incidence of kidney stones has continued to rise worldwide, and conventional treatments have limited efficacy in treating stones associated with recurrent or metabolic abnormalities. The microbiome, as the 'second genome' of the host, is involved in the development of kidney stones through metabolic regulation, immune homeostasis and inflammatory response. Studies have shown that the urinary microbiome of healthy people is dominated by commensal bacteria such as Lactobacillus and Streptococcus, which maintain microenvironmental homeostasis, whereas patients with renal stones have a significantly reduced diversity of intestinal and urinary microbiomes, with a reduced abundance of oxalic acid-degrading bacteria (e.g., Bifidobacterium oxalicum, Bifidobacterium bifidum), and a possible concentration of pathogenic bacteria (e.g., Proteus mirabilis). The microbiome regulates stone formation through mechanisms such as metabolites (e.g., short-chain fatty acids), changes in urine physicochemical properties (e.g., elevated pH), and imbalances in the inflammatory and immune microenvironments. For example, urease-producing bacteria promote magnesium ammonium phosphate stone formation through the breakdown of urea, whereas dysbiosis of the intestinal flora increases urinary oxalic acid excretion and exacerbates the risk of calcium oxalate stones. Microbiome-based diagnostic markers (e.g., elevated abundance of Aspergillus phylum) and targeted intervention strategies (e.g., probiotic supplementation, faecal bacteria transplantation) show potential for clinical application. However, technical bottlenecks (e.g., sequencing bias in low-biomass samples), mechanistic complexity (e.g., multistrain synergism), and individual heterogeneity remain major challenges for future research. Integration of multi-omics data, development of personalised therapies and interdisciplinary research will be the core directions to decipher the relationship between microbiome and kidney stones.},
}

@article {pmid40546239,
year = {2025},
author = {Liang, J and Dong, X and Yang, J and Hu, N and Luo, X and Cong, S and Chen, J and Zhao, W and Liu, B},
title = {Buyang Huanwu Decoction Modulates the Gut Microbiota-C/EBPβ/AEP Axis to Ameliorate Cognitive Impairment in Alzheimer's Disease Mice.},
journal = {CNS neuroscience & therapeutics},
volume = {31},
number = {6},
pages = {e70480},
doi = {10.1111/cns.70480},
pmid = {40546239},
issn = {1755-5949},
support = {2024yjscx013//Innovative Research Project for Postgraduate Students of Heilongjiang University of Traditional Chinese Medicine/ ; LH2022H059//Natural Science Foundation of Heilongjiang Province of China/ ; LH2023H073//Natural Science Foundation of Heilongjiang Province of China/ ; },
abstract = {BACKGROUND: Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and behavioral disturbances. Buyang Huanwu Decoction (BYHWD), a traditional Chinese herbal formulation, has demonstrated potential neuroprotective effects. This study aims to evaluate the therapeutic impact of BYHWD on cognitive impairments in 3×Tg mice and to investigate its underlying mechanism through modulation of the gut microbiota-C/EBPβ/AEP signaling pathway.

METHODS: In two independent experiments, we assessed the effects of BYHWD and its derived fecal microbiota transplantation (FMT-BYHWD) on behavioral performance, neuropathological alterations, and signaling pathways in 3×Tg mice.

RESULTS: Treatment with BYHWD significantly improved cognitive function in 3×Tg mice and mitigated AD-like pathological changes. By suppressing the C/EBPβ/AEP signaling pathway, BYHWD reduced pathological Aβ plaque deposition, diminished tau hyperphosphorylation, and inhibited the release of pro-inflammatory cytokines. Further analysis revealed that BYHWD restored gut microbiota balance and suppressed the activation of the C/EBPβ/AEP pathway in the hippocampus. Moreover, transplanting FMT-BYHWD from BYHWD-treated mice to germ-free 3×Tg mice also ameliorated their cognitive deficits and AD-like pathology, suggesting that the anti-AD effects of BYHWD are mediated through the gut-brain axis by regulating the interplay between gut microbiota and the C/EBPβ/AEP signaling pathway.

CONCLUSION: This study uncovers the mechanism by which BYHWD improves cognitive deficits and neuropathological changes in 3×Tg mice via the gut-brain axis, mediated by the modulation of the gut microbiota-C/EBPβ/AEP signaling pathway, providing a novel therapeutic strategy for AD.},
}

@article {pmid40544256,
year = {2025},
author = {Mannavola, CM and De Maio, F and Marra, J and Fiori, B and Santarelli, G and Posteraro, B and Sica, S and D'Inzeo, T and Sanguinetti, M},
title = {Bloodstream infection by Lactobacillus rhamnosus in a haematology patient: why metagenomics can make the difference.},
journal = {Gut pathogens},
volume = {17},
number = {1},
pages = {47},
pmid = {40544256},
issn = {1757-4749},
support = {PE00000007, INF-ACT//EU funding for the MUR PNRR Extended Partnership initiative on Emerging Infectious Diseases/ ; },
abstract = {BACKGROUND: Bloodstream infections (BSIs) pose a persistent threat to hospitalized patients, particularly those who are immunocompromised and susceptible to infections caused by anaerobic or facultative anaerobic bacteria. Alterations in gut microbiota composition can predispose individuals to intestinal domination by one or more pathobionts, increasing the risk of bacterial translocation into the bloodstream and subsequent bacteremia.

CASE PRESENTATION: We report the case of a 20-year-old female with multiple relapsed/refractory Philadelphia-negative B-cell acute lymphoblastic leukemia, initially referred to our hematology center for CAR-T cell therapy. The patient ultimately underwent allogeneic hematopoietic stem cell transplantation, which was complicated by infections, moderate-to-severe graft-versus-host disease, hepatic sinusoidal obstruction syndrome, and transplant-associated thrombotic microangiopathy, all contributing to a fatal outcome. Blood cultures obtained in the final week before the patient succumbed to multi-organ toxicity grew Lactobacillus rhamnosus. A fecal sample collected concurrently for intestinal microbiota characterization revealed a marked predominance of Bacillota (98.5%), with Lacticaseibacillus dominating at 47.9%, followed by Pediococcus (18.59%) and Staphylococcus (3.5%) at the genus level. We performed genomic comparison between the L. rhamnosus isolated from blood cultures and the best-matched strain detected in the intestinal microbiota.

CONCLUSIONS: We report the isolation of L. rhamnosus from blood cultures in a patient post hematopoietic cell transplantation, with genomic similarity to a gut-dominant L. rhamnosus strain. This case highlights the potential link between intestinal domination and subsequent bloodstream infection, supporting the value of gut microbiota profiling as an adjunctive tool for monitoring high-risk patients, such as hematopoietic cell transplant recipients.

SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13099-025-00722-3.},
}

@article {pmid40544212,
year = {2025},
author = {Lv, J and Hao, P and Zhou, Y and Liu, T and Wang, L and Song, C and Wang, Z and Liu, Z and Liu, Y},
title = {Role of the intestinal flora-immunity axis in the pathogenesis of rheumatoid arthritis-mechanisms regulating short-chain fatty acids and Th17/Treg homeostasis.},
journal = {Molecular biology reports},
volume = {52},
number = {1},
pages = {617},
pmid = {40544212},
issn = {1573-4978},
support = {2024ZKZ009//Southwest Medical University (SWMU) School-level Scientific Research Program/ ; },
abstract = {BACKGROUND: The pathogenesis of rheumatoid arthritis (RA), a chronic systemic autoimmune disease, is closely linked to the interactions between intestinal flora and metabolites. Recent research has shown that the "gut-joint axis" is an important regulator of immune homeostasis, gut microbiota dysbiosis not only causes pro-inflammatory bacteria to proliferate abnormally, but it also decreases the biosynthesis of short-chain fatty acids (SCFAs). This dual imbalance ultimately exacerbates synovial inflammation and encourages bone destruction by upsetting the balance of Th17/Treg cells, that is, the over-activation of Th17 cells and the impaired function of regulatory T cells (Treg).

OBJECTIVE: To clarify the molecular mechanism by which intestinal flora-derived SCFAs alter the pathogenic process of RA by controlling Th17/Treg balance, and to establish a theoretical foundation for targeted treatments.

METHODS: We integrated multidisciplinary evidence to create a "flora-SCFAs-immunity-joints" by conducting a systematic search of domestic and international literature in PubMed, Web of Science, and other databases over the past ten years, with a focus on intestinal flora composition, SCFA biosynthesis, Th17/Treg immunoregulation, and RA animal model research. We create a "flora-SCFAs-immunity-joint" network by integrating information from many disciplines.

OUTCOMES: Dietary fiber is broken down by intestinal flora to produce SCFAs (acetic, propionic, and butyric acids), which control Th17/Treg balance in two ways: (1) Encourage Treg differentiation: propionic acid activates the GPR43-cAMP/PKA-CREB pathway, which promotes Treg expansion and secretion of IL-10/TGF-β; (2) Inhibit Th17 polarization, SCFAs inhibited Th17 cell differentiation, down-regulated IL-23 secretion from dendritic cells, and blocked IL-6/STAT3 and RORγt signaling. Butyric acid also inhibits histone deacetylase (HDAC) activity, Foxp3 expression, and epigenetic stability. In a collagen-induced arthritis (CIA) paradigm, animal studies shown that fecal transplantation or SCFA supplementation dramatically decreased bone degradation and joint inflammatory scores. Its therapeutic translational potential was suggested by the negative correlation found between the Th17/Treg ratio and the amount of SCFAs in the gut of RA patients.

CONCLUSION: Through multi-target control of Th17/Treg balance, SCFAs show distinct benefits over conventional immunosuppression in the treatment of RA. Verification is still required for the pharmacokinetic constraints of SCFAs, variations in individual flora, and causative processes. To support the specific immune intervention in RA, it will be important in the future to integrate multi-omics technology to evaluate the trans-organ regulatory network of the "gut-joint axis" and to create nano-delivery methods or modified bacterial tactics to increase the targeting of SCFAs.},
}