@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.},
}

@article {pmid40542451,
year = {2025},
author = {Ji, S and Ahmad, F and Peng, B and Yang, Y and Su, M and Zhao, X and Vatanen, T},
title = {Engrafting gut bacteriophages have potential to modulate microbial metabolism in fecal microbiota transplantation.},
journal = {Microbiome},
volume = {13},
number = {1},
pages = {149},
pmid = {40542451},
issn = {2049-2618},
support = {U22A20365//Joint Funds of National Natural Science Foundation of China/ ; T2341019//National Natural Science Foundation of China/ ; 2023A1515012429//Natural Science Foundation of Guangdong Province/ ; 2024B03J1343//Guangzhou Science and Technology Plan Project/ ; },
abstract = {BACKGROUND: Fecal microbiota transplantation (FMT) is widely used to treat severe infections and investigated for the treatment of complex diseases. The therapeutic efficacy of FMT is related to the successful engraftment of bacteriophages from healthy donors to recipients. However, gut bacteriophage contributions to FMT engraftment and treatment outcomes remain unclear.

METHODS: The gut phageome from previously published metagenomes of donors and recipients across 23 FMT studies was assembled and functionally annotated for a meta-analysis.

RESULTS: Gut phageome profiles of FMT recipients, especially those with recurrent Clostridioides difficile infection (rCDI), shifted toward donor phageomes, accompanied by increased phageome alpha diversity. Engraftment of donor phages varied between recipient conditions with the highest engraftment rate, overrepresented by putative temperate phage, in patients with rCDI. Consistently, a higher proportion of auxiliary metabolic genes (AMGs), with the potential to support and modulate bacterial metabolism, were annotated on putative temperate phages.

CONCLUSIONS: FMT leads to significant taxonomic, functional, and lifestyle shifts in recipient phageome composition. Future FMT studies should include gut phageome characterization and consider it as a potential factor in microbial community shifts and treatment outcomes. Video Abstract.},
}

@article {pmid40540980,
year = {2025},
author = {Noviello, D and Amoroso, C and Vecchi, M and Facciotti, F and Caprioli, F},
title = {Curing inflammatory bowel diseases: breaking the barriers of current therapies- emerging strategies for a definitive treatment.},
journal = {Current opinion in immunology},
volume = {95},
number = {},
pages = {102593},
doi = {10.1016/j.coi.2025.102593},
pmid = {40540980},
issn = {1879-0372},
abstract = {Chronic intestinal inflammation in inflammatory bowel diseases (IBD) reflects the interplay of genetic predisposition, immune dysregulation, microbial imbalance, and epithelial barrier defects. Current therapies for IBD primarily focus on controlling inflammation necessitating lifelong treatment and face a 'therapeutic ceiling' due to primary and secondary loss of efficacy over time. Immune-mediated approaches do not address additional pathogenic mechanisms, such as impairment of epithelial barrier and gut microbial ecology. Thus, innovative strategies are required to foster the field closer to a definitive cure. This review discusses novel strategies to overcome current therapeutic limitations, including immune reset via hematopoietic stem cell transplantation and B cell-targeted therapies, antigen-specific interventions such as chimeric antigen receptor T cells and tolerogenic vaccines, and intestinal epithelial barrier restoration. We also explore microbiota-based strategies - ranging from fecal microbiota transplantation to engineered consortia and bacteriophages - and discuss the adjunctive role of diet. Together, we outline a potential research roadmap toward a potential cure for IBD.},
}

@article {pmid40538711,
year = {2025},
author = {Lathakumari, RH and Vajravelu, LK and Gopinathan, A and Vimala, PB and Panneerselvam, V and Ravi, SSS and Thulukanam, J},
title = {The gut virome and human health: From diversity to personalized medicine.},
journal = {Engineering microbiology},
volume = {5},
number = {1},
pages = {100191},
pmid = {40538711},
issn = {2667-3703},
abstract = {The human gut virome plays a crucial role in the gut and overall health; its diversity and regulatory functions influence bacterial populations, metabolism, and immune responses. Bacteriophages (phages) and eukaryotic viruses within the gut microbiome contribute to these processes, and recent advancements in sequencing technologies and bioinformatics have greatly expanded our understanding of the gut virome. These advances have led to the development of phage-based therapeutics, diagnostics, and artificial intelligence-driven precision medicine. The emerging field of phageomics shows promise for delivering personalized phage therapies that combat antimicrobial resistance by specifically targeting pathogenic bacteria while preserving beneficial microbes. Moreover, CRISPR-Cas systems delivered via phages have shown success in selectively targeting antibiotic resistance genes and enhancing treatment effectiveness. Phage-based diagnostics are highly sensitive in detecting bacterial pathogens, offering significant benefits for human health and zoonotic disease surveillance. This synthesis of the current knowledge highlights the pivotal role of the gut virome in regulating microbial communities and its transformative potential in personalized medicine, emphasizing its importance in advancing therapeutic and diagnostic strategies for improving health outcomes.},
}

@article {pmid40535532,
year = {2025},
author = {Wang, Q and Xu, G and Yan, O and Wang, S and Wang, X},
title = {Radiation-induced injury and the gut microbiota: insights from a microbial perspective.},
journal = {Therapeutic advances in gastroenterology},
volume = {18},
number = {},
pages = {17562848251347347},
pmid = {40535532},
issn = {1756-283X},
abstract = {Although radiotherapy is the second most effective cancer treatment, radiation injuries limit its use. About 80% of abdominal-pelvic radiotherapy patients develop acute radiation enteritis, with 20% discontinuing radiotherapy. The lack of effective mitigation measures restricts its clinical application. Recent studies have proposed gut microbiota as a potential biomarker for radiation injuries. However, the interaction between gut microbiota and radiation injuries remains poorly understood. This review summarizes two forms of interaction between gut microbiota and radiation injuries based on the location of the radiation field. One type of interaction, referred to as "direct interaction," involves changes in the diversity and composition of gut microbiota, alterations in microbiota-derived metabolites, disruption of the intestinal barrier, activation of inflammatory responses within the intestine, and involvement of the host's immune system. The second form, called "indirect interaction," includes the influence of the gut microbiota on various body systems, such as gut microbiota-brain axis, gut microbiota-cardiopulmonary axis, and gut microbiota-oral axis. Additionally, we examine promising interventions aimed at reshaping the gut microbiota, including the use of probiotics, prebiotics, and fecal microbiota transplantation. The interaction between radiation injuries and gut microbiota is more complex than previously understood. Therefore, further clarification of the underlying mechanisms will facilitate the application of gut microbiota in preventing and alleviating radiation injuries.},
}

@article {pmid40535011,
year = {2025},
author = {Wu, N and Ning, K and Liu, Y and Wang, Q and Li, N and Zhang, L},
title = {Relationship between high-fat diet, gut microbiota, and precocious puberty: mechanisms and implications.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1564902},
pmid = {40535011},
issn = {1664-302X},
abstract = {Precocious puberty (PP) is the second most common pediatric endocrine disorder globally and poses a growing public health concern, particularly among girls. While the exact biological mechanisms underlying PP remain unclear, unhealthy dietary patterns, particularly the consumption of a high-fat diet (HFD), are recognized as significant modifiable risk factors. The gut microbiota (GM) is an environmental factor that is disrupted by HFD and may modulate the onset and progression of PP. This review explored the intricate relationship between HFD, GM, and PP, and elucidated the potential mechanisms by which HFD may promote PP development by summarizing evidence from preclinical to clinical research, focusing on the role of GM and its derived metabolites, including short-chain fatty acids, bile acids, lipopolysaccharides, and neurotransmitters. Mechanistic exploration provides novel insights for developing microbiota-targeted therapeutic strategies, such as dietary and lifestyle interventions, fecal microbiota transplantation, probiotics, and traditional Chinese medicine, paving the way for promising approaches to prevent and manage PP.},
}

@article {pmid40534699,
year = {2025},
author = {Yu, JX and Wu, J and Chen, X and Zang, SG and Li, XB and Wu, LP and Xuan, SH},
title = {Gut microbiota in liver diseases: initiation, development and therapy.},
journal = {Frontiers in medicine},
volume = {12},
number = {},
pages = {1615839},
pmid = {40534699},
issn = {2296-858X},
abstract = {The gut microbiota plays a pivotal role in the pathogenesis and progression of various liver diseases, including viral hepatitis, alcoholic fatty liver disease, metabolic dysfunction-associated steatotic liver disease, drug-induced hepatitis, liver cirrhosis, hepatocellular carcinoma, and other hepatic disorders. Research indicates that dysbiosis of the gut microbiota can disrupt the integrity of the intestinal barrier and interfere with the immune functions of the gut-liver axis, thereby mediating the progression of liver diseases. Analysis of microbial composition and metabolites in fecal samples can assess the diversity of gut microbiota and the abundance of specific microbial populations, providing auxiliary diagnostic information for liver diseases. Furthermore, interventions such as fecal microbiota transplantation, probiotics, prebiotics, bacteriophages, and necessary antibiotic treatments offer multiple approaches to modulate the gut microbiota, presenting promising new strategies for the prevention and treatment of liver diseases. This review summarizes the latest research advances on the role of gut microbiota in liver diseases, offering novel theoretical foundations and practical directions for the diagnosis and treatment of hepatic disorders.},
}

@article {pmid40533850,
year = {2025},
author = {Ye, Q and Hu, Y and Jiang, H and Luo, T and Han, L and Chen, Y and Chen, J and Ma, L and He, Z and Yan, X},
title = {Maternal intestinal L. vaginalis facilitates embryo implantation and survival through enhancing uterine receptivity in sows.},
journal = {Microbiome},
volume = {13},
number = {1},
pages = {145},
pmid = {40533850},
issn = {2049-2618},
support = {32202700//National Natural Science Foundation of China/ ; 31925037//National Natural Science Foundation of China/ ; 2022YFD1300405//National Key Research and Development Program of China/ ; 2022YFD1300405//National Key Research and Development Program of China/ ; 2022YFD1300405//National Key Research and Development Program of China/ ; 2022020801020232//Knowledge Innovation Program of Wuhan-Shuguang Project/ ; AML2023B06//National Key Laboratory of Agricultural Microbiology/ ; 2662023DKPY002//Fundamental Research Funds for the Central University/ ; },
mesh = {Animals ; Female ; *Embryo Implantation/physiology ; Swine ; *Gastrointestinal Microbiome/physiology ; Pregnancy ; Mice ; *Uterus/physiology ; RNA, Ribosomal, 16S/genetics ; Litter Size ; Metabolomics ; Fecal Microbiota Transplantation ; },
abstract = {BACKGROUND: The embryo implantation quality during early pregnancy is the predominant factor for embryo survival and litter performance in sows. Gut microbiota is demonstrated to show a correlation to pregnancy outcomes by participating in regulating maternal metabolism. However, the specific functional microbiota and its mechanical effects on regulating embryo implantation and survival remain unclear. The objective of this study was to clarify whether embryo implantation and litter performance were affected by maternal intestinal microbiota, and to identify specific microbial communities and its mechanism in regulating embryo implantation.

RESULTS: In this study, we first conducted 16S rRNA sequencing and metabolomic analysis revealing the intestinal microbiota and metabolism of 42 sows with different litter size to select the potential functional microbiota that may contribute to embryo survival. Then, we explored the effects of that microbiota on embryo implantation and litter performance through microbiota transplantation in mice and sows. We found that maternal intestinal L. vaginalis exhibits enrichment in sows with higher litter size, which could facilitate embryo implantation and survival and ultimately increases litter size in mice. We further employed transcriptomic analysis to determine the characteristics of uterus, which found an enhanced uterine receptivity after L. vaginalis gavage. The plasma untargeted metabolomic analysis after L. vaginalis gavage in mice and targeted metabolomics analysis of in vitro cultured medium of L. vaginalis were used to evaluate the metabolic regulation of L. vaginalis and to reveal the underlying functional metabolites. Next, an increasing adhesion rate of endometrial-embryonic cells and an obvious increasing formation of pinopodes in cell surface of porcine endometrial epithelial cells were observed after treatments of L. vaginalis metabolites, especially galangin and daidzein. Also, the gene expression levels related to uterine receptivity were increased after treatments of L. vaginalis metabolites in porcine endometrial epithelial cells. Finally, we found that L. vaginalis or its metabolites supplementation during early gestation significantly increased the litter performance in sows.

CONCLUSIONS: Overall, intestinal microbial-host interactions can occur during early pregnancy and may be contribute to maternal metabolic changes and influence pregnancy outcomes in mammals. Our study provides insights of maternal intestinal L. vaginalis to enhance uterine receptivity and to benefit embryo/fetal survival through a gut-uterus axis, contributing to advanced concept and novel strategy to manipulate gut microbiota during early pregnancy, and in turn to improve embryo implantation and reduce embryo loss in sows. Video Abstract.},
}

Animals
Female
*Embryo Implantation/physiology
Swine
*Gastrointestinal Microbiome/physiology
Pregnancy
Mice
*Uterus/physiology
RNA, Ribosomal, 16S/genetics
Litter Size
Metabolomics
Fecal Microbiota Transplantation

@article {pmid40532535,
year = {2025},
author = {Wang, Z and He, Y and Luo, M and Liu, S and Hou, J and Cao, B and An, X},
title = {Transfer toxicity of polystyrene microplastics in vivo: Multi-organ crosstalk.},
journal = {Environment international},
volume = {202},
number = {},
pages = {109604},
doi = {10.1016/j.envint.2025.109604},
pmid = {40532535},
issn = {1873-6750},
abstract = {The accumulation of microplastics (MPs) within the environment caused serious ecological and health problems. Nevertheless, its systemic toxicity to organisms and its mechanisms lack effective evidence. This study established a model of MP exposure through the gavage of polystyrene (PS)-MPs particles to maternal mice on days 1 to 21 of lactation. The results demonstrated that PS-MPs were distributed widely in maternal mice, occurring mainly in the feces, colon, liver and mammary glands. Further experiments revealed that the gut and blood-milk barriers were disrupted, and pathological injury and inflammatory reactions were observed in the liver, gut, and mammary glands. Metabolomic and metagenome analysis indicated abnormalities in hepatic bile acid metabolism and significant alterations in the gut microbiota after exposure to PS-MPs. These alterations led to increased disruption of the intestine-liver axis. Notably, with fecal microbiota transplantation and antibiotic experiments, we observed that elimination of the intestinal microbiota reduced tissue inflammation and improved gut and blood-milk barrier leakage. These findings demonstrated that PS-MPs exaggerated intestine-liver axis disorders by inducing colonic injury, intestinal ecological dysregulation and abnormal hepatic bile acid metabolism. Furthermore, PS-MPs translocated via the intestine-liver axis and exerted broader toxic effects on mammary tissue. Overall, our study uncovered the transfer toxicity of PS-MPs in mice, proposing the possibility of a gut-liver-mammary axis.},
}

@article {pmid40532322,
year = {2025},
author = {Zhao, Y and Gong, N and Wang, S and Yuan, Q and Chen, X and Li, B and Zhang, L and Li, W and Zhu, R and Zhang, J and Zhang, W},
title = {Dynamic changes in intestinal microbiota mediate mechanical hyperalgesia in surgical menopause model: a potential mechanism of DRG neuroinflammation.},
journal = {International immunopharmacology},
volume = {161},
number = {},
pages = {115098},
doi = {10.1016/j.intimp.2025.115098},
pmid = {40532322},
issn = {1878-1705},
abstract = {The role of the intestinal microbiota in hyperalgesia in ovariectomized mice remains unclear. This study aimed to investigate pain behavior and dynamic changes in the intestinal microbiota and the levels of related metabolites in a model of surgical menopause and to verify the hypothesis that the intestinal microbiota mediates the occurrence and persistence of hyperalgesia through neuroinflammation. An ovariectomy (OVX) model was constructed to assess the intestinal microbiota composition, the levels of related metabolites, and inflammation levels in the spinal dorsal root ganglion (DRG). Fecal microbiota transplantation (FMT) was used to alter the intestinal microbiota, and its impact on pain-related behaviors and the level of inflammation in the DRG was evaluated. The mechanical pain threshold was significantly lower in the OVX group compared with the sham group at 4-8 w after surgery, and the thermal pain threshold was greater at 5 and 8 w after surgery. A decrease in the mechanical pain threshold was observed in the OVX group 5, and 7-9 weeks after FMT, indicating hyperalgesia. PCoA and OPLS-DA revealed differences in the composition of the microbiota and the abundance of related metabolites between the OVX and sham groups. Correlation analysis revealed an association between pain thresholds and the levels and metabolites of certain bacterial genera. The expression of C/EBPβ and IL-1β in the OVX group was greater than that in the sham group, and the expression of IL-6, IL-1β, and TRPV1 in the sham group was greater than that in the OVX group after FMT. In conclusion, the dynamic changes in the intestinal microbiota in female mice induced by surgical menopause result in hyperalgesia, possibly due to an increase in the severity of inflammation in the spinal DRG.},
}

@article {pmid40531376,
year = {2025},
author = {Wu, Y and Wong, OWH and Chen, S and Ng, SC and Su, Q and Chan, FKL},
title = {Gastrointestinal health and nutritional strategies in autism spectrum disorder.},
journal = {Journal of gastroenterology},
volume = {},
number = {},
pages = {},
pmid = {40531376},
issn = {1435-5922},
support = {R4030-22//Research Grants Council-Research Impact Fund/ ; NCI202346//New Cornerstone Science Foundation/ ; PF22-77807//Hong Kong PhD Fellowship Scheme (HKPFS) of the Research Grants Council of Hong Kong/ ; },
abstract = {Beyond the hallmark social and sensory difficulties in autism spectrum disorder (ASD), the comorbid gastrointestinal (GI) conditions and their potential link to the severity of core symptoms require clinical attention. Although evidence indicates that autistic children face a greater risk of GI disorders and require more intensive nutritional management compared to neurotypical peers, standard guidelines for managing GI symptoms in this population remain lacking. This review seeks to pinpoint critical considerations for the implementation of nutrition-based strategies aimed at addressing GI dysfunction in individuals with ASD. By emphasizing clinical translation and the mechanistic understanding of these strategies, it highlights the importance of restoring gut homeostasis as a pathway to improve functional independence and overall well-being. Furthermore, we outline priorities for clinical research aimed at developing evidence-based nutritional recommendations to support GI health in autistic individuals, emphasizing personalized and population-specific needs.},
}

@article {pmid40530459,
year = {2025},
author = {Kabage, AJ and Haselhorst, PJ and Khoruts, A},
title = {Donor-centric administration of the stool donor program is vital to its feasibility and patient safety.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2508950},
doi = {10.1080/19490976.2025.2508950},
pmid = {40530459},
issn = {1949-0984},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods/ethics/adverse effects/standards ; *Clostridium Infections/therapy ; *Patient Safety ; *Feces/microbiology ; *Tissue Donors ; Gastrointestinal Microbiome ; Clostridioides difficile ; },
abstract = {Human stool-based products composed of fecal microbiota are a new frontier of medical therapeutics development. The development of standardized manufacturing protocols of donor microbiota has transformed fecal microbiota transplantation (FMT) from a crude and rarely used procedure to a widely accepted and highly effective option for treatment Clostridioides difficile infections. There is also a growing interest in using microbiota transplant therapies for multiple other clinical indications. In this manuscript, we review the logistical challenges experienced by various stool banks and our own group in establishing and administering a stool donor program. Furthermore, we explore and highlight the multiple ethical considerations that are ultimately essential to product safety and efficacy and propose basic principles that are necessary to maintain stool donor program integrity.},
}

Humans
*Fecal Microbiota Transplantation/methods/ethics/adverse effects/standards
*Clostridium Infections/therapy
*Patient Safety
*Feces/microbiology
*Tissue Donors
Gastrointestinal Microbiome
Clostridioides difficile

@article {pmid40529581,
year = {2025},
author = {Xu, D and Lu, Z and Li, Q and Cheng, Y and Yang, Z},
title = {Decoding the gut-sleep Nexus: a bibliometric mapping of gut microbiota and sleep disorders.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1598173},
pmid = {40529581},
issn = {1664-302X},
abstract = {BACKGROUND: An increasing number of studies have focused on the interaction between gut microbiota and sleep disorders. However, there is currently no bibliometric analysis of the literature on gut microbiota and sleep disorders. This study employs bibliometric methods to analyze the current research status and hotspots in the field of gut microbiota and sleep disorders, providing a reference for future research in this area.

METHODS: Articles related to gut microbiota and sleep disorders were retrieved from the WOS core database, covering the period from the database's inception to December 31, 2024. After rigorous screening, VOSviewer and CiteSpace were used to conduct analyses on quantity, collaboration networks, clustering, and citation bursts.

RESULTS: The number of articles on gut microbiota and sleep disorders has increased annually, with a significant surge after 2022. China has the highest number of publications, while the United States has the highest citation count. The institution with the most publications is Shanghai Jiao Tong University, and the institution with the most citations is Deakin University. The top 10 journals by publication volume are all ranked above Q2 in the JCR. The most cited article is "Gut microbiome diversity is associated with sleep physiology in humans" by Smith et al., published in PLOS ONE in 2019. The top 10 most frequent keywords are gut microbiota, sleep, depression, inflammation, chain fatty acids, anxiety, brain, oxidative stress, obesity, and health. The keyword cluster "obstructive sleep apnea" is a focal research direction, while fecal microbiota transplantation is a current research hotspot.

CONCLUSION: This study reveals the publication trends, collaboration relationships among countries, regions, and authors, and recent research hotspots in the field of gut microbiota and sleep disorders through bibliometric methods, providing an objective data reference for scientific research in this domain.},
}

@article {pmid40529577,
year = {2025},
author = {Wu, S and Chen, N and Wang, C and So, KF},
title = {Research focus and trends of the association between gut microbiota and neuroinflammation.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1564717},
pmid = {40529577},
issn = {1664-302X},
abstract = {BACKGROUND: The interaction between the gut microbiota and neuroinflammation plays a crucial role in the pathogenesis of many diseases, particularly neurodegenerative diseases, and has become one of the focal points of research in recent years. Despite the large number of related studies, there is currently a lack of comprehensive analysis and prediction of these data to drive the field forward. This study aims to systematically analyze the clinical practices and research hotspots of the underlying mechanisms in this field using bibliometric and visualization methods, and to explore the future development pathways.

METHODS: CiteSpace, VOSviewer, GraphPad Prism and other software were used to analyze 1,404 studies on gut microbiota and neuroinflammation collected by the core of the Web of Science since 2000, to visually present the collaborative network between literatures, structure of authors and countries, co-occurrence of keywords, emerging reference literature, and research hotspots.

RESULTS: From 2000 to 2024, the number of related papers on this topic showed an overall upward trend, and the annual citation peaked in 2020, with significant contributions from China and the United States. Research focused on the relationship between gut microbiota and neuroinflammation, with a particular emphasis on investigating the mechanisms of the microbiota-gut-brain axis through both basic and clinical research. Treatment strategies include probiotic therapy, fecal microbiota transplantation and traditional Chinese medicine.

CONCLUSION: This study comprehensively reviews the research progress on the association between gut microbiota and neuroinflammation, and discusses the current research focus and frontier directions of this relationship, so as to provide reference for the development of this field.},
}

@article {pmid40529304,
year = {2025},
author = {Chen, Z and Jin, D and Hu, J and Guan, D and Bai, Q and Gou, Y},
title = {Microbiota and gastric cancer: from molecular mechanisms to therapeutic strategies.},
journal = {Frontiers in cellular and infection microbiology},
volume = {15},
number = {},
pages = {1563061},
pmid = {40529304},
issn = {2235-2988},
mesh = {*Stomach Neoplasms/therapy/microbiology/pathology ; Humans ; *Gastrointestinal Microbiome ; Dysbiosis/complications/microbiology ; Tumor Microenvironment ; Probiotics/therapeutic use ; Fecal Microbiota Transplantation ; },
abstract = {Gastric cancer, a prevalent malignancy globally, is influenced by various factors. The imbalance in the gut microbiome and the existence of particular intratumoural microbiota could have a strong connection with the onset and progression of gastric cancer. High-throughput sequencing technology and bioinformatics analysis have revealed a close correlation between abnormal abundance of specific microbial communities and the risk of gastric cancer. These microbial communities contribute to gastric cancer progression through mechanisms including increasing cellular genomic damage, inhibiting DNA repair, activating abnormal signaling pathways, exacerbating tumor hypoxia, and shaping a tumor immune-suppressive microenvironment. This significantly impacts the efficacy of gastric cancer treatments, including chemotherapy and immunotherapy. Probiotic, prebiotic, antibiotic, carrier-based, dietary interventions, fecal microbiota transplantation, and traditional Chinese medicine show potential applications in gastric cancer treatment. However, the molecular mechanisms regarding dysbiosis of microbiota, including gut microbiota, and intra-tumoral microbiota during the progression of gastric cancer, as well as the therapeutic efficacy of microbiota-related applications, still require extensive exploration through experiments.},
}

*Stomach Neoplasms/therapy/microbiology/pathology
Humans
*Gastrointestinal Microbiome
Dysbiosis/complications/microbiology
Tumor Microenvironment
Probiotics/therapeutic use
Fecal Microbiota Transplantation

@article {pmid40528217,
year = {2025},
author = {Ruszkowski, J and Kachlik, Z and Walaszek, M and Storman, D and Podkowa, K and Garbarczuk, P and Jemioło, P and Łyzińska, W and Nowakowska, K and Grych, K and Dębska-Ślizień, AM},
title = {Fecal microbiota transplantation from patients into animals to establish human microbiota-associated animal models: a scoping review.},
journal = {Journal of translational medicine},
volume = {23},
number = {1},
pages = {662},
pmid = {40528217},
issn = {1479-5876},
support = {"Medical University of Gdansk Excellence Initiative- Research University" program//Gdański Uniwersytet Medyczny/ ; },
mesh = {Animals ; Humans ; Mice ; *Disease Models, Animal ; *Fecal Microbiota Transplantation ; *Gastrointestinal Microbiome ; },
abstract = {BACKGROUND: Fecal microbiota transplantation (FMT) from humans with specific medical conditions to animal models can demonstrate causality by inducing or exacerbating pathophenotypes, linking the gut microbiota to health outcomes.

METHODS: We conducted a scoping review searching MEDLINE, EMBASE, Scopus, and Web of Science through July 2024 to identify human noninfectious diseases studied using FMT in animal models, investigate FMT methodologies, and assess the feasibility of systematic reviews on the role of the microbiota in specific diseases.

RESULTS: From 605 reports of 489 studies, we found that inflammatory bowel diseases, irritable bowel syndrome, obesity, colorectal cancer, and depression were the most commonly studied, with cancer research focusing on immunotherapy non-responsiveness. In a random sample of studies, gastrointestinal outcomes were most frequently reported, with remarkably high rates (> 80%) of successful induction of disease-specific alterations for intestinal barrier function, gastrointestinal inflammation, circulating immune parameters, and fecal metabolites. Most studies used C57BL/6 mice and oral gavage administration, with recipients being either germ-free or antibiotic-pretreated. We created tables linking conditions with publications to facilitate future systematic reviews.

CONCLUSIONS: Although human-to-animal FMT studies cover diverse conditions, methodological heterogeneity and inconsistent reporting hinder comparability. Standardized protocols and guidelines are needed. For several conditions, sufficient literature exists to assess the role of the gut microbiota in human health through systematic reviews.},
}

Animals
Humans
Mice
*Disease Models, Animal
*Fecal Microbiota Transplantation
*Gastrointestinal Microbiome

@article {pmid40528179,
year = {2025},
author = {Chen, K and Wang, H and Yang, Y and Tang, C and Sun, X and Zhou, J and Liu, S and Li, Q and Zhao, L and Gao, Z},
title = {Common mechanisms of Gut microbe-based strategies for the treatment of intestine-related diseases: based on multi-target interactions with the intestinal barrier.},
journal = {Cell communication and signaling : CCS},
volume = {23},
number = {1},
pages = {288},
pmid = {40528179},
issn = {1478-811X},
support = {82274343//National Natural Science Foundation of China/ ; 82405302//National Natural Science Foundation of China/ ; ZR2024QH032//Shandong Provincial Natural Science Foundation/ ; 24-4-4-zrjj-111-jch//Qingdao Natural Science Foundation/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome ; Animals ; *Intestinal Mucosa/microbiology/metabolism ; Probiotics/therapeutic use ; *Intestinal Diseases/microbiology/therapy ; Fecal Microbiota Transplantation ; },
abstract = {The concurrent occurrence and exacerbation of multiple diseases, including geriatric diseases and chronic diseases, impose a heavy burden on human health and medical expenses. Clarifying the common mechanisms of related multifarious diseases and developing preventive and therapeutic strategies with synergistic effects for multiple diseases are of great significance in alleviating the burden on the medical system and reducing patients' burden of drug metabolism. Recent studies have revealed that gut microbiota disorders and intestinal barrier damage, which consequently cause metabolic and immunological disorders, may be a common pathological basis underlying various intestinal-related diseases. In this review, we focus on the intestinal barrier function, summarizing the multi-target interactions and common mechanisms involved in diseases related to the gut such as ulcerative colitis, colorectal cancer, and type 2 diabetes. We identified gut microbe-based strategies, including probiotics, prebiotics, synbiotics, postbiotics, as well as potential targets in faecal microbiota transplant and berberine. The common mechanisms and key targets in the treatment of these diseases mainly include increasing the abundance of beneficial genera Bifidobacterium and Lactobacillus, increasing the levels of Short Chain Fatty Acids, restoring the intestinal mechanical barrier, and suppressing gut inflammation infiltration. We aim to provide a crucial basis and direction for the development of novel drugs with therapeutic effects for multiple diseases, thereby alleviating the patients' burden of medication and enhancing the efficacy of treatment.},
}

Humans
*Gastrointestinal Microbiome
Animals
*Intestinal Mucosa/microbiology/metabolism
Probiotics/therapeutic use
*Intestinal Diseases/microbiology/therapy
Fecal Microbiota Transplantation

@article {pmid40527176,
year = {2025},
author = {Wang, Z and Wang, Y and Zhang, J and Yin, K and Luo, H and Huang, W},
title = {Multi-omics approaches to explore the therapeutic mechanism for ginsenoside Rg1 against MASLD.},
journal = {Biochemical and biophysical research communications},
volume = {776},
number = {},
pages = {152161},
doi = {10.1016/j.bbrc.2025.152161},
pmid = {40527176},
issn = {1090-2104},
abstract = {Ginsenoside Rg1 (G-Rg1), a traditional Chinese medicine, alleviates metabolic dysfunction-associated steatotic liver disease (MASLD). However, the mechanism by which G-Rg1 improves metabolic disorders in MASLD by regulating the gut microbiota remains ambiguous‌. We constructed a diet-induced murine MASLD model and employed 16S rRNA sequencing and non-targeted metabolomic analysis to ‌investigate the mechanism of G-Rg1 in treating MASLD, focusing on its regulatory effect on the gut microbiota. Our results revealed that G-Rg1 significantly increased the 5-hydroxyindoleacetic acid levels and activated the aryl hydrocarbon receptor (AHR) by enhancing intestinal permeability, modulating the gut microbiota composition, and influencing tryptophan metabolism. Therefore, G-Rg1 improved immune function and reduced liver inflammation and lipid deposition in the MASLD mouse model. In contrast, the effect of G-Rg1 was impaired upon removal of the gut microbiota. Furthermore, fecal microbiota transplantation in G-Rg1-treated mice improved MASLD. These finding s suggest that regulating the gut microbiota may play an important role in G-Rg1's ability to protect against MASLD. G-Rg1 may exert its anti-MASLD effects through the gut microbiota, tryptophan metabolism, AHR activation, and interleukin-22 signaling, offering a novel approach for G-Rg1-mediated MASLD treatment.},
}

@article {pmid40523286,
year = {2025},
author = {Juul, FE and Bretthauer, M and Johnsen, PH and Samy, F and Tonby, K and Berdal, JE and Hoff, DAL and Ofstad, EH and Abraham, A and Seip, B and Wiig, H and Rognstad, ØB and Glad, IF and Valeur, J and Nissen-Lie, AE and Ness-Jensen, E and Lund, KMA and Skjevling, LK and Hanevik, K and Skudal, H and Melsom, EJ and Boyar, R and Cooper, TJ and Ranheim, TE and Riise, EM and Adami, HO and Kalager, M and Løberg, M and Garborg, KK},
title = {Fecal Microbiota Transplantation Versus Vancomycin for Primary Clostridioides difficile Infection : A Randomized Controlled Trial.},
journal = {Annals of internal medicine},
volume = {},
number = {},
pages = {},
doi = {10.7326/ANNALS-24-03285},
pmid = {40523286},
issn = {1539-3704},
abstract = {BACKGROUND: Fecal microbiota transplantation (FMT) is recommended for recurrent Clostridioides difficile infection (CDI), but its role in primary CDI is unclear.

OBJECTIVE: To investigate the efficacy and safety of FMT in primary CDI.

DESIGN: Randomized, open-label, noninferiority, multicenter trial. (ClinicalTrials.gov: NCT03796650).

SETTING: Hospitals and primary care facilities in Norway.

PATIENTS: Adults with CDI (C difficile toxin in stool and ≥3 loose stools daily) and no previous CDI within 365 days before enrollment.

INTERVENTION: FMT without antibiotic pretreatment versus oral vancomycin, 125 mg 4 times daily for 10 days.

MEASUREMENTS: The primary end point was clinical cure (firm stools or <3 bowel movements daily) at day 14 and no disease recurrence within 60 days with the assigned treatment alone.

RESULTS: Of 104 randomly assigned patients, 100 received FMT or the first dose of vancomycin and were eligible for analysis. Clinical cure and no disease recurrence within 60 days without additional treatment was observed in 34 of 51 patients (66.7%) with FMT versus 30 of 49 (61.2%) with vancomycin (difference, 5.4 percentage points [95.2% CI, -13.5 to 24.4 percentage points]; P for noninferiority < 0.001, rejecting the hypothesis that response to FMT is 25 percentage points lower than response to vancomycin). Eleven patients in the FMT group and 4 in the vancomycin group had additional C difficile treatment. Clinical cure at day 14 and no recurrence with or without additional treatment was observed in 40 of 51 patients (78.4%) with FMT and 30 of 49 (61.2%) with vancomycin (difference, 17.2 percentage points [95.2% CI, -0.7 to 35.1 percentage points]). No significant differences in adverse events were observed between groups.

LIMITATIONS: Open-label design and reliance on clinical end points.

CONCLUSION: FMT may be considered as first-line therapy in primary CDI.

PRIMARY FUNDING SOURCE: South-East Norway Health Trust.},
}

@article {pmid40522165,
year = {2025},
author = {Huang, JN and Wen, B and Wang, ZN and Gao, JZ and Chen, ZZ},
title = {Microplastics Change the Food Utilization of Filter-Feeding Fish via Gut Microbiota.},
journal = {Environmental science & technology},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.est.5c02067},
pmid = {40522165},
issn = {1520-5851},
abstract = {Microplastics (MPs) are ubiquitous in aquatic environments, while their effects on filter-feeding fish are poorly understood. This study aims to explore how MPs change the feeding of planktivorous silver carp. After exposure to MPs, the utilization efficiency of zooplankton by carp increased from 28.45% to 38.63-40.20%, while that of phytoplankton decreased from 50.64% to 40.47-43.32%. MPs did not cause changes in the phytoplankton and zooplankton communities that carp consumed but altered its gut microbiota, leading to increased abundance of genes encoding proteases but decreased carbohydrase genes. Gut metabolomics further showed corresponding metabolic changes especially with increased levels of l-tyrosine, citrulline, succinic acid, and propionic acid, which are significantly correlated with the isotopic signatures of carp utilizing zooplankton. Germ-free zebrafish transplanted with feces of MPs-exposed carp showed metabolic changes like those of carp, verifying that the gut microbiota mediated the effects induced by MPs, while silver carp transplanted with feces of MPs-exposed carp exhibited increased protease activity and enhanced zooplankton utilization efficiency, confirming that MPs could alter its food utilization via gut microbiota. Our findings fill a knowledge gap regarding the ecological risk of MPs to the feeding of planktivorous fish, with potential cascading effects on aquatic ecosystems.},
}

@article {pmid40520768,
year = {2025},
author = {Feng, Z and Burgermeister, E and Philips, A and Zuo, T and Wen, W},
title = {The gut virome in association with the bacteriome in gastrointestinal diseases and beyond: roles, mechanisms, and clinical applications.},
journal = {Precision clinical medicine},
volume = {8},
number = {2},
pages = {pbaf010},
pmid = {40520768},
issn = {2516-1571},
abstract = {The gut virome, an essential component of the intestinal microbiome, constitutes ∼0.1% of the total microbial biomass but contains a far greater number of particles than bacteria, with phages making up 90%-95% of this virome. This review systematically examines the developmental patterns of the gut virome, focusing on factors influencing its composition, including diet, environment, host genetics, and immunity. Additionally, it explores the gut virome's associations with various diseases, its interactions with gut bacteria and the immune system, and its emerging clinical applications.},
}

@article {pmid40520290,
year = {2025},
author = {Meng, D and Kong, W and Cheng, S and Liu, H and Huang, C},
title = {Gut-brain-liver axis in growth hormone deficiency: role of microbiota-derived short-chain fatty acids in ethnic variability and therapeutic development.},
journal = {Frontiers in public health},
volume = {13},
number = {},
pages = {1541654},
pmid = {40520290},
issn = {2296-2565},
mesh = {Humans ; *Fatty Acids, Volatile/metabolism ; *Gastrointestinal Microbiome/physiology ; *Liver/metabolism ; *Human Growth Hormone/deficiency ; Animals ; *Brain/metabolism ; },
abstract = {Growth hormone deficiency (GHD) is a pediatric endocrine disorder characterized by dysregulated growth hormone/insulin-like growth factor-1 (GH/IGF-1) axis activity and gut microbiota imbalance. Emerging evidence highlights the gut-brain-liver axis as a critical modulator of growth, with microbiota-derived short-chain fatty acids (SCFAs) playing dual roles in GH suppression and IGF-1 enhancement. This review synthesizes preclinical and clinical data to address ethnic variability in microbiota composition and therapeutic challenges. Key findings reveal that Chinese GHD cohorts exhibit reduced Bifidobacterium and fecal butyrate, whereas Spanish cohorts show minimal differences, potentially due to dietary fiber intake (e.g., Prevotella-enriched diets in Asia) or methodological variations in microbiota sequencing. Mechanistically, propionate (>500 μM) inhibits pituitary GH synthesis via GPR41/43-cAMP signaling, while butyrate enhances hepatic IGF-1 through GPR109A-mediated IL-6 secretion and osteoblastic histone deacetylase (HDAC) inhibition. Interventions such as probiotics (e.g., Lactobacillus plantarum increased IGF-1 by 1.2-1.8-fold in murine models) and high-fiber diets demonstrate preclinical efficacy but face clinical barriers, including poor adherence (<30%) and limited GHD-specific trials. Fecal microbiota transplantation (FMT) shows hormonal restoration in animal models but induces gastrointestinal adverse effects (22% bloating, 15% diarrhea) in humans. Multi-omics approaches are proposed to identify biomarkers (e.g., low butyrate + elevated trimethylamine N-oxide). These approaches also aim to optimize precision therapies, such as nanoparticle-delivered SCFAs. This review underscores the need for multicenter randomized controlled trials to validate synbiotics or engineered microbial consortia, bridging mechanistic insights into the microbiota-SCFA-endocrine axis with clinical translation for GHD management.},
}

Humans
*Fatty Acids, Volatile/metabolism
*Gastrointestinal Microbiome/physiology
*Liver/metabolism
*Human Growth Hormone/deficiency
Animals
*Brain/metabolism

@article {pmid40519780,
year = {2025},
author = {Marrocco, F and Khan, R and Reccagni, A and Lin, X and Delli Carpini, M and Iebba, V and D'Alessandro, G and Limatola, C},
title = {Fecal or bacterial transplantation in mice transfer environment-induced brain plasticity and associated behavioral changes.},
journal = {Frontiers in physiology},
volume = {16},
number = {},
pages = {1572854},
pmid = {40519780},
issn = {1664-042X},
abstract = {INTRODUCTION: Recent studies have shown that lifestyle factors, including diet and environmental stimuli, significantly alter the composition of gut microbiota and the metabolites they produce. Specifically, housing mice in an enriched environment (EE) enhances the production of short-chain fatty acids, which in part mediate the effects of EE on brain plasticity. In this study, we tested the hypothesis that the gut microbial composition of EE-exposed mice could be transplanted into mice housed in a standard environment (SE) to replicate the environmental effects on behavior, gene expression and neurogenesis.

METHODS: To test this hypothesis, we transplanted either a specific bacterial mixture or fecal material from EE-housed mice into SE-housed mice.

RESULTS: Our data show that both bacterial and fecal transplants reduce anxiety-like behaviors in mice. Additionally, we observed increased expression of hippocampal neurotrophins and enhanced neurogenesis.

DISCUSSION: These findings support the idea that gut microbiota influence brain functions, including anxiety-like behavior. Further research is necessary to clarify the underlying mechanisms. Moreover, the results suggest that fecal material transplantation (FMT) from individuals with healthy lifestyles may represent a promising strategy for the treatment of mood disorders.},
}

@article {pmid40519640,
year = {2025},
author = {You, W and Ji, J and Wen, D and Wang, C and Sun, X and Zhao, P},
title = {Unlocking therapeutic potential of amlexanox in MASH with insights into bile acid metabolism and microbiome.},
journal = {Npj gut and liver},
volume = {2},
number = {},
pages = {},
pmid = {40519640},
issn = {3004-9806},
abstract = {Metabolic dysfunction-associated steatohepatitis (MASH) has become a global health issue associated with obesity and diabetes. It is becoming a leading cause of end-stage liver diseases such as cirrhosis and hepatocellular carcinoma (HCC). Despite its increasing prevalence, effective pharmacotherapies for MASH remain limited, underscoring the urgent need for novel interventions. Amlexanox, an inhibitor of noncanonical IκB kinases, has demonstrated potential in restoring insulin sensitivity and glucose homeostasis in obese mice and human patients, as shown in our earlier studies. Here, we aimed to assess the therapeutic potential of amlexanox in dyslipidemia-associated diseases, particularly MASH and HCC, and to elucidate the underlying mechanism. We employed GAN diet-fed Ldlr [-/-] mice, which simultaneously develop obesity, MASH, and atherosclerosis, to recapitulate human metabolic syndrome and associated complications. Amlexanox was administrated orally to these mice after disease onset to examine its therapeutic efficacy. Our study demonstrates that even a low dose of amlexanox significantly reversed MASH and nearly completely prevented the progression from MASH to HCC. Both phenotypic and transcriptomic studies revealed that amlexanox markedly improved MASH-related dyslipidemia, hepatic steatosis, inflammation, liver injury, and hepatic fibrosis. Furthermore, multi-omics analysis revealed that amlexanox enhances hepatic bile acid synthesis and promotes fecal bile acid excretion. Notably, amlexanox reprogrammed gut microbiota, robustly increasing the abundance of Akkermansia muciniphila, a probiotic known to improve metabolic dysfunction. These findings uncover the multifaceted therapeutic potential of amlexanox in treating MASH and atherosclerosis by targeting bile acid metabolism, gut microbiota, hepatic inflammation, and fibrosis. Our study highlights amlexanox as a promising candidate for clinical applications.},
}

@article {pmid40519616,
year = {2025},
author = {Zhang, Y and Liang, S and Choi, S and Li, G},
title = {Effects of maternal rumen microbiota on the development of the microbial communities in the gastrointestinal tracts of neonatal sika deer.},
journal = {Journal of animal science and technology},
volume = {67},
number = {3},
pages = {619-635},
pmid = {40519616},
issn = {2055-0391},
abstract = {This study investigated whether the microbial assemblages in the gastrointestinal tracts (GITs) of sika deer calves can be manipulated by maternal rumen microbiota transplantation (MRMT). The results suggest that MRMT had no significant effect on the growth of calves but markedly lowered the duration of diarrhea and increased rumen fermentation in sika deer calves. Sequencing analysis of 16S rRNA gene amplicons revealed that MRMT increased the ability of some microbial taxa to colonize the GIT or enabled the colonization of others, which caused the ruminal microbial communities in sika deer calves to shift such that they resembled those of their mothers and promoted the temporal development of gut microbial diversity in deer calves. Moreover, after inoculation, 7 inoculum-dominant taxa (Butyrivibrio, Tenericutes, RFP12, SR1, Verrucomicrobia, Verruco_5, and WCHB1_41) and one inoculum-dominant taxon (Butyrivibrio) were significantly enriched in the rumen and feces of the sika deer calves, respectively. These data suggest that MRMT may be an effective approach for promoting microbial establishment in the GIT and preventing diarrhea in sika deer calves.},
}

@article {pmid40519460,
year = {2025},
author = {Suvvari, TK and Vallurupalli, V and Koneru, KS and Ingawale, S and Yegurla, RR},
title = {The Lasting Imprint of Antibiotics on Gut Microbiota: Exploring Long-Term Consequences and Therapeutic Interventions.},
journal = {Cureus},
volume = {17},
number = {5},
pages = {e84114},
pmid = {40519460},
issn = {2168-8184},
abstract = {The widespread use of antibiotics has significantly impacted gut microbiota, often leading to long-term dysbiosis with profound health consequences. Antibiotics not only target pathogenic bacteria but also disrupt beneficial microbial communities, reducing diversity and increasing susceptibility to metabolic disorders, immune dysfunction, and opportunistic infections like Clostridioides difficile. The antibiotic-induced microbiota alterations can persist for weeks or even months post-treatment, contributing to ongoing health challenges. Restorative strategies, including probiotics, prebiotics, fecal microbiota transplantation, and dietary modifications, offer potential solutions to mitigate these effects. A balanced approach to antibiotic use, coupled with targeted interventions, is essential to preserving gut microbial health and minimizing long-term complications. Further research is needed to optimize therapeutic strategies and enhance patient outcomes. So, this editorial aims to examine the long-term consequences of antibiotic-induced gut microbiota disruption, highlight clinical and subclinical implications, and evaluate emerging therapeutic interventions aimed at microbiota restoration.},
}

@article {pmid40518557,
year = {2025},
author = {Oppenheimer, M and Tao, J and Moidunny, S and Roy, S},
title = {Anxiety-like behavior during protracted morphine withdrawal is driven by gut microbial dysbiosis and attenuated with probiotic treatment.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2517838},
doi = {10.1080/19490976.2025.2517838},
pmid = {40518557},
issn = {1949-0984},
mesh = {Animals ; *Probiotics/administration & dosage/therapeutic use ; *Dysbiosis/microbiology ; *Gastrointestinal Microbiome/drug effects ; *Substance Withdrawal Syndrome/microbiology/psychology ; Mice ; *Anxiety/microbiology/etiology ; *Morphine/adverse effects ; Male ; Mice, Inbred C57BL ; Fecal Microbiota Transplantation ; Disease Models, Animal ; Behavior, Animal ; Morphine Dependence ; },
abstract = {The development of anxiety during protracted opioid withdrawal heightens the risk of relapse into the cycle of addiction. Understanding the mechanisms driving anxiety during opioid withdrawal could facilitate the development of therapeutics to prevent negative affect and promote continued abstinence. Our lab has previously established the gut microbiome as a driver of various side effects of opioid use, including analgesic tolerance and somatic withdrawal symptoms. We therefore hypothesized that the gut microbiome contributes to the development of anxiety-like behavior during protracted opioid withdrawal. In this study, we first established a mouse model of protracted morphine withdrawal, characterized by anxiety-like behavior and gut microbial dysbiosis. Next, we used fecal microbiota transplantation (FMT) to show that gut dysbiosis alone is sufficient to induce anxiety-like behavior. We further demonstrated that probiotic therapy during morphine withdrawal attenuated the onset of anxiety-like behavior, highlighting its therapeutic potential. Lastly, we examined transcriptional changes in the amygdala of morphine-withdrawn mice treated with probiotics to explore mechanisms by which the gut-brain axis mediates anxiety-like behavior. Our results support the use of probiotics as a promising therapeutic strategy to prevent gut dysbiosis and associated anxiety during opioid withdrawal, with potential implications for improving treatment outcomes in opioid recovery programs.},
}

Animals
*Probiotics/administration & dosage/therapeutic use
*Dysbiosis/microbiology
*Gastrointestinal Microbiome/drug effects
*Substance Withdrawal Syndrome/microbiology/psychology
Mice
*Anxiety/microbiology/etiology
*Morphine/adverse effects
Male
Mice, Inbred C57BL
Fecal Microbiota Transplantation
Disease Models, Animal
Behavior, Animal
Morphine Dependence

@article {pmid40518001,
year = {2025},
author = {Xu, Y and Mo, Y and Zhou, W and Qin, M and Li, M and Yin, G and Yu, H and Chen, Y and Du, H and Jin, Y and Huang, H and Ma, C and Xia, J and Li, H and Xie, Z and Wang, P and Hong, Y},
title = {Sorafenib induces intestinal toxicity by disturbing gut microbiota and activating the LPS/TLR4/NF-κB signaling pathway in mice.},
journal = {Toxicology},
volume = {},
number = {},
pages = {154220},
doi = {10.1016/j.tox.2025.154220},
pmid = {40518001},
issn = {1879-3185},
abstract = {Sorafenib is a multitargeted tyrosine kinase inhibitor approved by the FDA as a standard first-line therapy for advanced hepatocellular carcinoma. Nevertheless, the high incidence rate of gastrointestinal (GI) adverse effects substantially limits its clinical application. The molecular mechanisms underlying the GI damage remain poorly understood. In this study, we explored the critical role of gut microbiota in sorafenib-induced intestinal toxicity using a mouse model and proposed a potential therapeutic intervention strategy. Sorafenib administration caused intestinal pathological damage, systemic inflammation, and oxidative stress in mice. Antibiotic (ABX) treatment and fecal microbiota transplantation (FMT) experiments demonstrated that the GI toxicity induced by sorafenib was mediated by the gut microbiota. 16S rRNA sequencing analysis revealed that sorafenib dramatically disturbed gut microbial homeostasis, leading to an increased abundance of Gram-negative bacteria and upregulated biosynthesis of lipopolysaccharide (LPS). Intestinal transcriptomic sequencing further indicated that sorafenib induced Gram-negative bacterial-derived LPS leakage via the compromised intestinal barrier and exacerbated inflammation via TLR4/NF-κB pathway activation. Notably, the TLR4-specific inhibitor TAK-242 effectively attenuated sorafenib-induced intestinal damage. Taken together, our study unveils a novel mechanism by which sorafenib exacerbates intestinal injury through gut microbiota dysbiosis and LPS/TLR4/NF-κB signaling pathway, while proposing TAK-242 as a promising therapeutic strategy. This study underscores the critical role of the gut microbiota in sorafenib-induced intestinal damage and offers new avenues for clinical intervention.},
}

@article {pmid40517921,
year = {2025},
author = {Wang, Y and Huang, J and Tong, H and Jiang, Y and Jiang, Y and Ma, X},
title = {Nutrient Acquisition of Gut Microbiota: Implications for Tumor Immunity.},
journal = {Seminars in cancer biology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.semcancer.2025.06.003},
pmid = {40517921},
issn = {1096-3650},
abstract = {The gut microbiota is essential in colorectal cancer (CRC) development, progression, and therapeutic responsiveness through its metabolic acquisitions and immunomodulatory functions. The composition of gut microbiota is shaped by habitat filters such as oxygen availability, dietary components, and host-derived factors, which influence both bacterial colonization and metabolic strategies. Furthermore, microbial metabolism of carbohydrates, proteins, and lipids produces metabolites, including short-chain fatty acids (SCFAs), polyamines, ammonia, hydrogen sulfide, and secondary bile acids (BAs). These microbial metabolites can either support anti-tumor immune surveillance or promote tumorigenesis depending on their type, concentration, and the host context. Consequently, interventions such as high-fiber diets, prebiotic and probiotic supplementation, and fecal microbiota transplantation (FMT) have emerged as promising strategies to reshape the gut ecosystem and improve CRC treatment efficacy. This review summarizes current insights into microbial nutrient metabolism, discusses the immune-regulatory effects of key microbial metabolites, and explores microbiota-targeted strategies for enhancing antitumor efficacy. Understanding these interactions offers new therapeutic opportunities for cancer prevention and treatment.},
}

@article {pmid40517506,
year = {2025},
author = {Li, Y and Yue, D and Zhao, Y and Liu, P and Li, M and Chen, J and Yan, X and Fan, L and Song, G and Tian, X and Lv, Y and Zhao, Q and Qiu, Y and Yan, X},
title = {Fecal microbiota transplantation alleviates female offspring's ovarian inflammation in arsenic and fluoride co-exposed rats through the PI3K/ Akt /NF-κB pathway.},
journal = {Ecotoxicology and environmental safety},
volume = {301},
number = {},
pages = {118508},
doi = {10.1016/j.ecoenv.2025.118508},
pmid = {40517506},
issn = {1090-2414},
abstract = {Numerous studies have shown that exposure to arsenic (As) or fluoride(F) can damage the reproductive system, but limited evidence exists regarding the combined toxicity and pathogenesis of As and F co-exposure in female reproduction. Moreover, the role of gut microbiota in mediating such toxicity remains unclear. This study investigated the effects of As and F co-exposure on ovarian development and the potential protective role of fecal microbiota transplantation (FMT). We established an animal model of ovarian injury induced via co-exposure to NaAsO2 and NaF from birth to postnatal day 120(PND120) and introduced FMT from PND60. Co-exposure reduced serum levels of estradiol(E2) and luteinizing hormone (LH), along with morphological alterations in ovarian tissue. Meanwhile, the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/nuclear transcription factor-κB (NF-κB) pathway, a known mediator of inflammation-related ovarian dysfunction, was significantly upregulated. Interestingly, with prolonged exposure, the inflammatory indicators (Akt, IL-1β, IL-6, TNF-α) on PND120 were significantly higher than those on PND60. Notably, FMT alleviated ovarian inflammation, potentially by improving colonic barrier function, thereby indirectly mitigating ovarian damage. Taken together, this study reveals that NaAsO2 and NaF co-exposure induces progressive ovarian inflammation via the PI3K/Akt/NF-κB pathway, and that FMT may offer protective effects. Our findings provide new insights into the environmental risks to female reproductive health.},
}

@article {pmid40516560,
year = {2025},
author = {Assmann, SL and Keszthelyi, D and Kimman, ML and Breukink, SO and , },
title = {Faecal incontinence core outcome set: an international Delphi consensus exercise among patients, health-care professionals, and researchers.},
journal = {The lancet. Gastroenterology & hepatology},
volume = {},
number = {},
pages = {},
doi = {10.1016/S2468-1253(25)00013-5},
pmid = {40516560},
issn = {2468-1253},
abstract = {Faecal incontinence is a debilitating anorectal disorder that can severely affect a person's quality of life. The variability in reported outcomes in studies on treatments for faecal incontinence complicates the synthesis of evidence, thereby weakening treatment recommendations. Furthermore, the emphasis on clinical outcomes often neglects outcomes that are crucial to patients' daily lives. Incorporating diverse stakeholder perspectives, we aimed to develop a core outcome set (COS)-a minimum set of outcomes that should be measured in future studies evaluating the efficacy of a treatment in adults with faecal incontinence. Following guidelines from the COMET initiative, this study proceeded through three steps: identifying outcomes via patient interviews and a systematic literature review; ranking and refining outcomes through two rounds of Delphi surveys involving patients, health-care professionals, and researchers; and finalising the COS through a consensus meeting with relevant stakeholders. Round 1 of the Delphi survey included 109 participants (73 health-care professionals and researchers and 36 patients) and round 2 involved 74 participants (54 and 20, respectively). In both rounds, participants ranked the importance of potential outcomes on a 9-point Likert scale. Of the 58 outcomes that entered round 1 and the three that were later added, 27 outcomes were voted out and the remaining 34 were discussed during a consensus meeting to finalise the COS. The final COS encompasses 13 outcomes: seven quality of life-related outcomes (quality of life, influence on daily activities, social functioning, treatment satisfaction, enjoyment in life, embarrassment, and peace of mind) and six clinical outcomes (severity of faecal incontinence, number of faecal incontinence episodes, urgency, stool consistency, adverse events, and adherence to therapy). This study establishes what outcomes should be included in a COS for use in faecal incontinence research, but future research is needed to identify the appropriate measurement instruments for each outcome and to establish appropriate timing for their assessment, which will further refine outcome definitions before this COS can be implemented. Once these aspects are clarified, the COS can be adopted into faecal incontinence research, which we hope will ultimately improve clinical care.},
}

@article {pmid40514640,
year = {2025},
author = {Almulla, AF and Maes, M},
title = {Peripheral Immune-Inflammatory Pathways in Major Depressive Disorder, Bipolar Disorder, and Schizophrenia: Exploring Their Potential as Treatment Targets.},
journal = {CNS drugs},
volume = {},
number = {},
pages = {},
pmid = {40514640},
issn = {1179-1934},
support = {RA66/016//FF66 grant and a Sompoch Endowment Fund (Faculty of Medicine), MDCU/ ; BG-RRP-2.004-0007-С01//Strategic Research and Innovation Program for the Development of MU - PLOVDIV-(SRIPD-MUP)", Creation of a network of research higher schools, National plan for recovery and sustainability, European Union - NextGenerationEU/ ; },
abstract = {Major depressive disorder (MDD), bipolar disorder (BD), and schizophrenia (SCZ) are major mental disorders linked to substantial morbidity. Traditional monoamine-based pharmacotherapies frequently produce inadequate outcomes for many patients. The elevated levels of treatment resistance require the exploration of new pharmacological targets. Evidence indicates that peripheral immune-inflammatory dysregulation, characterized by an imbalance between immunological responses and compensatory immune-regulatory systems (IRS/CIRS), together with increased oxidative and nitrosative stress (O&NS), significantly contributes to the pathogenesis of these disorders. This review examines IRS/CIRS/O&NS pathways as new drug targets and highlights novel pharmacological trials. Antiinflammatory drugs have been repurposed as augmentation strategies for the treatment of MDD/BD and SCZ, including nonsteroidal antiinflammatory medications, such as cyclooxygenase-2 (COX-2) inhibitors; cytokine-targeting biologics, such as tumor necrosis factor-α monoclonal antibodies; and minocycline, an antibiotic that attenuates neuroinflammation. N-acetylcysteine, curcumin, and omega-3 polyunsaturated fatty acids demonstrate some efficacy as augmentation therapies in MDD, likely by diminishing IRS activation and O&NS. Strategies aimed at the gut-brain axis and gut dysbiosis, including fecal microbiota transplantation, are under investigation for their capacity to restore immunological homeostasis by improving gut barrier integrity and microbiome composition. This review examines new potential therapeutic targets arising from recent discoveries in neuro-immune interactions and oxidative stress, including particular lymphocyte surface markers, the CIRS, and intracellular network molecules in both affective and psychotic disorders. The evidence underscores the clinical importance of immune-targeted augmentation treatments in psychiatric disorders and supports the ongoing development of these novel pharmacotherapies within a precision medicine paradigm.},
}

@article {pmid40513921,
year = {2025},
author = {Zhang, X and Sheng, N and Wang, Z and Cao, Y and Jiang, X and Yan, H and Cheng, F and Geng, T and Wei, K and Zhang, L and Gao, M and Zhou, G and Chen, P},
title = {Exploring the mechanism of Carbonized Typhae Pollen in treating blood stasis syndrome through metabolic profiling: the synergistic effect of hemostasis without blood stasis.},
journal = {Journal of ethnopharmacology},
volume = {},
number = {},
pages = {120124},
doi = {10.1016/j.jep.2025.120124},
pmid = {40513921},
issn = {1872-7573},
abstract = {Removing blood stasis and stopping bleeding traditional Chinese medicines (RBSB-TCM) formed a unique class of TCM, characterized by vasodilating, removing stasis and hemostatic effects. Carbonized Typhae Pollen (CTP), derived from Typhae Pollen (TP) through carbonization, has emerged as a particularly valuable therapeutic agent. It has been widely used in clinical practice to treat hemorrhagic disorders caused by blood stasis syndrome (BSS). However, the potential mechanism for CTP to achieve the dual synergistic effect of promoting blood flow and hemostasis remains unclear.

AIM OF THE STUDY: From the standpoint of metabolite profiles, this study attempts to investigate the fundamental mechanism of CTP in the elimination of blood stasis and the cessation of bleeding.

MATERIALS AND METHODS: First, chemical constituents, absorbed constituents and metabolites in rats following oral administration of CTP were identified by ultra-high performance liquid chromatography coupled with the quadrupole time-of-flight mass spectrometry (UHPLC-Q-TOF-MS) method combined with MetabolitePilot 2.0.4 software. Subsequently, the pharmacological effects of CTP were systematically investigated using rat models with BSS and zebrafish with cerebral hemorrhage. Specifically, the impact on coagulation function and histopathology in rats, as well as the effect on cerebral hemorrhage in zebrafish, were thoroughly evaluated. Untargeted metabolomics based on rat plasma was applied to analyze the metabolic profile changes, revealing the potential action mechanism. The underlying mechanism was furtherly confirmed by gut microbiome analysis and systemic molecular biology experiments.

RESULTS: 34 prototype chemicals and 71 metabolites from the liver, heart, spleen, lung, kidney, small intestine, uterus, and serum were found. CTP improved the abnormal coagulation system, promoted blood circulation, and reduced pathological damage caused by BSS. Plasma metabolomics revealed that BSS significantly altered bile acid (BA) metabolism and arachidonic acid (AA) metabolism. Gut microbiome analysis and fecal microbiota transplantation (FMT) experiments further demonstrated that CTP modulated the gut microbiota. This modulation promoted BA production and activated endothelial nitric oxide synthase (eNOS), leading to increased nitric oxide (NO) levels. These changes contributed to the therapeutic effect of CTP in removing blood stasis. Systemic molecular biology experiments showed that CTP activated key components of the AA metabolic pathway. It promoted PLCγ1 phosphorylation, increased intracellular Ca[2+] levels, and upregulated COX-2 expression. In addition, CTP enhanced the production of AA-related metabolites, including 6-keto-prostaglandin F1α (6-keto-PGF1α), prostaglandin E2 (PGE2), and thromboxane B2 (TXB2). It also increased the transcription of AA metabolism-related genes, such as PLCγ1, PTGS2a, PTGS2b, PTGIS, PTGES, TXBAS, and vWF.

CONCLUSIONS: CTP could promote the generation of AA metabolites through PLCγ1/Ca[2+]/COX-2 to stop bleeding, while also enhancing eNOS activity and NO synthesis through gut microbiota-bile acid axis to remove blood stasis. These two effect were balanced to achieve hemostasis without blood stasis.},
}

@article {pmid40511533,
year = {2025},
author = {Mo, X and Shen, L and Wang, X and Ni, W and Li, L and Xia, L and Liu, H and Cheng, R and Wen, L and Xu, J and Liu, L},
title = {Melatonin Mitigates Sarcopenic Obesity via Microbiota and Short-Chain Fatty Acids: Evidence From Epidemiologic and In Vivo Studies.},
journal = {Journal of cachexia, sarcopenia and muscle},
volume = {16},
number = {3},
pages = {e13869},
pmid = {40511533},
issn = {2190-6009},
support = {82230112//National Natural Science Foundation of China/ ; 82273631//National Natural Science Foundation of China/ ; 2024M761026//China Postdoctoral Science Foundation/ ; 2022YFA0806100//National Key Research and Development Program of China/ ; },
mesh = {Animals ; *Melatonin/pharmacology/therapeutic use ; *Sarcopenia/drug therapy/epidemiology/etiology ; *Obesity/drug therapy/epidemiology ; *Fatty Acids, Volatile/metabolism ; *Gastrointestinal Microbiome/drug effects ; Humans ; Male ; Rats ; Middle Aged ; Female ; Case-Control Studies ; Aged ; },
abstract = {INTRODUCTION: Gut dysbiosis is closely related to the development of sarcopenic obesity (SO). Melatonin (MLT) regulates gut microbiota and promotes the production of short-chain fatty acids (SCFAs). However, whether MLT affects SO through the gut microbiota and SCFAs remains unclear. This study aimed to investigate the effect and mechanism of MLT in SO induced by a high-fat diet (HFD).

METHODS: First, a case-control study was conducted to explore the potential association between serum MLT levels and SO-related parameters in 31 patients. Next, rats fed with a HFD were orally administered with MLT for 16 weeks, and obesity-related metabolic disorders and muscle atrophy were measured. 16S rRNA gene sequencing and gas chromatography-mass spectrometry were used to detect gut microbiota and SCFAs, respectively. Gut barrier integrity was assessed by the expression of the Muc-2 protein and tight junction proteins. Finally, faecal microbiota transplantation and SCFAs administration were performed to confirm the causal role of the gut microbiota and SCFAs in the effect of MLT on SO.

RESULTS: The serum levels of MLT decreased in patients with SO (29.87 ± 6.71 vs. 24.94 ± 5.68, p < 0.01) and were closely associated with appendicular skeletal muscle mass index (r = 0.3514, p < 0.01) and handgrip strength (r = 0.2824, p < 0.05). MLT ameliorated obesity-related metabolic disorders (p < 0.05), poor muscle mass (p < 0.05), strength (p < 0.05) and function (p < 0.05) and muscle atrophy (p < 0.05) in HFD-fed rats. MLT regulated HFD-induced gut dysbiosis, which was mainly characterized by increases in SCFAs-related bacteria and SCFAs (p < 0.05). MLT recovered HFD-induced impairment of gut barrier integrity by promoting the expression levels of Muc-2, claudin-1, occludin and zonula occluden-1 proteins in the colon (p < 0.05). Correlation analysis showed that SCFAs-related bacteria and SCFAs were negatively associated with SO. Faecal suspension from MLT-treated rats promoted the production of SCFAs in recipient rats (p < 0.05). In addition, faecal suspension from MLT-treated rats partially mitigated metabolic disorders (p < 0.05), poor muscle mass and function (p < 0.05) and muscle atrophy (p < 0.05) in recipient rats. SCFAs treatment alleviated the development of SO in HFD-fed rats by suppressing metabolic disorders (p < 0.05), reducing muscle oxidative stress and inflammation (p < 0.05) and promoting protein synthesis through the AKT/mTOR/p70S6k signalling pathway (p < 0.05).

CONCLUSIONS: MLT mitigated HFD-induced SO by regulating the gut microbiota and promoting the production of SCFAs. MLT might be a novel strategy for delaying the progression of SO.},
}

Animals
*Melatonin/pharmacology/therapeutic use
*Sarcopenia/drug therapy/epidemiology/etiology
*Obesity/drug therapy/epidemiology
*Fatty Acids, Volatile/metabolism
*Gastrointestinal Microbiome/drug effects
Humans
Male
Rats
Middle Aged
Female
Case-Control Studies
Aged

@article {pmid40510802,
year = {2025},
author = {Tan, S and Peng, C and Lin, X and Peng, C and Yang, Y and Liu, S and Huang, L and Bian, Y and Li, Y and Xu, C},
title = {Clinical efficacy of non-pharmacological treatment of functional constipation: a systematic review and network meta-analysis.},
journal = {Frontiers in cellular and infection microbiology},
volume = {15},
number = {},
pages = {1565801},
pmid = {40510802},
issn = {2235-2988},
mesh = {Humans ; Acupuncture Therapy/methods ; *Constipation/therapy ; Fecal Microbiota Transplantation/methods ; Randomized Controlled Trials as Topic ; Treatment Outcome ; },
abstract = {INTRODUCTION: The purpose of this study is to compare the relative effectiveness and safety of non-pharmacological interventions for the treatment of functional constipation (FC).

METHODS: We searched Pubmed, Embase, Cochrane, and Web of Science databases for randomized controlled trials published from 2010 to November 2024. The quality of the included studies was evaluated using the Cochrane bias risk tool and Review Manager 5.4, and the evidence was graded using GRADEPro. A network meta-analysis (NMA) was conducted using R Studio, and the surface under the cumulative ranking curve (SUCRA) was used to rank the included drugs for each outcome measure to compare the clinical efficacy of different treatment methods for chronic functional constipation.

RESULTS: A total of 29 RCT studies were included, with a total of 4389 patients with functional constipation who were randomly assigned to receive placebo or one of the nine different non-pharmacological treatment methods. The assessment of bias risk showed that the bias risk of most included studies was low. The results showed that the first-ranked treatment method for clinical efficacy was acupuncture; the first-ranked treatment method for changes in spontaneous bowel movement (SBM) and complete spontaneous bowel movement (CSBM) was fecal microbiota transplantation (FMT); the first-ranked treatment method for changes in the Bristol Stool Form Scale (BSFS) score was FMT; the first-ranked treatment method for changes in the Patient Assessment of Constipation Quality of Life (PAC-QOL) score after treatment was the Vibration capsule; the first-ranked treatment method for changes in the Patient Assessment of Constipation Symptoms (PAC-SYM) score after treatment was percutaneous electrical stimulation; and the treatment method with the lowest incidence of adverse reactions was probiotics.

CONCLUSION: Based on the SUCRA values and NMA results, we found that FMT showed better effects and higher safety on BSFS scores, SBM, and CSBM. In addition, acupuncture showed a good clinical efficacy. We hypothesize that the combination of FMT and acupuncture may be an effective and safe treatment option for functional constipation, but further high-quality clinical studies are needed to confirm this.

https://www.crd.york.ac.uk/prospero/, identifier CRD42024625747.},
}

Humans
Acupuncture Therapy/methods
*Constipation/therapy
Fecal Microbiota Transplantation/methods
Randomized Controlled Trials as Topic
Treatment Outcome

@article {pmid40510588,
year = {2025},
author = {He, S and Chen, H and Xi, H and Sun, G and Du, B and Liu, X},
title = {Gut Microbiota-Derived Butyric Acid Alleviates Glucocorticoid-Associated Osteonecrosis of the Femoral Head via Modulating Inflammatory Cytokines in Bone Marrow Mesenchymal Stem Cells.},
journal = {Mediators of inflammation},
volume = {2025},
number = {},
pages = {8742817},
pmid = {40510588},
issn = {1466-1861},
mesh = {Animals ; *Butyric Acid/metabolism/therapeutic use/pharmacology ; *Gastrointestinal Microbiome/physiology/drug effects ; Rats, Sprague-Dawley ; Rats ; *Mesenchymal Stem Cells/metabolism/drug effects ; *Glucocorticoids/adverse effects ; *Cytokines/metabolism ; Male ; *Osteonecrosis/chemically induced/metabolism/drug therapy ; },
abstract = {Background: The role of gut microbiota and its metabolites in regulating bone metabolism has been well established, with inflammatory immune responses potentially playing a critical role. Glucocorticoid-associated osteonecrosis of the femoral head (GA-ONFH), caused by high-dose glucocorticoid use for inflammatory or immune-related diseases, is a prevalent condition of bone metabolic imbalance. However, the regulatory role and mechanisms of gut microbiota and its metabolites in the development and progression of GA-ONFH remain unclear. This study aims to investigate the intervention effects of gut microbiota and its metabolite butyric acid on GA-ONFH through a series of multi-omics in vitro and in vivo experiments. Methods: Sprague Dawley rats were randomly divided into four groups. The gut microbial composition of the groups was analyzed through 16S rDNA sequencing. Targeted metabolomics was employed to assess differences in short-chain fatty acids (SCFAs) among the groups. Butyric acid, identified as a key differential metabolite, was then selected for further exploration of its effects on bone marrow mesenchymal stem cells (BMSCs) and GA-ONFH rat models through in vitro and in vivo experiments. Results: 16S rDNA sequencing revealed alterations in gut microbiota structure in GA-ONFH rats. Micro-CT and HE staining demonstrated that depletion of gut microbiota with broad-spectrum antibiotics prior to GA-ONFH modeling exacerbated the disease's development. In contrast, fecal microbiota transplantation (FMT) was shown to alleviate GA-ONFH progression. Targeted metabolomics indicated that FMT mitigated the reduction in butyric acid levels induced by dexamethasone (DXM). Subsequent in vitro cell experiments confirmed that butyric acid promotes BMSC proliferation, migration, and osteogenic differentiation. RNA sequencing revealed that butyric acid regulates T cell-mediated inflammatory cytokine genes in BMSCs, while Western blot and immunofluorescence assays confirmed that butyric acid modulates the expression of TNF-α and IL-2/IL-4 in BMSCs. Finally, in vivo experiments demonstrated that butyric acid supplementation attenuated the progression of GA-ONFH and improved the expression of inflammation-related cytokines in femoral head tissue. Conclusions: Our study demonstrates that gut microbiota depletion exacerbates GA-ONFH, while FMT restores butyric acid levels and alleviates disease severity. Butyric acid reduced the expression of TNF-α and IL-2 while increasing the level of IL-4 in vivo and in vitro, thereby improving the local inflammatory environment of the femoral head and alleviating the progression of GA-ONFH. These findings highlight that reduction in butyric acid levels due to gut microbiota dysbiosis is a crucial factor in the progression of GA-ONFH.},
}

Animals
*Butyric Acid/metabolism/therapeutic use/pharmacology
*Gastrointestinal Microbiome/physiology/drug effects
Rats, Sprague-Dawley
Rats
*Mesenchymal Stem Cells/metabolism/drug effects
*Glucocorticoids/adverse effects
*Cytokines/metabolism
Male
*Osteonecrosis/chemically induced/metabolism/drug therapy

@article {pmid40509521,
year = {2025},
author = {Zhang, M and Wang, W and Li, W and Wang, Z and Bi, K and Li, Y and Wu, Y and Zhao, Y and Yang, R and Du, Q},
title = {Ultrasonic-Assisted Extraction of Polysaccharides from Brassica rapa L. and Its Effects on Gut Microbiota in Humanized Mice.},
journal = {Foods (Basel, Switzerland)},
volume = {14},
number = {11},
pages = {},
doi = {10.3390/foods14111994},
pmid = {40509521},
issn = {2304-8158},
support = {32260586//the National Natural Science Foundation of China - Regional Fund Project/ ; },
abstract = {This study optimized ultrasound-assisted extraction (UAE) for polysaccharide isolation from Brassica rapa L. using Box-Behnken design, achieving a maximum yield of 41.12% under conditions of 60 °C, 60 min, 175 W ultrasonic power, and 30 mL/g liquid-solid ratios. The crude polysaccharide (BRAP) was purified via DEAE-52 cellulose and Sephadex G-100 chromatography, yielding BRAP1-1 with the highest recovery rate. Structural analyses (FT-IR, HPGPC, SEM, SEC-MALLS-RI) identified BRAP1-1 as a β-glycosidic pyranose polysaccharide (32.55 kDa) composed of fucose, rhamnose, arabinose, galactose, and galacturonic acid (molar ratio 0.81:4.30:3.61:1.69:89.59). In a humanized mouse model via fecal microbiota transplantation (FMT), BRAP1-1 significantly increased α-diversity indices (ACE, Chao1; p < 0.05) and altered β-diversity, with PCA explaining 73% variance (PC1: 60.70%, PC2: 13.53%). BRAP1-1 elevated beneficial genera (Lysinibacillus, Solibacillus, Bacteroides, etc.) while suppressing pathogens (Treponema, Flavobacterium, etc.). Six genera, including [Eubacterium]_coprostanoligenes_group and Bacteroidales (p < 0.05), correlated with acetic/propionic acid production. These findings demonstrate BRAP1-1's potential to modulate gut microbiota composition and enhance intestinal homeostasis.},
}

@article {pmid40509464,
year = {2025},
author = {Gong, H and Zhao, H and Mao, X},
title = {Sea Cucumber Hydrolysates Alleviate Cognitive Deficits in D-Galactose-Induced C57BL/6J Aging Mice Associated with Modulation of Gut Microbiota.},
journal = {Foods (Basel, Switzerland)},
volume = {14},
number = {11},
pages = {},
doi = {10.3390/foods14111938},
pmid = {40509464},
issn = {2304-8158},
support = {2023YFF1104502//National Key R&D Program of China/ ; },
abstract = {As the global elderly population is rising, concerns about cognitive decline and memory loss are becoming urgent. This study evaluated the potential of sea cucumber hydrolysates (SCH) from Stichopus japonicus in alleviating cognitive deficits using a D-galactose-induced murine aging model. The effects of SCH on behavior, hippocampal morphology, gut microbiota, hippocampal cholinergic system, brain-derived neurotrophic factor (BDNF) signaling, and neuroinflammatory pathways were investigated. Results showed that SCH ameliorated learning and memory deficits and reduced neuronal damage in aging mice. SCH also modulated gut microbiota, along with increased fecal short-chain fatty acids levels. Functional prediction revealed that alterations in gut microbiota were related to signal transduction. Further, SCH enhanced hippocampal cholinergic function through elevating acetylcholine (ACh) levels and inhibiting acetylcholinesterase (AChE) activity and activated BDNF signaling, consistent with predictions of gut microbiota function. Restoration of cholinergic homeostasis and transmission of the BDNF pathway might contribute to the inhibition of hippocampal neuroinflammation via suppressing microglial activation and the nuclear factor kappa-B (NF-κB) pathway. In summary, SCH attenuated cognitive deficits through suppressing neuroinflammation, which might be correlated with the signal transduction caused by regulating gut microbiota. Further validation will be conducted through microbiota depletion and fecal microbiota transplantation. These findings suggest that SCH is a promising functional component for counteracting aging-related cognitive deficits.},
}

@article {pmid40509391,
year = {2025},
author = {Zang, R and Zhou, R and Li, Y and Liu, Z and Wu, H and Lu, L and Xu, H},
title = {Oleuropein Regulates Bile Acid Metabolism via Modulating the Gut Microbiota, Thereby Alleviating DSS-Induced Ulcerative Colitis in Mice.},
journal = {Foods (Basel, Switzerland)},
volume = {14},
number = {11},
pages = {},
doi = {10.3390/foods14111863},
pmid = {40509391},
issn = {2304-8158},
abstract = {The pathogenesis of ulcerative colitis (UC) involves genetic, immunological, and environmental factors as well as gut microbiota dysbiosis. As a natural antioxidant with various pharmacological activities widely present in Oleaceae plants, oleuropein (OLE) exhibits anti-inflammatory, anti-tumor, antiviral, hypoglycemic, and cardioprotective effects. It has been validated that OLE extracted from olive oil can ameliorate UC. However, it remains unclear if and how OLE modulates the gut microbiota in the alleviation of UC. Therefore, this study was conducted to explore the mechanisms for OLE to alleviate UC induced by dextran sulfate sodium (DSS), with the focus placed on its regulatory function in the gut microbiota. The results indicated that OLE mitigated DSS-induced UC by enhancing the intestinal barrier function, reshaping the gut microbiota, and modulating bile acid metabolism. The fecal microbiota transplantation (FMT) experiment results further confirmed that the protective effect of OLE against UC could be mediated by alterations in the gut microbiota and their metabolites induced by OLE. Additionally, OLE increased the abundance of Lactobacillus and certain bile acid metabolites in the colon, including hyodeoxycholic acid (HDCA). HDCA could upregulate the expression of ZO-1 and claudin-3, restoring intestinal barrier integrity. Simultaneously, HDCA could inhibit the activation of the nuclear factor kappa-B (NF-κB) signaling pathway in the colon and relieve colonic inflammation. Overall, it was corroborated that OLE alleviated DSS-induced UC by modulating the gut microbiota and altering bile acid metabolism.},
}

@article {pmid40508089,
year = {2025},
author = {Ai, P and Xu, S and Yuan, Y and Xu, Z and He, X and Mo, C and Zhang, Y and Yang, X and Xiao, Q},
title = {Targeted Gut Microbiota Modulation Enhances Levodopa Bioavailability and Motor Recovery in MPTP Parkinson's Disease Models.},
journal = {International journal of molecular sciences},
volume = {26},
number = {11},
pages = {},
doi = {10.3390/ijms26115282},
pmid = {40508089},
issn = {1422-0067},
support = {82171246//National Natural Science Foundation of China/ ; 82371251//National Natural Science Foundation of China/ ; 2022YFE0210100//National Key R&D Program of China/ ; 22QA1405700//Shanghai Rising-Star Program/ ; },
mesh = {*Gastrointestinal Microbiome/drug effects ; Animals ; *Levodopa/pharmacokinetics/pharmacology/therapeutic use ; Mice ; Fecal Microbiota Transplantation ; Biological Availability ; Male ; Humans ; Disease Models, Animal ; *Parkinson Disease/drug therapy/metabolism ; Dopamine/metabolism ; Mice, Inbred C57BL ; Female ; },
abstract = {Emerging evidence highlights the gut microbiota as a pivotal determinant of pharmacological efficacy. While Enterococcus faecalis (E. faecalis)-derived tyrosine decarboxylases (tyrDCs) are known to decarboxylate levodopa (L-dopa), compromising systemic bioavailability, the causal mechanisms underlying microbiota-mediated pharmacodynamic variability remain unresolved. In our study, we employed antibiotic-induced microbiota depletion and fecal microbiota transplantation (FMT) to interrogate microbiota-L-dopa interactions in MPTP-induced Parkinson's disease (PD) mice. The study demonstrated that antibiotic-mediated microbiota depletion enhances L-dopa bioavailability and striatal dopamine (DA) level, correlating with improved motor function. To dissect clinical heterogeneity in the L-dopa response, PD patients were stratified into moderate responders and good responders following standardized L-dopa challenges. In vitro bioconversion assays revealed greater L-dopa-to-DA conversion in fecal samples from moderate responders versus good responders. FMT experiments confirmed mice receiving good-responder microbiota exhibited enhanced L-dopa bioavailability, higher striatal DA concentrations, and a heightened therapeutic effect of L-dopa relative to moderate-responder recipients. Collectively, our study provided evidence that the gut microbiota directly modulates L-dopa metabolism and microbial composition determines interindividual therapeutic heterogeneity. Targeted microbial modulation-through precision antibiotics or donor-matched FMT-is a viable strategy to optimize PD pharmacotherapy, supporting the potential for microbiota-targeted adjuvant therapies in PD management.},
}

*Gastrointestinal Microbiome/drug effects
Animals
*Levodopa/pharmacokinetics/pharmacology/therapeutic use
Mice
Fecal Microbiota Transplantation
Biological Availability
Male
Humans
Disease Models, Animal
*Parkinson Disease/drug therapy/metabolism
Dopamine/metabolism
Mice, Inbred C57BL
Female

@article {pmid40507919,
year = {2025},
author = {Belvončíková, P and Macáková, K and Tóthová, N and Babál, P and Tarabčáková, L and Gardlík, R},
title = {Investigating the Role of Gut Microbiota in the Pathogenesis and Progression of Rheumatoid Arthritis in a Collagen-Induced Arthritis Mouse Model.},
journal = {International journal of molecular sciences},
volume = {26},
number = {11},
pages = {},
doi = {10.3390/ijms26115099},
pmid = {40507919},
issn = {1422-0067},
support = {APVV-21-0370//Slovak Research and Development Agency/ ; VEGA 1/0706/25//Ministry of Education, Science, Research and Sport of the Slovak Republic/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome ; *Arthritis, Rheumatoid/microbiology/pathology/therapy/etiology ; *Arthritis, Experimental/microbiology/pathology/therapy ; Mice ; Disease Models, Animal ; RNA, Ribosomal, 16S/genetics ; Disease Progression ; Humans ; Mice, Inbred DBA ; Male ; Fecal Microbiota Transplantation ; Female ; },
abstract = {Rheumatoid arthritis (RA) is a chronic systemic autoimmune disorder whose precise etiology remains unclear, though growing evidence implicates gut microbiota in its pathogenesis. This study aimed to investigate the role of gut microbiota in the onset and progression of RA by employing fecal microbiota transplantation (FMT) in a collagen-induced arthritis (CIA) mouse model using DBA/1J and Aire[-]/[-] strains. Mice received FMT from healthy donors, treatment-naïve RA patients, or treated RA patients in relapse, followed by assessment of microbiota composition via 16S rRNA sequencing, arthritis severity scoring, histological evaluations, and systemic inflammatory markers. The findings revealed distinct microbiota clustering patterns post-FMT across experimental groups, highlighting strain-specific colonization effects. Notably, genera such as Bifidobacterium and Paraprevotella correlated positively with arthritis severity in DBA/1J mice, whereas Corynebacterium, Enterorhabdus, and Odoribacter exhibited negative correlations, suggesting potential protective roles. Despite these microbial differences, minor variations in arthritis scores, paw inflammation, or systemic inflammation were observed among FMT groups. This indicates that although gut microbiota alterations are associated with RA pathogenesis, further investigation with larger cohorts and comprehensive sequencing approaches is essential to elucidate the therapeutic potential of microbiome modulation in autoimmune diseases.},
}

Animals
*Gastrointestinal Microbiome
*Arthritis, Rheumatoid/microbiology/pathology/therapy/etiology
*Arthritis, Experimental/microbiology/pathology/therapy
Mice
Disease Models, Animal
RNA, Ribosomal, 16S/genetics
Disease Progression
Humans
Mice, Inbred DBA
Male
Fecal Microbiota Transplantation
Female

@article {pmid40506454,
year = {2025},
author = {Runge, S and von Zedtwitz, S and Maucher, AM and Bruno, P and Osbelt, L and Zhao, B and Gernand, AM and Lesker, TR and Gräwe, K and Rogg, M and Schell, C and Boerries, M and Strowig, T and Andrieux, G and Hild, B and Rosshart, SP},
title = {Laboratory mice engrafted with natural gut microbiota possess a wildling-like phenotype.},
journal = {Nature communications},
volume = {16},
number = {1},
pages = {5301},
pmid = {40506454},
issn = {2041-1723},
support = {491676693//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 256073931//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 446316360//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 431984000//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 241702976//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 438496892//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 501370692//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 256073931//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 256073931//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 491676693//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 259373024//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 431984000//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 441891347//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 471011418//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 493802833-P7//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 390874280//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 2023.010.1//Wilhelm Sander-Stiftung (Wilhelm Sander Foundation)/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/immunology/physiology ; Mice ; Phenotype ; Specific Pathogen-Free Organisms ; Mice, Inbred C57BL ; Male ; Female ; *Fecal Microbiota Transplantation/methods ; Models, Animal ; },
abstract = {Conventional laboratory mice housed under specific pathogen-free (SPF) conditions are the standard model in biomedical research. However, in recent years, many rodent-based studies have been deemed irreproducible, raising questions about the suitability of mice as model organisms. Emerging evidence indicates that variability in SPF microbiota plays a significant role in data inconsistencies across laboratories. Although efforts have been made to standardize microbiota, existing microbial consortia lack the complexity and resilience necessary to replicate interactions in free-living mammals. We present a robust, feasible and standardizable approach for transplanting natural gut microbiota from wildlings into laboratory mice. Following engraftment, these TXwildlings adopt a structural and functional wildling-like microbiota and host physiology toward a more mature immune system, with characteristics similar to those of adult humans. We anticipate that adopting wild mouse-derived microbiota as standard for laboratory mouse models will improve the reproducibility and generalizability of basic and preclinical biomedical research.},
}

Animals
*Gastrointestinal Microbiome/immunology/physiology
Mice
Phenotype
Specific Pathogen-Free Organisms
Mice, Inbred C57BL
Male
Female
*Fecal Microbiota Transplantation/methods
Models, Animal

@article {pmid40500780,
year = {2025},
author = {Liu, J and Jing, C and Guo, Y and Shang, Z and Zhang, B and Zhou, X and Zhang, J and Lian, G and Tian, F and Li, L and Chen, Y},
title = {The central signaling pathways related to metabolism-regulating hormones of the gut-brain axis: a review.},
journal = {Journal of translational medicine},
volume = {23},
number = {1},
pages = {648},
pmid = {40500780},
issn = {1479-5876},
support = {ZR2022MH085//Natural Science Foundation of Shandong Province/ ; ZR2022MH070//Natural Science Foundation of Shandong Province/ ; 202134027//Jinan Science and Technology Bureau/ ; },
abstract = {Obesity is a widespread metabolic disorder linked to various conditions, including type 2 diabetes, hypertension, fatty liver disease, sleep apnea, and hyperuricemia. It significantly impacts quality of life and economic productivity. Traditional methods like diet and lifestyle changes often fail to produce substantial weight loss. Consequently, emerging treatments such as anti-obesity medications, bariatric surgery, and fecal microbiota transplantation are becoming more prominent. Recent research emphasizes the role of hormones that communicate with the hypothalamus through the gut-brain axis, affecting appetite, insulin secretion, and body weight via specific signaling pathways. This review explores the role of key gastrointestinal hormones (GLP-1, PYY, ghrelin, CCK, GIP, leptin, and bile acids) and their signaling pathways in metabolic regulation. The present research systematically evaluates the impact of bariatric surgery on appetite modulation and certain metabolic functions through key signaling pathways, including GLP-1R, GHS-R1a, and FXR/TGR5.},
}

@article {pmid40505989,
year = {2025},
author = {Mehta, N and Little, K and Woodworth, MH and Goodenough, D and Dhonau, R and Fridkin, SK},
title = {Evaluating Disparities in Recurrent Clostridioides difficile Infection (CDI) and Fecal Microbiota Transplant (FMT) Treatment using Geospatial and Social Vulnerability Analytic Tools.},
journal = {Gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.1053/j.gastro.2025.05.028},
pmid = {40505989},
issn = {1528-0012},
}

@article {pmid40505847,
year = {2025},
author = {Yadav, A and Tadas, M and Kale, M and Wankhede, N and Umekar, M and Kotagale, N and Taksande, B},
title = {Gut Microbiota and Behavioral Ontogeny in Autism Spectrum Disorder: A Pathway to Therapeutic Innovations.},
journal = {Physiology & behavior},
volume = {},
number = {},
pages = {114989},
doi = {10.1016/j.physbeh.2025.114989},
pmid = {40505847},
issn = {1873-507X},
abstract = {Autism Spectrum Disorder (ASD) is a multifaceted neurodevelopmental condition characterized by deficits in social communication, repetitive behaviors, and restricted interests. Emerging evidence suggests that gut-brain axis a dynamic, bidirectional communication network between gut microbiota and central nervous system, is critical in shaping behavioral ontogeny in ASD. Dysbiosis of gut microbiota, commonly observed in individuals with ASD, has been associated with alterations in neurodevelopmental trajectories and symptom severity. Furthermore, disturbances in maternal microbiome during pregnancy are increasingly recognized as key factors influencing fetal brain development, potentially heightening risk of ASD and behavioral manifestations. Mechanistic research reveals that gut-derived metabolites modulate blood-brain barrier integrity, neuroinflammatory processes, and neuronal circuit formation, contributing to behavioral outcomes. These findings emphasize gut microbiota's profound influence on emergence and progression of ASD-related behaviors. Promising therapeutic strategies, including probiotics, prebiotics, fecal microbiota transplantation, and dietary interventions, have demonstrated potential in modulating the gut microbiome and improving behavioral symptoms in ASD. However, challenges such as individual variability in microbiome composition, limited clinical evidence, and an incomplete understanding of causative mechanisms remain significant barriers to clinical translation. This review explores the interplay between gut microbiota and ASD-associated behaviors, focusing on key mechanisms such as microbial regulation of neurotransmitter production, immune signaling, and neuroinflammation. It further highlights gut microbiota's potential as a modifiable factor influencing neurodevelopmental and behavioral outcomes in ASD. By advancing our understanding of gut-brain axis, we can pave the way for personalized and targeted interventions aimed at improving behavioral ontogeny and developmental trajectories in individuals with ASD.},
}

@article {pmid40505719,
year = {2025},
author = {Zhu, X and Xu, Y},
title = {Gut microbiome contributes to 6PPD-Quinone induced cognitive impairment through PI3K/Akt signaling.},
journal = {Toxicology},
volume = {},
number = {},
pages = {154217},
doi = {10.1016/j.tox.2025.154217},
pmid = {40505719},
issn = {1879-3185},
abstract = {Studies show that N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine-quinone (6PPD-Q) accumulates in the central nervous system, but its role in cognitive impairment and underlying mechanisms remain unclear. Morris water maze assay revealed that 6-PPDQ significantly impairs cognitive function, particularly learning and memory. HE staining revealed alterations in the hippocampal DG and CA3 regions of exposed mice, including sparse cell arrangement, blurred boundaries, nuclear condensation, and a reduction in Nissl bodies. Fecal microbiota transplantation from 6-PPDQ-exposed mice to normal mice induced cognitive deficits and hippocampal pathological damage. Western Blot assay showed that 6-PPDQ exposure resulted in inhibition of PI3K/AKT signaling. Moreover, blunted PI3K/AKT signaling was observed in mice transplanted with 6-PPDQ-associated mice fecal microbiota. Further analysis of 16S rDNA assay identified a total of 30 differential bacteria at the genus level, including 8 upregulated bacteria such as g_Helicobacter and 22 downregulated bacteria such as g_Prevotellaceae_NK3B31_group. In conclusion, this study uncovers gut microbiome mediates 6PPD-Q-induced cognitive impairment through inhibiting of PI3K/Akt signaling, and provides a basis for further investigation into gut microbiome's protective effects on 6-PPDQ-induced nervous system injury.},
}

@article {pmid40502301,
year = {2025},
author = {Bhandari, P and Berezovskiy, R and Makhani, S and Gausman, V and Rastogi, N and Braude, S},
title = {Discordance in Clinical Indicators With Sequential Fecal Microbiota Transplantation: A Case of Fulminant Clostridioides Difficile Infection.},
journal = {ACG case reports journal},
volume = {12},
number = {6},
pages = {e01731},
pmid = {40502301},
issn = {2326-3253},
abstract = {Fulminant Clostridioides difficile infection (CDI) is a rare, severe type of CDI, often associated with extended hospitalizations, significant healthcare costs, and elevated mortality rates. Fecal microbiota transplantation remains an effective treatment modality for patients with fulminant CDI, with high cure rates reported after multiple treatments. Stool frequency, pseudomembrane resolution, and inflammatory markers are routinely monitored to evaluate disease severity and treatment responsiveness. Our case highlights a discordance in these indicators and demonstrates C-reactive protein as an important marker in assessing residual colitis and disease resolution. Comprehensive scoring systems should consider incorporating C-reactive protein and other biomarkers to optimize CDI management.},
}

@article {pmid40502184,
year = {2025},
author = {Verna, G and De Santis, S and Islam, B and Sommella, EM and Licastro, D and Zhang, L and De Almeida Celio, F and Merciai, F and Caponigro, V and Campiglia, P and Pizarro, TT and Chieppa, M and Cominelli, F},
title = {A missense mutation in Muc2 promotes gut microbiome- and metabolome-dependent colitis-associated tumorigenesis.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.05.31.657160},
pmid = {40502184},
issn = {2692-8205},
abstract = {UNLABELLED: Colitis-associated cancer (CAC) arises from a complex interplay between host and environmental factors, including the gut microbiome. Since ulcerative colitis (UC), a significant risk factor for CAC, is rising in prevalence worldwide, an integrative approach is essential to identify potential triggers linking inflammation to cancer. In the present study, we investigated the role of the gut microbiome using Winnie mice, a UC-like model with a relevant missense mutation in the Muc2 gene. Upon transfer from a conventional (CONV) to a specific-pathogen-free (SPF) facility, Winnie mice exhibited a more severe colitis phenotype, and notably, spontaneous CAC as early as four weeks of age, which progressively worsened over time. In contrast, CONV Winnie developed only mild colitis but with no overt signs of tumorigenesis. Notably, when rederived into germ-free (GF) conditions, SPF Winnie mice were protected from colitis or colon tumor development, indicating an essential role for the gut microbiome in the initiation and progression of CAC in these mice. Using shotgun metagenomics, metabolomics, and lipidomics, we identified a distinct pro-inflammatory microbial and metabolic signature that potentially drives the transition from colitis to CAC. Fecal microbiota transplantation (FMT), using either SPF Winnie or WT (Bl/6) donors into GF Winnie recipients, demonstrated that while colitis developed regardless of donor, only FMT from SPF Winnie donors resulted in CAC, revealing a microbiota-driven, host-specific susceptibility to tumorigenesis in Winnie mice. Our studies present a novel and relevant model of CAC, providing further evidence that the microbiome plays a key role in the pathogenesis of CAC, thereby challenging the concept of colon cancer as a strictly non-transmissible disease.

LAY SUMMARY: This study reveals a distinct metagenomic, metabolomic, and lipidomic profile associated with tumorigenesis in a murine model of ulcerative colitis, highlighting the risks of specific intestinal dysbiosis in genetically predisposed subjects.

WHAT YOU NEED TO KNOW: Background and context: Colitis-associated colorectal cancer arises from complex host-environment interactions, including gut microbiome influences, driving chronic inflammation, with the intestinal lumen environment remaining a largely unexplored potential risk factor in cancer development.New findings: Winnie mice in specific pathogen-free conditions developed severe colitis, and a novel juvenile colon dysplasia and cancer, with gut microbiome changes driving colitis-associated cancer initiation and progression.Limitations: We identified a pro-inflammatory microbial/metabolic signature promoting colitis-to-CAC transition in Winnie mice, with FMT confirming microbiota-driven tumor susceptibility. However, further research is needed to pinpoint the key bacteria-metabolite-lipid combination driving CAC.Clinical research relevance: This newly characterized microbiota-metabolome-based model of CAC, challenges the dogma of cancer as a non-transmittable disease, providing a foundation for developing microbiota-based strategies for CAC prevention and treatment.Basic research relevance: Unlike genetic or chemically induced models, the Winnie mouse model uniquely serves as a dual model for spontaneous colitis and juvenile CAC, offering a fast, 100% penetrant phenotype that enhances reliability, accelerates research, and provides valuable insights into IBD and CAC.},
}