@article {pmid41782164,
year = {2026},
author = {Sørensen, KM and Jensen, CH and Möller, S and Qvist, N and Andersen, DC and Sørensen, JA},
title = {Repairing Peri-Anal Fistulas with regenerative cell therapeutics: study protocol for a double-blinded randomized controlled phase I-II trial from Denmark (REP-PAF).},
journal = {Trials},
volume = {27},
number = {1},
pages = {},
pmid = {41782164},
issn = {1745-6215},
support = {NNF21OC0071847//Novo Nordisk Fonden/ ; NNF19OC0055353//Novo Nordisk Fonden/ ; },
mesh = {Humans ; *Rectal Fistula/surgery/physiopathology/diagnosis ; Double-Blind Method ; Denmark ; *Adipose Tissue/cytology/transplantation ; Treatment Outcome ; Randomized Controlled Trials as Topic ; Clinical Trials, Phase II as Topic ; Quality of Life ; Time Factors ; Debridement/adverse effects ; Wound Healing ; *Stem Cell Transplantation/adverse effects/methods ; Transplantation, Autologous ; Female ; *Anal Canal/surgery/physiopathology/diagnostic imaging ; },
abstract = {BACKGROUND: Surgical treatment of high anal fistulas is challenging and associated with a relatively high rate of complications and failure. Stem cell therapy has shown promising results for fistulas associated with Crohn's disease but remains less studied in cryptoglandular fistulas. This clinical trial is being performed to evaluate the outcome of treating complex cryptoglandular perianal fistulas (PAFs) using minimal surgical debridement combined with either non-cultured (autologous) or cultured (allogeneic) adipose-derived regenerative cells (ADRCs). The primary outcome is the clinical healing rate after 12 months. Secondary outcomes include functional outcomes regarding quality of life and anal continence (measured by the 36-Item Short Form Health Survey [SF-36] and the Wexner Fecal Incontinence Score), risk factors for fistula recurrence, radiological healing assessed by magnetic resonance imaging, and comparison of autologous versus allogeneic ADRCs with respect to cell characterization, immune responses, and efficacy.

METHODS: This is a double-blinded, randomized interventional non-inferiority, phase I-II clinical trial using two approved investigational medicinal products. The study will be conducted at the surgical department, Odense University Hospital OUH, in Odense, Denmark. Inclusion criterion is an adult patient (≥ 18 years) with complex PAF (high transsphincteric or suprasphincteric), involving more than 30% of the anal sphincter. Key exclusion criteria are ongoing suppuration, simple anal fistula, ano- or rectovaginal fistula, inflammatory bowel disease, body mass index (BMI) of < 18.5 kg/m[2], known allergy to penicillin or streptomycin, pregnancy, and verified syphilis, human immunodeficiency virus (HIV), or hepatitis on screening test. The primary investigator (PI) is responsible for participants' recruitment. Eligible patients will undergo 1-day surgery, including debridement of the fistula tract and closure of the internal orifice, liposuction from the anterior abdominal wall, injection of 30-40 mL of autologous microfat around the fistula tract, and injection of 30 million stem cells (either autologous ADRCs or allogeneic ADRC001) according to randomization (1:1 allocation ratio). Patients who receive treatment will attend follow-up visits at 3, 6, and 12 months postoperatively. Serious adverse events will be reported including large abscess formation, wound dehiscence causing fecal incontinence, sepsis, major bleeding, and serious allergic reactions. The trial has been approved by the European Medicines Agency EMA and is monitored by the Good Clinical Practice (GCP) Unit at OUH. A total of 75 patients will be included. Recruitment began in October 2024, with a planned duration of 3 years.

DISCUSSION: The trial intervention is designed as a minimally invasive treatment with the potential to shorten and ease recovery, enable a quicker return to daily activities and work, and avoid sphincter damage, thereby preserving function. The trial is expected to provide evidence on whether allogeneic ADRCs combined with microfat are a viable alternative to autologous ADRCs with microfat for the treatment of PAF.

TRIAL REGISTRATION: Clinical Trials Information System (CTIS) EU CT 2022-502659-73-01. Registered on 18 November 2023.

CLINICALTRIALS: org NCT0 6303752. Registered on 25 February 2024.},
}

Humans
*Rectal Fistula/surgery/physiopathology/diagnosis
Double-Blind Method
Denmark
*Adipose Tissue/cytology/transplantation
Treatment Outcome
Randomized Controlled Trials as Topic
Clinical Trials, Phase II as Topic
Quality of Life
Time Factors
Debridement/adverse effects
Wound Healing
*Stem Cell Transplantation/adverse effects/methods
Transplantation, Autologous
Female
*Anal Canal/surgery/physiopathology/diagnostic imaging

@article {pmid41856839,
year = {2026},
author = {Suchodolski, JS and Toresson, L},
title = {Microbiome Modulation in Veterinary Medicine: From Diet to Fecal Microbiota Transplantation.},
journal = {The Veterinary clinics of North America. Small animal practice},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cvsm.2026.01.009},
pmid = {41856839},
issn = {1878-1306},
abstract = {The intestinal microbiome plays a crucial role in host health. As intestinal dysbiosis can have different underlying causes, multimodal therapeutic approaches are often necessary. Dietary modulation potentially combined with fibers should be the first-line approaches in all patients with acute or chronic enteropathy and help modulate the microbiome. A subset of animals with chronic intestinal disease have marked dysbiosis that results in abnormal microbial function and reflects underlying mucosal pathology, which often persists in chronic inflammatory enteropathy. Fecal microbiota transplantation can be a useful adjunct treatment of chronic disorders, but in patients with severe dysbiosis, repeated treatments are likely needed.},
}

@article {pmid41858792,
year = {2026},
author = {Raber, J and Sharpton, TJ},
title = {Diet, gut microbiome, and cognition in neurodegeneration: a review and methodological framework.},
journal = {Frontiers in aging neuroscience},
volume = {18},
number = {},
pages = {1771904},
pmid = {41858792},
issn = {1663-4365},
abstract = {The gut microbiome influences brain function through the gut-brain axis via synthesis of neurotransmitters, production of metabolites affecting epithelial barrier integrity and immune modulation and signaling through the vagus nerve. In humans, microbiome diversity reflects healthy aging and predicts survival, while dysbiosis is increasingly implicated in neurodegenerative conditions including Alzheimer's disease, Parkinson's disease, multiple sclerosis, and ALS. Fecal transplant studies in germ-free mice demonstrate that microbiome alterations are sufficient to induce cognitive and neuropathological phenotypes, supporting causality in preclinical models. Genetic risk factors and environmental exposures affect both neurodegeneration risk and microbiome composition. In this review, we synthesize evidence from human cohorts and preclinical models on the gut-brain axis in cognitive health and disease. We then present a methodological framework for diet-microbiome-cognition research, addressing causal inference through mediation analysis, supervised approaches for deriving diet scores, validation strategies, and individual heterogeneity. This framework can guide development of microbiome-targeted dietary interventions to improve cognitive outcomes.},
}

@article {pmid41859112,
year = {2026},
author = {Chen, H and Lou, G and Meng, F and Zhang, Y and Kuang, H and Yang, D},
title = {Critical role of reproductive tract microbiota and derived metabolites in inflammation, tumor immunity, and tumorigenesis of gynecological cancers: a narrative review.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1734792},
pmid = {41859112},
issn = {1664-3224},
mesh = {Humans ; Female ; *Genital Neoplasms, Female/metabolism/immunology/microbiology/therapy/etiology ; Animals ; *Microbiota/immunology ; *Carcinogenesis/immunology ; Inflammation/immunology/metabolism/microbiology ; *Gastrointestinal Microbiome/immunology ; *Genitalia, Female/microbiology/immunology ; },
abstract = {Gynecological malignancies, including ovarian, cervical, and endometrial cancers, present significant clinical challenges due to the epidemiological complexity and limitations in current therapeutic strategies. Emerging evidence highlights the critical role of the microbiome and its metabolites in modulating tumor initiation, progression, and treatment responses. This review explores the intricate mechanisms through which gut and reproductive tract microbiota influence gynecological cancers via immune regulation, metabolic reprogramming, and epigenetic modifications. Key microbial metabolites, such as short-chain fatty acids, bile acids, and estrogen-metabolizing intermediates, serve as molecular bridges in host-microbe communication, impacting chemotherapy resistance and immunotherapy efficacy. Furthermore, we discuss the translational potential of microbiome-targeted interventions, including probiotics, fecal microbiota transplantation, and precision microbial therapies, as innovative approaches for diagnosis, prognosis, and treatment. Understanding the microbiota-reproductive axis offers novel insights into overcoming therapeutic resistance and improving patient outcomes in gynecologic oncology.},
}

Humans
Female
*Genital Neoplasms, Female/metabolism/immunology/microbiology/therapy/etiology
Animals
*Microbiota/immunology
*Carcinogenesis/immunology
Inflammation/immunology/metabolism/microbiology
*Gastrointestinal Microbiome/immunology
*Genitalia, Female/microbiology/immunology

@article {pmid41859191,
year = {2026},
author = {Su, Y and Xia, Y},
title = {Gut microbiota dysbiosis and depression: Bidirectional interactions, mediating pathways, and microecological therapeutics.},
journal = {Current research in food science},
volume = {12},
number = {},
pages = {101372},
pmid = {41859191},
issn = {2665-9271},
abstract = {The microbiota-gut-brain axis (MGBA) is increasingly recognized as a key target for ameliorating major depressive disorder (MDD). This review systematically synthesizes evidence on the bidirectional relationship between gut microbiota dysbiosis and MDD, and delineates the core mechanisms-such as neuroinflammation, neurotransmitter metabolism, and hypothalamic-pituitary-adrenal (HPA) axis dysregulation-through which this axis influences depressive pathogenesis. Further, the intestinal microbiota characteristics related to MDD, the main regulatory pathways, and the potential efficacy of microbiome-targeted intervention measures-including psychobiotics, prebiotics, fecal microbiota transplantation (FMT), and dietary strategies-were sorted out. In the clinical assessment and drug research of depression, the assessment tools are mainly divided into two categories: clinician-rated and self-reported. These two types are often used together to provide multi-dimensional evidence of therapeutic efficacy. Evidence suggests that stress-related intestinal permeability may initiate gut dysbiosis, which in turn can impair barrier function, promote neuroinflammation, disrupt neurotransmitter synthesis, and overactivate the HPA axis, potentially exacerbating depressive symptoms. Interventions targeting the gut microbiota may help reshape microbial communities, increase short-chain fatty acids (SCFAs) and 5-Hydroxytryptamine (5-HT), and dampen inflammatory and stress responses, thereby offering a promising, non-pharmacological avenue for alleviating MDD. This review not only offers a theoretical foundation for microbiota-based therapeutics in MDD but also highlights pathways toward developing safe, effective non-pharmacological strategies for depression management.},
}

@article {pmid41859453,
year = {2026},
author = {Cao, L and Zhu, W},
title = {Insights from the high-altitude animal gut adaptation model: mechanisms of obesity regulation via microbiota-derived metabolite homeostasis and the gut-X axis.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1795452},
pmid = {41859453},
issn = {1664-302X},
abstract = {The unique environmental conditions at high altitudes drive the gut microbiota of resident animals to develop distinct structural and functional traits, thereby offering an ideal natural model for investigating the synergistic adaptation of hosts and microorganisms to extreme environmental stressors. This review systematically expounds the mechanism of metabolic adaptation of gut microbiota to high-altitude through the phenotypic characteristics of "high productivity and low inflammation," and understands the mediating effect of short-chain fatty acids and secondary bile acids, which are derived metabolites of flora. SCFAs can enhance the intestinal barrier, regulate the function of immune cells, act on the gut-brain axis, and then affect the feeding behavior. SBAs, as signal molecules, regulate the lipid and energy metabolism of the host through the gut-liver axis. This division of labor and coordination, driven by different metabolites and achieved through specific gut-X axis pathways, constitutes a microecological regulatory network that enables the host to maintain metabolic homeostasis in high-altitude areas. Understanding this natural model can reveal the role of "flora metabolite organ axis" in maintaining health. It can also provide reference direction for obesity intervention caused by high-fat diet (HFD) and other factors, such as regulating the function of gut microbiota through strategies such as dietary regulation, probiotics and prebiotics supplementation, and fecal microbiota transplantation (FMT), and regulating the specific gut-X axis pathway, so as to restore metabolic balance.},
}

@article {pmid41860558,
year = {2026},
author = {Bloom, P and Khanna, S},
title = {Fecal microbiota transplantation in chronic liver disease: Current and future state of the art.},
journal = {Hepatology communications},
volume = {10},
number = {4},
pages = {},
doi = {10.1097/HC9.0000000000000927},
pmid = {41860558},
issn = {2471-254X},
mesh = {*Fecal Microbiota Transplantation/methods/trends/adverse effects ; Humans ; Gastrointestinal Microbiome ; *Liver Diseases/therapy ; Chronic Disease ; },
abstract = {Chronic liver diseases are associated with changes in gut microbiome composition and function. Early data suggest that fecal microbiota transplantation (FMT) may treat several chronic liver diseases, especially cirrhosis, hepatic encephalopathy, and alcohol-associated liver disease. Well-powered and multisite studies are needed to better understand which indications and subpopulations hold promise for FMT. At present, there is variability in the screening, processing, and administration of FMT. Some of this variability is inherent to the nature of FMT, but some of the variability could be standardized to optimize safety and efficacy. Ultimately, we may find that narrowed and donor-independent microbiome therapeutics are superior tools to provide a consistently effective result in chronic liver disease. Regulation of FMT for chronic liver disease indications in the United States will continue to require the rigid regulatory framework of other drugs, requiring an Investigational New Drug (IND) application.},
}

*Fecal Microbiota Transplantation/methods/trends/adverse effects
Humans
Gastrointestinal Microbiome
*Liver Diseases/therapy
Chronic Disease

@article {pmid41861682,
year = {2026},
author = {Ding, WL and Wang, L and Xu, BW and Lu, YN and Yue, TJ and Zhang, ZQ and Guo, FF and Han, RL and Huang, SC},
title = {Strontium chelate with Achyranthes bidentata polysaccharide as a carrier promotes bone regeneration through mediating the gut-liver-bone axis in TD chickens.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {155},
number = {},
pages = {158077},
doi = {10.1016/j.phymed.2026.158077},
pmid = {41861682},
issn = {1618-095X},
abstract = {BACKGROUND: Tibial dyschondroplasia (TD), characterized by impaired angiogenesis and abnormal chondrocyte maturation in the tibial growth plate (TGP), is a common bone disorder in commercial broilers. Strontium (Sr), a trace element with osteogenic and angiogenic properties that plays a crucial role in bone health, exhibits low bioavailability. Achyranthes bidentata polysaccharides, a major extract from Achyranthes bidentata with the function of "guiding the medicine downward", has been used to enhance drug delivery to the lower extremity meridians.

PURPOSE: This study aimed to prepare a novel Achyranthes bidentata polysaccharides-strontium (ABPS-Sr) chelate to enhance Sr bioavailability and investigate its therapeutic effects on tibial damage in TD broilers from the perspective of the gut-bone axis.

METHODS: The ABPS-Sr chelate was synthesized and optimized using response surface methodology, followed by structural characterization. A thiram-induced TD broiler model was established to evaluate the therapeutic efficacy of the ABPS-Sr chelate using qRT-PCR, Western blot, immunoprecipitation, micro-CT, histological staining, and biochemical assays. 16S rRNA sequencing and targeted and non-targeted metabolomics were employed to characterize alterations in gut microbiota, intestinal metabolites and plasma lipid metabolites. Experiments involving phosphatidylcholine (PC)-exposed broilers and fecal microbiota transplantation (FMT) in mice were performed to verify the mediate role of gut microbiota and tibia-damaging effects of PC.

RESULTS: The one-pot synthesis of ABPS-Sr chelate was optimized to achieve a yield of 27.7 %, with structural characterization confirming Sr[2+] coordination-induced conformational changes and porous architecture. Dietary supplementation with ABPS-Sr chelate significantly improved growth performance, restored tibial microstructure, and promoted vessel density in the TGP in TD broilers. Moreover, ABPS-Sr chelate promoted angiogenesis in the TGP by upregulating VEGF expression and restored osteogenic differentiation by activating the ITGB1/FAK/PI3K/AKT1 signaling pathway. Furthermore, ABPS-Sr chelate reshaped gut microbiota composition, restored intestinal barrier function, and corrected hepatic lipid metabolism disorders, particularly by reducing plasma glycerophospholipid (e.g., PC) accumulation that exerts negative effects on bone health.

CONCLUSION: This study demonstrated that ABPS-Sr chelate restores tibial injury in TD broilers by enhancing osteogenesis and angiogenesis via modulation of the gut-liver-bone axis, which provides a promising nutritional intervention strategy for improving poultry bone health.},
}

@article {pmid41850677,
year = {2026},
author = {Mi, X and Liu, R and Jiang, Z and Tang, M and Yan, J and Liu, J and Li, Y and Zheng, J and Yang, W and Gong, L and Shi, J},
title = {Gut Microbiota-Derived Propionate Governs Hepatic N2 Neutrophils in Wilson's Disease.},
journal = {Cellular and molecular gastroenterology and hepatology},
volume = {},
number = {},
pages = {101770},
doi = {10.1016/j.jcmgh.2026.101770},
pmid = {41850677},
issn = {2352-345X},
abstract = {BACKGROUND AND AIMS: Neutrophil functions play a pivotal role in hepatic pathogenesis. Our previous work has established that N2-polarized neutrophils promote hepatic fibrogenesis in Wilson's disease depends on hepatic TGF-β1 production. However, the regulators governing TGF-β1 production in orchestrating disease-associated N2 neutrophils remain elusive. In this study, we investigated the immunomodulatory effects of gut microbiota-derived short-chain fatty acids (SCFAs) on neutrophil polarization.

APPROACH AND RESULTS: We report that Akkermansia muciniphila was markedly reduced in the gut microbiota of mice with Wilson's disease, accompanied by decreased SCFA levels, especially propionate. Additionally, transplantation of fecal bacteria from wild-type mice or A. muciniphila could promote an antifibrotic effect, elevate propionate levels, reduce TGF-β1 secretion, and decrease hepatic N2 neutrophils in mice with Wilson's disease. Moreover, administration of propionate also significantly enhanced antifibrotic immunity. Mechanistically, propionate reduced the production of TGF-β1 in hepatocytes by inhibiting histone deacetylase activity, increasing the acetylation of DNAJA3 at sites K134 and K385, thus decreasing expression of DNAJA3. Consistently, gut-derived propionate inversely correlated with hepatic injury severity in Wilson's disease patients, which could be functionally mediated by TGF-β1.

CONCLUSIONS: Gut microbiota are pivotal for hepatic neutrophil polarization and liver fibrosis in Wilson's disease. Our findings suggest that therapeutic modulation of gut microbiota, SCFA profiles, and TGF-β1 production, particularly when combined with histone deacetylase inhibitors, may represent promising therapeutic approaches for Wilson's disease.},
}

@article {pmid41851729,
year = {2026},
author = {Zhu, W and Han, L and He, L and Wei, S and Li, J and Xin, L and Zhang, H and Shen, J and Song, Y and Zhou, J and Chang, CJ and Zhou, J},
title = {Parabacteroides goldsteinii-derived outer membrane vesicles alleviate acute lung injury via modulation of bile acid metabolism.},
journal = {Journal of nanobiotechnology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12951-026-04288-3},
pmid = {41851729},
issn = {1477-3155},
support = {JSZK2019A01//Shanghai Jinshan Municipal Health Commission/ ; 20DZ2261200//Science and Technology Commission of Shanghai Municipality/ ; 20DZ2254400//Science and Technology Commission of Shanghai Municipality/ ; 82470069//National Natural Science Foundation of China/ ; 2022YFA0806200//National Key Research and Development Program of China/ ; ZD2021CY001//Shanghai Municipal Science and Technology Major Project/ ; },
abstract = {BACKGROUND: Acute respiratory distress syndrome (ARDS) is a severe clinical syndrome with limited therapeutic options. Acute lung injury (ALI) is widely used as an experimental animal model that recapitulates the key pathological features of human ARDS. Parabacteroides goldsteinii, a newly identified Gram-negative probiotic, exhibits anti-inflammatory effects in certain disease models. Gram-negative bacteria release nanoscale structures called outer membrane vesicles (OMVs), which show varying composition across species. The role of P. goldsteinii-derived OMVs (Pg-OMVs) in ALI or ARDS remains to be elucidated.

RESULT: In this study, we investigated the therapeutic potential of Pg-OMVs in a bleomycin (BLM)-induced ALI mouse model and explored their effects on pulmonary inflammation and gut microbiota composition. Compared to mice receiving BLM alone, Pg-OMV-treated mice exhibited significantly reduced inflammatory cell infiltration and lower levels of pro-inflammatory cytokines. Notably, Pg-OMV treatment significantly altered the gut microbiota composition, characterized by an increased abundance of Akkermansia muciniphila and a decreased abundance of Clostridia_bacterium. Fecal microbiota transplantation (FMT) experiments confirmed that the protective effects of Pg-OMVs were mediated via gut-lung axis. Further analysis revealed elevated cholic acid (CA) levels in the peripheral blood and bronchoalveolar lavage fluid following Pg-OMV treatment. CA was shown to suppress BLM-induced macrophage pyroptosis in the lung. Pharmacological inhibition of CA reversed the protective effects of Pg-OMVs, further confirming its pivotal role.

CONCLUSIONS: In summary, Pg-OMVs increased the abundance of Akkermansia muciniphila while decreasing the abundance of Clostridia_bacterium in the gut, elevated systemic CA levels, and suppressed macrophage pyroptosis via inhibition of the NF-κB pathway, thereby attenuating pulmonary inflammation and ultimately alleviating ALI. These findings highlight a novel therapeutic strategy for the treatment of ALI or ARDS by targeting the gut-lung axis.},
}

@article {pmid41852385,
year = {2025},
author = {Ataei, P and Kalantari, H and Bodnar, TS and Turner, RJ},
title = {The gut-brain connection: microbes' influence on mental health and psychological disorders.},
journal = {Frontiers in microbiomes},
volume = {4},
number = {},
pages = {1701608},
pmid = {41852385},
issn = {2813-4338},
abstract = {The human gut microbiome has emerged as a pivotal modulator of brain function and mental health, acting through intricate bidirectional communication along the gut-brain axis. Mounting evidence suggests that microbial communities influence neurodevelopment, neurotransmission, and behavior via pathways involving the vagus nerve, immune signaling, and microbiota-derived metabolites such as short-chain fatty acids and neurotransmitter precursors. This review critically examines the mechanistic underpinnings of microbiota-brain communication and evaluates current findings linking dysbiosis to psychiatric conditions, including depression, anxiety, schizophrenia, autism spectrum disorder, and bipolar disorder. In addition, it assesses the therapeutic potential of microbiome-targeted interventions-such as probiotics, fecal microbiota transplantation (FMT), and precision dietary modulation-in ameliorating neuropsychiatric symptoms. While the field holds considerable promise, limitations, including correlational study designs, small sample sizes, and a lack of standardized methodologies, underscore the need for rigorous, large-scale clinical trials. A deeper understanding of host-microbe interactions may catalyze a paradigm shift in psychiatric treatment, paving the way for novel, personalized microbiome-based therapeutics.},
}

@article {pmid41852399,
year = {2025},
author = {Tillotson, G},
title = {Editorial: Live Biotherapeutic Products: where are we?.},
journal = {Frontiers in microbiomes},
volume = {4},
number = {},
pages = {1664282},
pmid = {41852399},
issn = {2813-4338},
}

@article {pmid41852409,
year = {2025},
author = {Bailey, A and Leuther, KK and Robinson, LA},
title = {The microbiome and lung cancer: microbial effects on host immune responses and treatment outcomes.},
journal = {Frontiers in microbiomes},
volume = {4},
number = {},
pages = {1606551},
pmid = {41852409},
issn = {2813-4338},
abstract = {The human microbiome plays a critical role in shaping physiological processes, immune system function, metabolism, and disease development. Recent research has highlighted the microbiome's profound cancer impact, particularly on lung cancer. This review explores how microbial communities in lung and gut influence tumor progression, immune responses, and treatment outcomes as well as describing the interactions between the microbiome and the host immune system in modulating the efficacy of cancer therapies. Emerging evidence from preclinical and clinical studies investigating the role of the lung and gut microbiome in lung cancer focus on alterations in the microbiota that influence the tumor microenvironment, modulate immune responses, and potentially enhance/hinder treatment effectiveness such as chemotherapy, targeted therapies, and immunotherapy. Microbial diversity plays a significant role in immune regulation, and specific microbial species may activate/suppress immune cells such as T-cells, dendritic cells, and macrophages. Furthermore, this review examines the therapeutic implications of microbiome modulation, including the use of probiotics, antibiotics, and fecal microbiota transplantation in enhancing cancer therapies. Alterations in the lung and gut microbiome and their interaction in the recently described gut-lung axis with its bidirectional communication significantly influence the tumor microenvironment and systemic immune responses. These findings suggest that microbial diversity can regulate immune functions, with specific species capable of activating or suppressing immune cell activity. Furthermore, microbiome-targeted interventions show potential in improving the effectiveness of treatments including chemotherapy, targeted therapies, and immunotherapy, underscoring the importance of the microbiome as a key factor in lung cancer pathogenesis and treatment.},
}

@article {pmid41852427,
year = {2025},
author = {Al-Kuwari, A and Al-Karbi, H and Al-Khuzaei, A and Baroudi, D and Bendriss, G},
title = {Beyond antibiotics: leveraging microbiome diversity to combat antimicrobial resistance.},
journal = {Frontiers in microbiomes},
volume = {4},
number = {},
pages = {1618175},
pmid = {41852427},
issn = {2813-4338},
abstract = {The best way to fight harmful microbes may not lie in new antibiotics, but rather in leveraging the power of microbes themselves. Antimicrobial resistance (AMR) is a growing global concern, where the overuse of antibiotics has led to the emergence of resistant strains. This paper explores the potential of increasing diversity in gut microbiomes as natural approaches to fight AMR. The promotion microbial diversity is proposed as a promising strategy to reduce dependency on antibiotics by fostering a resilient microbial community. Strategies are discussed to address the loss of diversity caused by antibiotics including diet, probiotics, fecal transplants (FMT) and fermentation of animal/plant products. Preliminary findings from an experiment with camel milk fermentation suggest that fermentation can increase microbial diversity, potentially affecting resistance to common antibiotics such as tetracycline, streptomycin, penicillin, and chloramphenicol, and enhancing microbiome resilience, allowing it to naturally resist pathogens without additional antibiotic use. The results highlight both the benefits and potential risks fermented products. Additionally, FMT, naturally occurring in the animal world, is a promising method to restore microbiome balance and mitigating the impact of AMR. A mechanistic model is discussed to underscore the importance of maintaining microbial balance as an effective strategy for mitigating AMR and promoting long-term health. Further research are needed to better understand the mechanisms behind these changes and their implications for public health. This perspective paper calls for a shift in the approach to AMR, advocating for microbiome-based solutions as a sustainable alternative to traditional pharmaceutical interventions.},
}

@article {pmid41852522,
year = {2026},
author = {Luo, Y and Cao, J and Li, B and Wang, J and Geng, T and Luo, Z and Xie, J},
title = {Global landscape analysis of clinical trials on gut microbiota modulation therapies for irritable bowel syndrome.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1737537},
pmid = {41852522},
issn = {2296-858X},
abstract = {OBJECTIVE: Systematically analyze the global landscape of interventional clinical trials on gut microbiota modulation (GMM) therapies for irritable bowel syndrome (IBS).

METHODS: Searched the Trialtrove database (1998-July 2025) with the key term combination "(Disease is Autoimmune/Inflammation: Irritable Bowel Syndrome) AND (Mechanism of Action: Microbiome modulator)", included 305 interventional trials (excluded 15 observational studies). Descriptive analysis was done via SPSS 26.0, adhering to TITAN Guidelines 2025.

RESULTS: Asia was the most active region; trials peaked in 2021, with Phase II (44.3%) and IV (33.3%) dominant. Probiotics led (single-strain: Lactobacillus/Bifidobacterium; multi-strain: Lactobacillus + Bifidobacterium), followed by fecal microbiota transplantation (FMT). IBS-D (49.6%) was the main subtype (IBS-C: 26.1%); probiotics were the most frequently studied for both, FMT for IBS-D, and prebiotics for IBS-C.

CONCLUSION: GMM therapies for IBS are relatively mature. Personalized therapies are necessary; multiomics and emerging therapies (e.g., Akkermansia muciniphila) will promote IBS precision medicine.},
}

@article {pmid41853345,
year = {2023},
author = {Huang, Q and Yang, L and Cai, G and Huang, Y and Zhang, S and Ye, Z and Yang, J and Gao, C and Lai, J and Lin, L and Wang, J and Liu, T},
title = {Comparison of the gut microbiota of college students with the nine balanced and unbalanced traditional Chinese medicine constitutions and its potential application in fecal microbiota transplantation.},
journal = {Frontiers in microbiomes},
volume = {2},
number = {},
pages = {1292273},
pmid = {41853345},
issn = {2813-4338},
abstract = {Fecal microbiota transplantation (FMT) has been tested for the prevention and treatment of various intestinal and extra-intestinal diseases, but its efficacy is not stable, which may be due to the lack of an optimized method for screening high-quality donors. The low efficiency and high cost of donor screening are also obstacles to the clinical application of FMT. In this study, we tested the efficiency of the constitution theory of traditional Chinese medicine (TCM) in screening high-quality FMT donors. College student volunteers were sorted into either the balanced TCM constitution (BC) or unbalanced TCM constitution (UBC) groups, with the latter group comprising eight different constitution types, and the gut microbiota profiles of each UBC were compared with that of BC. Subsequently, the success rates of the qualified donors of BC and UBC volunteers were compared. Finally, the anti-obesity effect of FMT, obtained using the fecal microbiota of BC and UBC donors, was tested on mice with high fat diet-induced obesity. The results showed that the gut microbiota of BC and UBC volunteers were significantly different. There was a higher proportion of qualified FMT donors in the BC volunteer group than in the UBC volunteer group. Moreover, the experiment in mice showed that the fecal microbiota of BC and UBC volunteers conferred different anti-obesity effects. Overall, TCM constitution could be a reference for FMT practice. Our study presents a new idea, namely, using TCM constitution theory to efficiently screen high-quality FMT donors.},
}

@article {pmid41853353,
year = {2023},
author = {Ortiz-Olvera, N and Fernández-Figueroa, EA and Argueta-Donohué, J and Miranda-Ortíz, H and Ruiz-García, E},
title = {Case Report: Oral and fecal microbiota in a super-donor: the healthy microbiota paradigm for fecal transplantation.},
journal = {Frontiers in microbiomes},
volume = {2},
number = {},
pages = {1219960},
pmid = {41853353},
issn = {2813-4338},
abstract = {Despite the numerous fecal microbiota transplantation trials that have been carried out, knowledge about the actual composition of a "healthy microbiota" remains scarce. The aim of this research was to describe the differences in the composition of oral and fecal microbiotas in a super-donor. The microbiota analysis was done using next-generation sequencing of the V3 and V4 regions of the bacterial 16S rRNA gene. The biodiversity found in the mouth was very rich, with 56 species identified, and there was a predominance of the genera Veillonella, Haemophilus, and Streptococcus. It is worth mentioning the presence (2.33%) of Fusobacterium nucleatum in the mouth. In feces, the genera Bacteroides and Faecalibacterium predominated, with the species F. prausnitzii being the most abundant. This analysis shows that the diversity of the microbiota of a super-donor plays a fundamental role in the effectiveness of its product in fecal matter transplantation. This suggests that transplanted gut microorganisms have the ability to maintain or recover health in a dynamic process between the microbiota and the host. Our findings encourage further research which will result in the development of bacterial therapies in infectious and inflammatory diseases.},
}

@article {pmid41853374,
year = {2023},
author = {Gudka, R and Nyinoh, IW},
title = {Fecal microbial transplantation as a novel therapeutic for autism spectrum disorders: a review of the current literature.},
journal = {Frontiers in microbiomes},
volume = {2},
number = {},
pages = {1222089},
pmid = {41853374},
issn = {2813-4338},
abstract = {BACKGROUND: Autism spectrum disorders (ASDs) are complex neurobiological conditions with poor long-term outcomes and limited treatment options. The microbiota-gut-brain axis indicates a pathway by which the gut microbiota links to ASDs. Fecal microbial transplantation (FMT), whereby the gut microbiota is replaced with that of a healthy individual, shows promise for the treatment of neurobiological conditions. This review examines the current evidence for the use of FMT as a therapeutic for ASD.

DISCUSSION: ASDs and their associated gastrointestinal symptoms are improved with FMT, potentially due to the engraftment of features of a healthy gut. Longer treatment regimens that include daily maintenance doses appear to be the most effective long-term therapeutic option, with benefits persisting 2 years post-intervention. Evidence is mixed regarding the use of preparatory treatments. Considering the sex bias in ASD research, small sample sizes and the lack of placebo control arms, randomized controlled trials would be of benefit to the evidence base regarding the use of FMT as a therapeutic option for ASD.

CONCLUSION: FMT is a promising new therapeutic for ASD, but the evidence base is in its infancy.},
}

@article {pmid41853519,
year = {2024},
author = {Li, Y and Yang, Y and Yang, N and Wu, Q and Yang, J and Guo, J and Zhang, H},
title = {Recent advances in fecal microbiota transplantation for Clostridium difficile infection-associated diarrhea after kidney transplantation.},
journal = {Frontiers in microbiomes},
volume = {3},
number = {},
pages = {1409967},
pmid = {41853519},
issn = {2813-4338},
abstract = {Kidney transplantation is considered to be the best treatment for end-stage renal disease. To reduce the incidence of rejection and improve the survival of recipients and kidney grafts, kidney transplant recipients must take immunosuppressive agents, and some patients require them for the rest of their lifetime. These treatment regimens can result in susceptibility to opportunistic infections and disrupt the intestinal microbiota, thereby leading to diarrhea, which causes water and electrolyte metabolism disorder, nutrient malabsorption, and instability in the blood concentrations of the immunosuppressive agents. Fluctuating blood concentration levels of these agents necessitate frequent laboratory monitoring and dose adjustments to avoid poor adherence and increase the risk of graft rejection. Furthermore, severe diarrhea can cause kidney transplant failure or death. Clostridium difficile infection (CDI) is the leading cause of diarrhea after renal transplantation. Traditional antibiotics can kill C. difficile; however, spores can remain in the gut. Disruption of the intestinal flora caused by antibiotherapy increases the risk of developing recurrent CDI (rCDI). Fecal microbiota transplantation (FMT) has been proven to be a safe and effective treatment for CDI and is recommended for rCDI owing to its convenient material acquisition method, high efficacy, and low incidence of adverse reactions. This review summarizes the recent progress in FMT for CDI-associated diarrhea after renal transplantation.},
}

@article {pmid41853530,
year = {2024},
author = {Suo, Z and Yu, Y and Shi, F and Tian, J and Hao, Z and Zhang, J and Zou, J},
title = {Effects of oral liquiritigenin inoculation on gut microbiota and gene expression in intestinal and extraintestinal tissues of mice.},
journal = {Frontiers in microbiomes},
volume = {3},
number = {},
pages = {1380152},
pmid = {41853530},
issn = {2813-4338},
abstract = {INTRODUCTION: Liquiritigenin (LQ), a natural flavonoid found in traditional Chinese medicine and often administered orally, holds potential to affect both the gut and its microbiota, that potentially mediating or influencing its biological and pharmacological effects. However, the effects of LQ on gut microbiota composition and intestinal function remain poorly understood. In this study, we aimed to explore the impact of LQ on gut microbiota and gene expression in both intestinal and extraintestinal tissues.

METHODS: We orally inoculated six-week-old SPF C57BL/6 mice with either LQ (a concentration of 4 mg/ml diluted in dimethylsulfoxide, (DMSO)) or DMSO, and administered daily for a duration of 2 weeks. At the end of the experimental period, all mice were euthanized. Fresh fecal samples, as well as samples from the intestine, lung, and liver, were collected for subsequent microbiota analysis, RNA-seq, or histochemical and immunohistochemical (IHC) staining.

RESULTS: Findings show that LQ alters gut microbiota composition, enhancing microbial correlations in the colon but causing some dysbiosis, evidenced by increased pathobionts, decreased beneficial bifidobacteria, and reduced microbiota diversity. Gene expression analysis reveals LQ upregulates mucosal immune response genes and antiinfection genes in both the intestine and lung, with histology confirming increased Paneth cells and antimicrobial peptides in the intestine. Additionally, LQ affects tissue-specific gene expression, triggering hypersensitivity genes in the colon, downregulating metabolic genes in the small intestine, and reducing cell motility and adhesion genes in the lung.

DISCUSSION: These results suggest LQ's potential to modulate common mucosal immunity but also highlight possible risks of gut dysbiosis and hypersensitivity, particularly in vulnerable individuals. Our study, while informative about the effects of LQ on gut health, lacks direct evidence on whether changes in gut microbiota and gene expression caused by LQ impact inflammatory diseases or are causally linked. Future research should investigate this through fecal microbiota transplantation to explore the causal relationships and LQ's potential effects on immune responses and disease outcomes in relevant models.},
}

@article {pmid41853542,
year = {2024},
author = {Daharsh, L and Lohani, SC and Ramer-Tait, AE and Li, Q},
title = {Characterization of double humanized BLT-mice with stable engraftment of a human gut bacterial microbiome.},
journal = {Frontiers in microbiomes},
volume = {3},
number = {},
pages = {1404353},
pmid = {41853542},
issn = {2813-4338},
abstract = {Humanized mice with human-like immune systems are commonly used to study immune responses to human-specific pathogens. However, one limitation of using humanized mice is their native murine gut microbiota, which significantly differs from that in humans. Given the importance of the gut microbiome to human health, these differences may profoundly impact the ability to translate results from humanized mouse studies to humans. Further, there is a critical need for improved pre-clinical models to study the complex in vivo relationships of the gut microbiome, immune system, and human disease. We previously created double humanized mice with a functional human immune system and a stable, human-like gut microbiome. Here, we characterized the engrafted human gut bacterial microbiome in our double humanized mouse model generated by transplanting fecal material from healthy human donors into the gut of humanized mice. Analysis of bacterial microbiomes in fecal samples from double humanized mice revealed they had unique 16S rRNA gene profiles consistent with those of the individual human donor samples. Importantly, transplanted human-like gut microbiomes were stable in mice for the duration of the study, extending up to 14.5 weeks post-transplant. Microbiomes of double humanized mice also harbored predicted functional capacities that more closely resembled those of the human donors than humanized mice. In conclusion, our study highlights the successful engraftment of human fecal microbiota in BLT humanized mice and underscores the stability of this model, offering a valuable platform for investigating the intricate interplay among the human gut microbiome, immune system, and various diseases in vivo.},
}

@article {pmid41853554,
year = {2024},
author = {Sehgal, K and Feuerstadt, P},
title = {Live biotherapeutic products: a capstone for prevention of recurrent Clostridiodes difficile infection.},
journal = {Frontiers in microbiomes},
volume = {3},
number = {},
pages = {1399440},
pmid = {41853554},
issn = {2813-4338},
abstract = {Clostridiodes difficile infection (CDI) continues to be one of the leading causes of healthcare-acquired diarrhea and infections, and recurrence is the biggest challenge in its management. As technology and research have led to a better understanding of the pathophysiology of C. difficile, we have come to appreciate the role that the gastrointestinal microbiota plays in infection onset and the prevention of recurrence. The gut microbiota is disrupted in those with CDI, which allows further propagation of the infection leading to recurrence, if the microbiota deficiency is unable to regrow itself. While antimicrobial therapy is necessary for treatment of any CDI, these therapeutics do not address the underlying disturbance of microbiota. Microbial remodulation therapies have been developed supplementing the microbiota deficiency that exists after the standard of care antimicrobial resulting in a reduction of recurrence. Fecal microbiota transplantation (FMT) was the initial attempt for this type of therapeutic and proved to be safe and effective, however never achieved FDA approval. In light of this, live biotherapeutic products (LBPs) were developed by pharmaceutical companies through a more standardized and regulated process. These products are safe and efficacious in reducing CDI recurrence when given after a standard of care antimicrobial, eventually leading to FDA approval of two products that can now be used widely in clinical practice.},
}

@article {pmid41853797,
year = {2026},
author = {Zhou, M and Du, K and Wang, H and Zhang, Z and Zhao, R and Ma, C and Huang, Q and Zhang, W and Chen, W},
title = {Ananalysis of the effects of Treg cell therapy intervention on the gut microbiota of type 1 diabetic mice using 16S rRNA gene sequencing.},
journal = {Experimental biology and medicine (Maywood, N.J.)},
volume = {251},
number = {},
pages = {10701},
pmid = {41853797},
issn = {1535-3699},
mesh = {Animals ; *Gastrointestinal Microbiome/genetics ; *RNA, Ribosomal, 16S/genetics ; *T-Lymphocytes, Regulatory/transplantation/immunology ; Male ; Mice, Inbred C57BL ; *Diabetes Mellitus, Type 1/therapy/microbiology ; *Diabetes Mellitus, Experimental/therapy/microbiology ; Mice ; Feces/microbiology ; },
abstract = {This study established a type 1 diabetes (T1DM) mouse model via intraperitoneal injection of streptozotocin (STZ) and examined the effect of regulatory T (Treg) cells on the gut microbiota by comparing its composition and diversity across three groups: control, T1DM, and Treg-treated mice. Forty-one 8-week-old male C57BL/6 mice under specific pathogen-free conditions were divided into a healthy control group, an untreated T1DM group, and a Treg treatment group (receiving low, medium, or high doses). T1DM was induced by administering a low-dose STZ injection over five consecutive days, with diabetes confirmation defined as a blood glucose level ≥300 mg/dL. CD4+CD25+ Treg cells isolated from spleens of healthy mice were used for treatment. Fecal samples collected on days 0, 14, and 34 from three randomly selected mice per group were subjected to 16S rRNA gene sequencing targeting the V3-V4 regions. The results showed significant differences in both alpha and beta diversity among the groups. Dominant bacterial families varied: Ruminococcaceae and others were enriched in the Treg treatment group, Muribaculaceae in the control group, and Lactobacillaceae in the untreated T1DM group. Genus-level abundances also shifted over time. Firmicutes abundance positively correlated with Treg levels (r = 0.70, p = 0.0433) but negatively with IFN-γ, whereas Cyanobacteria exhibited the opposite correlation. The Firmicutes/Bacteroidetes ratio was higher in T1DM mice than in controls and lower in the Treg-treated group. Metabolic pathway analysis indicated that two-component systems and ABC transporters were more prevalent in T1DM mice. In summary, Treg cell treatment altered the diversity, composition, dominant taxa, and Firmicutes/Bacteroidetes ratio of the gut microbiota compared with untreated T1DM mice.},
}

Animals
*Gastrointestinal Microbiome/genetics
*RNA, Ribosomal, 16S/genetics
*T-Lymphocytes, Regulatory/transplantation/immunology
Male
Mice, Inbred C57BL
*Diabetes Mellitus, Type 1/therapy/microbiology
*Diabetes Mellitus, Experimental/therapy/microbiology
Mice
Feces/microbiology

@article {pmid41854281,
year = {2026},
author = {Masi, L and Troisi, S and Petito, V and Puca, P and Pane, C and Biamonte, F and Migliore, G and Emoli, V and Lopetuso, LR and Gasbarrini, A and Papa, A and Scaldaferri, F},
title = {Fecal microbiota transplantation in murine models of colitis and short bowel syndrome: lessons learned, limitations, and translational perspectives.},
journal = {Minerva gastroenterology},
volume = {72},
number = {1},
pages = {104-116},
doi = {10.23736/S2724-5985.26.04136-7},
pmid = {41854281},
issn = {2724-5365},
mesh = {*Fecal Microbiota Transplantation/methods ; Animals ; Disease Models, Animal ; Mice ; *Short Bowel Syndrome/therapy/microbiology ; Gastrointestinal Microbiome ; *Colitis/therapy/microbiology ; Translational Research, Biomedical ; Humans ; },
abstract = {Fecal microbiota transplantation (FMT) has become a powerful experimental tool for dissecting microbiota-driven mechanisms in murine models of gastrointestinal and systemic disease. This review provides a comprehensive methodological and translational overview of FMT in mice, focusing on lessons learned from inflammatory bowel disease (IBD) research and emerging perspectives in short bowel syndrome (SBS). We first outline the fundamental role of the gut microbiota in immune regulation, metabolic homeostasis, and maintenance of epithelial barrier integrity, establishing the rationale for modulating microbial communities through FMT. A detailed methodological analysis follows, highlighting how donor selection, recipient conditioning, sample handling, administration route, and environmental variables critically influence microbial engraftment and experimental reproducibility. The review then synthesizes current evidence from key murine IBD models, demonstrating that FMT can restore epithelial integrity, rebalance adaptive immunity, modulate cytokine networks, and enrich beneficial short-chain fatty-acid-producing taxa. Concepts such as functional engraftment, viability of transferred communities, and host-microbe metabolic interactions are discussed as central determinants of FMT efficacy. Finally, we address the emerging but challenging application of FMT in SBS. Profound alterations in intestinal anatomy, transit, oxygen tension, and substrate availability limit the integration of donor microbiota in SBS models, necessitating adapted strategies such as anaerobic handling, pre-conditioned consortia, synbiotics, and optimized delivery systems. Piglet models and computational approaches for donor-recipient matching are highlighted as promising translational tools. Overall, this review underscores the need for methodological standardization and physiologically tailored approaches to advance the reliability, mechanistic insight, and translational potential of FMT in both IBD and SBS.},
}

*Fecal Microbiota Transplantation/methods
Animals
Disease Models, Animal
Mice
*Short Bowel Syndrome/therapy/microbiology
Gastrointestinal Microbiome
*Colitis/therapy/microbiology
Translational Research, Biomedical
Humans

@article {pmid41854683,
year = {2026},
author = {Wang, J and Shi, Y and Jia, Y and Peng, J},
title = {Effect of Diosmetin on Gut Microbiota and Serum Metabolites in Acute Pancreatitis Mice: A Metagenomic and Metabolomic Study.},
journal = {FASEB journal : official publication of the Federation of American Societies for Experimental Biology},
volume = {40},
number = {6},
pages = {e71679},
doi = {10.1096/fj.202503650RRR},
pmid = {41854683},
issn = {1530-6860},
support = {2023DK2002//Key Project of Research and Development Plan of Hunan Province/ ; 82170661//MOST | National Natural Science Foundation of China (NSFC)/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Flavonoids/pharmacology ; Mice ; *Pancreatitis/drug therapy/metabolism/microbiology/blood/chemically induced ; Male ; Metabolomics/methods ; Metagenomics/methods ; Fecal Microbiota Transplantation ; Mice, Inbred C57BL ; *Metabolome/drug effects ; },
abstract = {Diosmetin is a bioactive flavonoid that exhibits well-documented antioxidant, anti-inflammatory, and anti-tumor properties. However, its potential to attenuate acute pancreatitis (AP) progression through gut microbiota modulation has not yet been elucidated. In this study, mice were pretreated with varying oral doses of diosmetin for 1 week before AP induction via intraperitoneal (i.p.) caerulein injections. The therapeutic efficacy and optimal dosage were determined through histopathological analysis of pancreatic tissue and serological biomarker assessment. Additionally, transcriptomic profiling and western blot were employed to elucidate the underlying signaling pathways. Furthermore, based on integrated metagenomic and metabolomic analyses, a core gut microbiota-metabolite-gene interaction network modulated by diosmetin was constructed. Finally, fecal microbiota transplantation (FMT) experiments validated the critical role of gut microbiota in the effects of diosmetin against AP. The results showed that medium-dose diosmetin treatment significantly attenuated pancreatic histopathological damage and acinar cell apoptosis in AP mice, while suppressing the activation of the MAPK inflammatory signaling pathway. Notably, diosmetin treatment was associated with restored microbial diversity, altered bacterial community structure, and changes in key metabolic pathways, reversing gut microbiota dysbiosis. Specifically, a diosmetin-responsive interaction network was constructed, highlighting associations between core bacterial taxa (Butyricimonas faecalis, Enterocloster bolteae, Roseburia intestinalis), key metabolites (3-indoleacrylic acid, 2-methoxy-4-vinylphenol, nitrite), and MAPK pathway-related genes. Finally, the protective effect of diosmetin was further substantiated by FMT, suggesting a potential role of the gut microbiota in this process. In conclusion, diosmetin ameliorated pancreatic injury in a murine model of caerulein-induced AP by modulating gut microbiota composition and associated metabolic profiles. These findings suggested that diosmetin represented a promising therapeutic option for AP, offering a scientific foundation for its clinical application and the underlying mechanisms involved.},
}

Animals
*Gastrointestinal Microbiome/drug effects
*Flavonoids/pharmacology
Mice
*Pancreatitis/drug therapy/metabolism/microbiology/blood/chemically induced
Male
Metabolomics/methods
Metagenomics/methods
Fecal Microbiota Transplantation
Mice, Inbred C57BL
*Metabolome/drug effects

@article {pmid41844477,
year = {2026},
author = {Hui, H and Guzailiayi, A and Sirui, H and Danping, L and Xiaoyan, L and Abudukelimu, A and Pengbo, W},
title = {Sleep deprivation exacerbates hepatic steatosis by promoting hepatic inflammation and oxidative stress through gut microbiota dysbiosis in metabolic dysfunction-associated fatty liver disease rat.},
journal = {Biochemical and biophysical research communications},
volume = {813},
number = {},
pages = {153588},
doi = {10.1016/j.bbrc.2026.153588},
pmid = {41844477},
issn = {1090-2104},
abstract = {OBJECTIVE: The study aimed to explore the impact of sleep deprivation on hepatic steatosis in metabolic dysfunction-associated fatty liver disease (MASLD) and its possible mechanisms.

METHODS: Forced exercise was used to establish sleep deprivation(SD) models in Sprague-Dawley rats. After 8 weeks of modeling, lipid profile, liver function, pathological feature, inflammatory cytokines, oxidative stress markers, and gut microbiota were determined.

RESULTS: Sleep deprivation exacerbated hepatic steatosis in MASLD rats, as evidenced by significant alteration in morphological analysis and pathological features, accompanied by more severe metabolic disorders and liver injury. Moreover, sleep deprivation dramatically enhanced the secretion of pro-inflammatory cytokines and oxidative stress damage in the liver of MASLD rats. The results of 16S rRNA analysis confirmed a novel causal role of gut microbiota dysbiosis in driving the development of MASLD. Furthermore, sleep deprivation exacerbated gut microbiota dysbiosis in MASLD rats, especially reducing beneficial bacteria including s_roseburia hominis, s_Bacteroides vulgatus, and s_Akkermansia muciniphila. Interestingly, fecal microbiota transplantation (FMT) had demonstrated potential to restore gut microbiota dysbiosis induced by the synergism of high-fat diet (HFD) and sleep deprivation. After partially counteracting the impact of the synergistic effects on gut microbial homeostasis by FMT, hepatic steatosis, hepatic inflammation, and oxidative stress damage in rats of the HFD + SD group were substantially improved.

CONCLUSIONS: These results reveal that sleep deprivation exacerbates hepatic steatosis in MASLD by disrupting gut microbial homeostasis, thereby aggravating hepatic inflammation and oxidative stress, providing novel insights into the potential therapeutic strategies for MASLD and other sleep deprivation-related disorders.},
}

@article {pmid41844930,
year = {2026},
author = {Kumari, N and Pal, G and Chawak, K and Arbi, SH and Anand, S},
title = {Current trends and updates on the emerging role of fecal microbiota transplantation in the treatment of neurodegenerative diseases.},
journal = {Antonie van Leeuwenhoek},
volume = {119},
number = {4},
pages = {},
pmid = {41844930},
issn = {1572-9699},
mesh = {*Fecal Microbiota Transplantation/trends/methods ; Humans ; *Neurodegenerative Diseases/therapy/microbiology ; Gastrointestinal Microbiome ; Animals ; Feces/microbiology ; },
abstract = {Fecal microbiota consists of a consortium of bacterial populations that reside in the human body, particularly in the gastrointestinal system, and are crucial to numerous physiological processes. Due to its promising clinical potential and acceptable safety profile, FMT has been the subject of numerous investigations as a possible therapeutic method for curing diverse disorders. Neurodegenerative diseases (NDs) are one among them and warrant immediate attention. There is a lack of efficient treatments for many ailments, and despite decades of research, we still don't fully understand their mechanisms and causes. The lack of advancement has prompted the research community to focus more on investigating novel or different elements that may impact the etiology or management of these disorders. The gut-brain axis, which embraces the two-way communication between the gut and brain via immunological, neurological, endocrine, and metabolic pathways, is one such element. Since NDs are frequently linked to aberrant gut microbiome compositions, it is not surprising that altering the gut microbiome can be a promising strategy in the treatment and management of neurological disorders. Fecal microbiota transplantation (FMT) is a technique employed for modulating microbiome composition and is becoming more and more common. FMT or recolonizing the ''diseased'' gut with a normal microbiome is one way to restore a dysbiotic gut. Traditionally used to treat Clostridium difficile-linked infections, FMT has lately been investigated as a probable treatment strategy for NDs. This review aims to systematically tap the current trends and updates on the employment of FMT in neurodegenerative research, whether as a treatment regimen or to look into the role of the microbiota in pathogenesis.},
}

*Fecal Microbiota Transplantation/trends/methods
Humans
*Neurodegenerative Diseases/therapy/microbiology
Gastrointestinal Microbiome
Animals
Feces/microbiology

@article {pmid41844942,
year = {2026},
author = {Thu, MS and Le, HBC and Duc, NP and Mai, VH and Walker, N and Hirankarn, N},
title = {Impact of microbiome-modulating strategies in cancer patients receiving immunotherapy (MSIT): A systematic review and meta-analysis.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-44743-7},
pmid = {41844942},
issn = {2045-2322},
support = {N42A680423//National Research Council of Thailand/ ; },
abstract = {The gut microbiota influences immune checkpoint inhibitors (ICIs) efficacy. Microbiome-modulating strategies (MMSs), including probiotics, synbiotics, and faecal microbiota transplantation (FMT), have emerged as promising adjuncts, but their clinical impact remains uncertain. We systematically reviewed PubMed, Embase, and CENTRAL to February 2025 for clinical cohorts evaluating MMS in cancer patients receiving ICIs. Thirty-six studies (25 trials/cohorts; n = 2,746) were included. Meta-analyses, and subgroup analyses were performed for efficacy along with microbiome shifts and safety. MMS plus ICIs achieved a pooled objective response rate (ORR) of 40% (95% CI: 31%-49%; I[2] = 63.4%; p = 0.0003; 95% PI: 15%-72%). Descriptive proportions showed ORR of 45% (95% CI: 32%-58%; I[2] = 72.5%; p = 0.0058) for probiotics and 33% (95% CI: 22%-48%; I[2] = 60.7%; p = 0.0064) for FMT; however, these findings are non-comparative and confounded by study differences. Exploratory subgroup signals were noted for probiotics in NSCLC (ORR 55%; 95%CI: 45%-64%; I[2] = 0%; p = 0.3683) and FMT in melanoma (ORR 39%; 95% CI: 15%-69%; I[2] = 72.5%; p = 0.0262). Dual ICI regimens showed the highest point estimate for ORR (43%; 95% CI: 17%-73%; I[2] = 68.5%; p = 0.0747) but increased toxicity. Microbiome analyses revealed enrichment of short-chain fatty acid-producing taxa and Bifidobacterium spp. among responders. Based on a limited pooled sample size (n = 143), MMS-related adverse events were mostly grade 1-2 (42%; 95% CI: 14%-77%, I[2] = 53.8%, p = 0.0210), with rare severe events (1%). Overall, MMS show promising, though preliminary, hypothesis-generating signals for modulating ICI response. Given high heterogeneity and reliance on early-phase, single-arm trials, the findings underscore urgent need for large, biomarker-driven randomized controlled trials to define optimal interventions and cautiously integrate microbiome modulation into immuno-oncology care.},
}

@article {pmid41845903,
year = {2026},
author = {Cao, H and Sun, J and Lv, Y and Ye, J and Wang, Y and Jiang, H},
title = {Targeting the gut-kidney axis to improve kidney transplantation prognosis: from mechanisms to clinical intervention strategies.},
journal = {Renal failure},
volume = {48},
number = {1},
pages = {2642487},
doi = {10.1080/0886022X.2026.2642487},
pmid = {41845903},
issn = {1525-6049},
mesh = {Humans ; *Kidney Transplantation/adverse effects ; *Gastrointestinal Microbiome/immunology ; *Graft Rejection/prevention & control/immunology ; Prognosis ; Fecal Microbiota Transplantation ; *Kidney/immunology ; *Kidney Failure, Chronic/surgery/immunology ; Intestinal Mucosa/immunology ; Immune Tolerance ; },
abstract = {Kidney transplantation is an important treatment for end-stage renal disease, but lifelong immunosuppression is needed to prevent immune rejection, but the immunosuppressive therapy increases the risk of post-transplant complications. Therefore, how to improve the long-term survival of transplanted kidneys and reduce rejection has become a hot spot in current research. Recently, the 'gut-kidney axis' has received widespread attention as an important pathway for immune regulation. It refers to the fact that changes in either side of the gastrointestinal tract and kidney will affect the other side through energy metabolism, immuno-inflammation, intestinal mucosa, intestinal flora, among others, up and including to adverse consequences, which can be mutually causative. With the theory of 'gut-kidney axis', more and more studies have found that intestinal immune cells and microbiota play an important role in maintaining immune homeostasis and regulating the immune microenvironment of renal transplant recipients. Some studies have found that intestinal immune cells and microbiota not only influence the systemic immune status, but also may regulate the immune response of transplanted kidneys through metabolites and inflammatory mediators. In this review, we summarize the potential mechanisms of intestinal immune cells and microbiota in immune tolerance and rejection after renal transplantation based on the theory of 'gut-kidney axis'. In addition, we highlight microbiome modulation strategies, particularly dietary interventions and fecal microbiota transplantation, as emerging approaches with potential to improve transplant outcomes. A deeper understanding of the mechanism of action of the gut-kidney axis will provide new ideas and therapeutic targets for immunomodulation after renal transplantation.},
}

Humans
*Kidney Transplantation/adverse effects
*Gastrointestinal Microbiome/immunology
*Graft Rejection/prevention & control/immunology
Prognosis
Fecal Microbiota Transplantation
*Kidney/immunology
*Kidney Failure, Chronic/surgery/immunology
Intestinal Mucosa/immunology
Immune Tolerance

@article {pmid41846062,
year = {2026},
author = {Zhu, Q and Gao, M and Yan, M and Ma, Z and Li, X and Yu, M and Niu, X and Wang, J},
title = {Naringin alleviates autoimmune hepatitis in mice via the gut-liver Axis through modulation of microbiota, metabolites, and immune responses.},
journal = {International immunopharmacology},
volume = {177},
number = {},
pages = {116498},
doi = {10.1016/j.intimp.2026.116498},
pmid = {41846062},
issn = {1878-1705},
abstract = {Autoimmune hepatitis (AIH) is an immune-mediated liver disease that could be impacted by gut microbiota dysbiosis. Naringin, a flavonoid derived from citrus fruits, has been reported to modulate gut microbial composition and alleviate liver diseases, but its role in AIH remains incompletely understood. In this study, we used multi-omics analysis and fecal microbiota transplantation (FMT) to examine the protective benefits of naringin in a ConA-induced AIH mouse model. To strengthen mechanistic conclusions, histopathological scoring, liver function indices, and immune cell profiling were determined. Naringin reduced IFN-γ and IL-17A, improved oxidative balance, remodeled hepatic transcriptome, and corrected microbial dysbiosis. Integrated multi-omics analysis revealed associations with altered MAPK, NF-κB, JAK-STAT, and autophagy pathways. Additional investigations revealed that naringin increased the expression of the tight junction proteins ZO-1 and occludin, improved intestinal barrier integrity, and decreased Th1/Th17 cell proportions without significantly altering Th2 cells, as validated by flow cytometry and immunohistochemistry. Importantly, FMT from naringin-treated donors provided hepatoprotective benefits in recipient mice. These findings shed fresh information on the gut-liver axis in AIH, highlighting naringin as a potential therapeutic agent through coordinated regulation of oxidative stress, immune responses, and gut microbiota-associated metabolic profiles.},
}

@article {pmid41846401,
year = {2026},
author = {Bogatic, D and Costello, SP and Bryant, RV},
title = {Letter: Dose and Donor Matter-Determining the Optimal Strategy for Faecal Microbiota Transplantation in Clostridioides difficile Infection.},
journal = {Alimentary pharmacology & therapeutics},
volume = {},
number = {},
pages = {},
doi = {10.1111/apt.70625},
pmid = {41846401},
issn = {1365-2036},
}

@article {pmid41847216,
year = {2026},
author = {Shi, H and Huang, L and Zhang, JH and Shen, C and Zhang, N and Lv, C and Shao, L and Li, M and Sun, Z and Shi, L and Yu, G and Chen, Y},
title = {Gut Microbiota Regulates Brain-Bone Axis to Influence Osteoporosis Pathogenesis and Treatment.},
journal = {Research (Washington, D.C.)},
volume = {9},
number = {},
pages = {1178},
pmid = {41847216},
issn = {2639-5274},
abstract = {Osteoporosis is a systemic skeletal disorder characterized by reduced bone mass, impaired microarchitecture, and increased fracture risk, primarily resulting from dysregulated bone remodeling. Increasing evidence highlights a close interaction between bone metabolism and the gut microbiota. Alterations in bone mineral density can influence gut microbial composition. Conversely, microbial dysbiosis disrupts bone homeostasis through multiple pathways, including microbial metabolites, immune regulation, and neuroendocrine signaling. Short-chain fatty acids suppress osteoclast differentiation and enhance intestinal calcium absorption, while gut dysbiosis promotes bone loss by impairing intestinal barrier integrity and increasing proinflammatory cytokines such as tumor necrosis factor-α and interleukin-6. The gut-brain-bone axis represents an important regulatory network linking the central nervous system, gut-derived signals, and skeletal remodeling. Chronic stress and neurodegenerative conditions activate the hypothalamic-pituitary-adrenal axis and bone-derived extracellular vesicle signaling, thereby favoring bone resorption. Estrogen deficiency further disrupts the receptor activator of nuclear factor κΒ ligand/osteoprotegerin signaling pathway and alters gut microbial composition, contributing to postmenopausal bone loss. Therapeutic strategies targeting this axis, including probiotics, prebiotics, fecal microbiota transplantation, dietary fiber supplementation, and pharmacological or natural compounds, show potential in restoring microbial balance and improving bone metabolism. Future studies integrating multiomics approaches and well-designed clinical trials are needed to clarify microbiome-bone interactions and support the development of targeted interventions for osteoporosis.},
}

@article {pmid41849251,
year = {2026},
author = {Chen, J and Shen, X and Chen, Y and Liang, J and Liu, Y and Cao, J and Wang, LS and Lu, B and Sun, C and Wang, Y},
title = {Finger Citron (Citrus medica L. var. sarcodactylis Swingle) and Its Characteristic Component Limettin Alleviated Diet-Induced Obesity via Modulating Gut Microbiota and Steroid Hormone Biosynthesis.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c15347},
pmid = {41849251},
issn = {1520-5118},
abstract = {This study investigated the antiobesity effects and underlying mechanisms of finger citron extract (FC) and its characteristic compound limettin (LMT) in high-fat diet (HFD)-induced obese mice. FC and LMT significantly reduced body weight gain and improved glucose and lipid homeostasis in obese mice. Fecal 16S rRNA sequencing revealed that both treatments reversed HFD-induced gut dysbiosis, enriching norank_f__norank_o__Clostridia_UCG-014, while FC uniquely increased Akkermansia and decreased Rikenella. Serum metabolomics indicated that FC and LMT markedly activated the steroid hormone biosynthesis pathway, elevating 11β-hydroxyprogesterone, 17α-hydroxyprogesterone, and 11-deoxycorticosterone. Colon transcriptomics further confirmed altered local steroid synthesis and metabolism in the colon. Antibiotic depletion and fecal microbiota transplantation verified the indispensable role of gut microbiota in FC/LMT-mediated metabolic protection. Collectively, FC and LMT ameliorated diet-induced obesity by modulating steroid hormone biosynthesis through gut microbiota regulation, highlighting their potential as functional dietary supplements for obesity prevention.},
}

@article {pmid41432256,
year = {2026},
author = {He, F and Liu, G and Wu, H and Elsabagh, M and Huang, Y and Wang, J and Wang, M and Zhang, H},
title = {Maternal intestinal and placental mitochondrial dysfunction, autophagy, and ferroptosis involving intestinal microbiota by gut microbiota transplantation from sheep to mice†.},
journal = {Biology of reproduction},
volume = {114},
number = {3},
pages = {1030-1044},
doi = {10.1093/biolre/ioaf253},
pmid = {41432256},
issn = {1529-7268},
support = {2024YFD1300203//Project of National Key Research and Development Program of China/ ; },
mesh = {Animals ; Female ; Pregnancy ; *Placenta/drug effects ; Mice ; *Autophagy/physiology/drug effects ; *Gastrointestinal Microbiome/physiology ; Sheep ; *Ferroptosis/physiology/drug effects ; *Mitochondria ; *Intestines/microbiology ; *Fecal Microbiota Transplantation ; Fetal Growth Retardation/chemically induced ; },
abstract = {Exposure to testosterone (T) in pregnant ewes resulted in placental dysfunction and fetal growth restriction (FGR). However, the impact of T on gut microbiota and its contribution to exacerbating intestinal and placental pathologies remains uncharacterized. Pregnant sheep received intramuscular injections of 100 mg T propionate or a control vehicle. To examine the gut microbiota' s role in T-induced FGR, gut microbiota transplantation (GMT) was conducted from T-exposed and control ewes into antibiotic-treated pregnant mice. The findings demonstrated that T exposure exacerbated mitochondrial impairment, autophagy, and ferroptosis in placental and intestinal tissues, alongside inducing gut microbial dysbiosis. GMT further revealed that pathological alterations were mechanistically linked to gut microbiota imbalance. The findings demonstrated that gut-placental axis play a central role in mediating T-induced mitochondrial dysfunction, autophagy, and ferroptosis in maternal intestinal and placental tissues. These results underscore novel therapeutic opportunities, which operate via the gut-placental axis to mitigate FGR.},
}

Animals
Female
Pregnancy
*Placenta/drug effects
Mice
*Autophagy/physiology/drug effects
*Gastrointestinal Microbiome/physiology
Sheep
*Ferroptosis/physiology/drug effects
*Mitochondria
*Intestines/microbiology
*Fecal Microbiota Transplantation
Fetal Growth Retardation/chemically induced

@article {pmid41839398,
year = {2026},
author = {Kawuribi, V and Awere-Duodu, A and Adjei, FA and Osman, AH and Bomansaan, H and Madadi, MM and Tampuri, JU and Adu-Amankwaah, J},
title = {The Gut-Tumor Metabolic Axis: A Comprehensive Exploration of Bidirectional Crosstalk in Cancer Immunotherapy.},
journal = {Critical reviews in oncology/hematology},
volume = {},
number = {},
pages = {105280},
doi = {10.1016/j.critrevonc.2026.105280},
pmid = {41839398},
issn = {1879-0461},
abstract = {The gut-tumor metabolic axis represents a bidirectional immunometabolic network in which tumor-derived metabolites reshape microbial ecology, while gut microbiome-derived metabolites recalibrate systemic and intratumoral immunity, ultimately influencing cancer progression and immunotherapy outcomes. Tumor aerobic glycolysis generates excess lactate and acidity that suppress cytotoxic immune function, remodel the tumor immune microenvironment, and indirectly perturb intestinal microbial composition. In turn, microbial metabolites including short-chain fatty acids, bile acid derivatives, tryptophan catabolites, inosine, and trimethylamine N-oxide signal through defined host pathways such as GPR109A, AHR, and adenosine A2A receptors to regulate antigen presentation, T-cell differentiation, macrophage polarization, and immune checkpoint sensitivity. Preclinical and emerging clinical evidence demonstrates that dietary modulation, rational probiotics, and fecal microbiota transplantation can enhance immune checkpoint inhibitor efficacy in selected contexts. However, metabolite effects are highly context dependent, with dose, timing, tumor type, and immune state critically shaping therapeutic benefit or resistance. This review integrates mechanistic insights and clinical evidence, highlights translational challenges including safety, donor heterogeneity, and biomarker validation, and proposes a framework for biomarker-guided microbiome-based strategies to advance precision cancer immunotherapy.},
}

@article {pmid41833674,
year = {2026},
author = {Wang, X and Shao, J and Dong, X and Ding, H and Ma, Z},
title = {Bletilla striata polysaccharide alleviates obesity by remodeling the gut microbiota-metabolite-liver axis and suppressing the hepatic AMPK-SREBP2/SQLE signaling pathway.},
journal = {International journal of biological macromolecules},
volume = {},
number = {},
pages = {151416},
doi = {10.1016/j.ijbiomac.2026.151416},
pmid = {41833674},
issn = {1879-0003},
abstract = {Obesity is a global health crisis, yet the precise biochemical relay underlying the anti-obesity effects of Bletilla striata polysaccharides (BSP) remains to be fully elucidated. We investigated the metabolic effects of BSP in a high-fat diet (HFD)-induced obese mouse model. Using an integrative multi-omics strategy combined with fecal microbiota transplantation (FMT) and functional validation, we aimed to decipher the "gut microbiota-metabolite-liver" regulatory axis. BSP supplementation significantly attenuated HFD-induced weight gain, improved glucose and lipid homeostasis, and mitigated systemic inflammation, oxidative stress, and hepatic steatosis in a dose-dependent manner. Multi-omics analyses revealed that BSP selectively remodeled the gut microbiota by suppressing obesity-associated genera while enriching beneficial taxa such as Allobaculum, Ileibacterium valens, and Dubosiella. These microbial shifts were accompanied by a reduction in deleterious bile acids and, crucially, a significant increase in the production and systemic circulation of short-chain fatty acids, providing a definitive physiological link between intestinal alterations and distal host responses. Hepatic transcriptomic and protein analyses further revealed that these gut-derived metabolites triggered the phosphorylation-mediated activation of AMPK signaling, which subsequently suppressed squalene epoxidase (SQLE)-mediated cholesterol biosynthesis. Causal evidence was established through FMT, where recipient mice phenocopied the metabolic benefits of BSP donors. Furthermore, loss- and gain-of-function experiments using pharmacological inhibitors and AAV8-mediated gene delivery confirmed that SQLE is a necessary mediator of BSP's anti-obesity action. Collectively, our findings demonstrate that BSP alleviates obesity by orchestrating a microbiota-metabolite-host axis connecting gut microbial remodeling to the hepatic AMPK-SREBP2/SQLE signaling cascade, highlighting its potential as a targeted functional dietary intervention.},
}

@article {pmid41833765,
year = {2026},
author = {Yang, C and Zhang, X and Bie, J and Kang, W and Sun, G and Qing, Z and Lihua, L and Qiaosheng, H},
title = {Gut microbiota drives dietary lignans to improve perimenopausal depression via activating hippocampal ERβ/GluN2A/PSD95 pathway.},
journal = {Pharmacological research},
volume = {},
number = {},
pages = {108161},
doi = {10.1016/j.phrs.2026.108161},
pmid = {41833765},
issn = {1096-1186},
abstract = {Dietary lignans (Diet-LIG) are a class of estrogenic plant polyphenols whose improve potential for perimenopausal depression (PMD), a condition driven by estrogen deficiency, remains unexplored. This study aims to investigate whether Diet-LIG intake can alleviate perimenopausal depressive symptoms and to explore the underlying mechanisms. The randomized controlled trial conducted in the study revealed that one-month supplementation significantly alleviated depressive and anxiety symptoms and elevated serum estradiol in perimenopausal women. This clinical benefit was associated with increased fecal levels of gut bacterial metabolites (enterolactone and enterodiol) the enzyme β-glucuronidase, and the enrichment of specific bacteria, notably Bacteroides ovatus. Animal studies showed that Diet-LIG upregulated ERβ protein expression in the hippocampal tissue of PMD mice. KEGG analysis of hippocampal proteomics showed that differentially expressed proteins between the Diet-LIG intervention and PMD groups were primarily enriched in the glutamatergic synapse pathway. Golgi staining and Western blot analysis confirmed that Diet-LIG supplementation improved neuronal plasticity, with significantly increased expression of GluN2A and PSD95 proteins. Humanized fecal microbiota transplantation experiments and in vitro cell interventions with Bacteroides ovatus monoculture medium revealed that the antidepressant effects of Diet-LIG are not directly mediated solely by the modulated gut microbiota, but instead rely on the bioactivity of metabolites produced through gut microbiota-driven conversion. In vitro validation experiments, the knockdown of ERβ in HT22 cells significantly suppressed GluN2A and PSD95 expression and blocked their induction by Diet-LIG metabolites. In conclusion, gut microbiota drives Diet-LIG to activate hippocampal ERβ, which regulates the GluN2A/PSD95 pathway and enhances hippocampal neuronal plasticity, thereby ameliorating perimenopausal depressive symptoms. (Chinese Clinical Trial Registry [ChiCTR], ID Number: ChiCTR2400082537.).},
}

@article {pmid41834217,
year = {2026},
author = {Yuan, X and Gong, H and Zhang, L and Liu, Y and Zhou, M and Liu, Y and Tang, J and Pan, S and Xu, X and Wang, Y and Zhang, X and Zhang, T and Song, J},
title = {T2DM-Induced Gut Dysbiosis Exacerbates Periodontitis Through Intestinal Barrier Disruption and Redox Imbalance.},
journal = {Journal of clinical periodontology},
volume = {},
number = {},
pages = {},
doi = {10.1111/jcpe.70116},
pmid = {41834217},
issn = {1600-051X},
support = {U22A20314//National Natural Science Foundation of China/ ; 82170968//National Natural Science Foundation of China/ ; 82301082//National Natural Science Foundation of China/ ; 2022YFC2504200//National Key Research and Development Program of China/ ; 2025MD774176//China Postdoctoral Science Foundation/ ; YXQN202401//Chongqing Youth Talent Support Program/ ; },
abstract = {AIM: To investigate the potential role and underlying mechanisms of gut microbiota in type 2 diabetes mellitus (T2DM)-exacerbated periodontitis.

MATERIALS AND METHODS: A T2DM-associated periodontitis model was established in C57BL/6 mice and analysed using multi-omics sequencing (16S rRNA, metagenomics and metabolomics). Faecal microbiota transplantation (FMT) from T2DM donors was carried out in recipient mice to investigate the impact of gut dysbiosis on periodontitis. FMT from healthy donors, supplementation of intestinal barrier protectant or the metabolite oleic acid (OA) was administered to mice with T2DM-associated gut dysbiosis to examine their ameliorative effects on periodontal damage.

RESULTS: T2DM-associated gut dysbiosis, independent of hyperglycaemia, triggered intestinal barrier disruption, which disturbed systemic redox-related metabolisms and elevated oral oxidative stress, thereby aggravating periodontitis. Restoring gut microbiota via FMT from a healthy donor or protecting the intestinal barrier ameliorated periodontitis. Exogenous supplementary metabolite OA rescued periodontal damage by activating the SIRT1/FoxO1 pathway and enhancing antioxidant enzymes in mice with T2DM-associated gut dysbiosis.

CONCLUSIONS: T2DM-induced gut dysbiosis exacerbates periodontitis through intestinal barrier disruption and redox imbalance. These findings provide new adjunctive therapeutic perspectives including microbiota restoration, intestinal barrier protection and antioxidant supplementation for managing patients with T2DM-induced periodontitis.},
}

@article {pmid41834408,
year = {2026},
author = {Zhu, R and Li, L and Zhao, M and Zhang, B and Zhang, Z and Li, M and Yu, L and Song, Z and Gu, N},
title = {Polysaccharide from Ribes nigrum L. Ameliorates Diabetic Kidney Injury in Mice by Modulating the GUDCA/GPBAR1 Axis through the Remodeling of the Gut Microbiota.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c16173},
pmid = {41834408},
issn = {1520-5118},
abstract = {Diabetic nephropathy (DN) is a major microvascular complication of diabetes, requiring effective therapies. This study showed polysaccharide from Ribes nigrum L. (blackcurrant polysaccharides (BCP)) exerted therapeutic effects in high-fat diet/streptozotocin-induced diabetic mice, improving glucose homeostasis and alleviating renal inflammation and fibrosis. 16S rRNA sequencing revealed BCP altered gut microbiota and notably enriched Akkermansia muciniphila, which was validated via fecal microbiota transplantation and exogenous A. muciniphila administration. Combined 16S rRNA sequencing and metabolomic analysis identified a positive correlation between A. muciniphila and glycoursodeoxycholic acid (GUDCA). Exogenous A. muciniphila supplementation significantly increased the level of serum GUDCA in DN mice. Elevated GUDCA activated the bile acid receptor GPBAR1 in the kidney, suppressing NF-κB/NLRP3 inflammasome and TGF-β-mediated fibrosis. BCP improves renal outcomes by regulating bile acid metabolism through gut microbiota modulation, supporting its potential as a novel dietary strategy for DN.},
}

@article {pmid41834856,
year = {2026},
author = {He, Z and Liu, B and Gong, A and Jia, X},
title = {The role of Western diet and gut microbiota in the pathogenesis of cardiovascular diseases.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1608563},
pmid = {41834856},
issn = {1664-302X},
abstract = {The Western diet (WD) is characterized by high fat, high sugar, high salt and low fiber. WD can disrupt the homeostasis of the intestinal flora and become an important factor in the occurrence and development of Cardiovascular Diseases (CVD). This review elucidates the core mechanism through which WD-induced intestinal flora dysbiosis contributes to the development of CVD. Specifically, the disruption of intestinal barrier function promotes the generation of pathogenic metabolites, such as trimethylamine-N-oxide (TMAO), while simultaneously suppressing the production of beneficial metabolites, including short-chain fatty acids (SCFAs). This metabolic shift subsequently triggers systemic inflammatory responses, oxidative stress, and metabolic disturbances, thereby accelerating the progression of CVD-related conditions, such as atherosclerosis and hypertension. Meanwhile, this review systematically summarizes key intervention strategies targeting the gut microbiota. Accumulating evidence indicates that interventions such as probiotics, prebiotics, the Mediterranean diet, and fecal microbiota transplantation (FMT) can effectively restore intestinal microbial homeostasis, enhance the production of SCFAs, and mitigate the risk of CVD. Notably, long-term dietary patterns have demonstrated significant efficacy in reshaping the gut ecosystem, underscoring the importance of sustainable lifestyle modifications. Therefore, this study aims to integrate current knowledge regarding the underlying molecular mechanisms and provide a theoretical basis for developing precise interventions to prevent and treat CVD through modulation of the gut microbiota.},
}

@article {pmid41834861,
year = {2026},
author = {Zhang, Z and Hu, X and Ma, Y},
title = {Gut microbiota and ulcerative colitis: a bibliometric analysis of knowledge structure, research hotspots, and future directions.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1765748},
pmid = {41834861},
issn = {1664-302X},
abstract = {BACKGROUND: Ulcerative colitis (UC), a globally prevalent immune-mediated colonic disorder, is fundamentally linked to intestinal dysbiosis. Despite the exponential growth in related papers, systematic, data-driven bibliometric analyses including global productivity trends, international collaboration networks, citation impact distributions, and the temporal evolution of research topics remain lacking.

METHODS: We conducted a comprehensive bibliometric analysis of 5,879 articles and reviews sourced from the Web of Science Core Collection (WOSCC) and Dimensions (2004-2025). Publication outputs, international collaboration networks, institutional productivity, and keyword evolution were visualized using R-bibliometrix, VOSviewer, and CiteSpace. Lotka's law and Bradford's law were applied to assess author and journal productivity distributions, respectively. Burst detection algorithms identified emerging research frontiers.

RESULTS: Annual publications demonstrated exponential growth, escalating from 36 in 2004 to a projected 819 in 2024. Geographically, China dominated absolute output (n = 2,559), followed by the USA (n = 1,181), with these two nations collectively accounting for 63.6% of global publications, justifying their prominence as the two major hubs in this research field. Harvard Medical School exhibited the highest citation efficiency (296.6 citations per publication), contrasting with volume leaders like Zhejiang University (92 publications). Co-occurrence clustering revealed 18 distinct knowledge domains, converging on five accelerating frontiers: "fecal microbiota transplantation (FMT)," "short-chain fatty acids," "traditional Chinese medicine," "intestinal barrier mechanisms," and "nanoparticle-based microbiota modulation." Burst analysis confirmed these themes-initiated citation surges post-2017, with "nanoparticles" and "intestinal barrier" exhibiting the strongest recent momentum (2023-2025), indicating a paradigm shift from descriptive microbiome profiling to mechanistic, precision-targeted interventions.

CONCLUSION: The UC-microbiome research agenda has transitioned from correlative association studies to multi-layered therapeutic modulation. Future efforts should prioritize standardizing FMT protocols through randomized controlled trials, establishing multi-ethnic longitudinal cohorts to address population-specific microbiome signatures, elucidating dose-response relationships of microbial metabolites, and converging nanodelivery systems with microbiome engineering to optimize therapeutic precision and sustain remission.},
}

@article {pmid41836291,
year = {2026},
author = {Mi, F and Guo, J and Zheng, W and Shen, J and Ye, H},
title = {Fecal microbiota transplantation alleviates steatosis and inflammation in high-fat and high-sugar diet-induced fatty liver in mice.},
journal = {Frontiers in cell and developmental biology},
volume = {14},
number = {},
pages = {1723128},
doi = {10.3389/fcell.2026.1723128},
pmid = {41836291},
issn = {2296-634X},
abstract = {AIM: To investigate whether fecal microbiota transplantation (FMT) could alleviate high-fat and high-sugar (HFCS) diet-induced metabolic dysfunction-associated fatty liver disease (MAFLD) in mice and explore potential mechanisms underlying gut microbiota modulation.

METHODS: A MAFLD mouse model was established by feeding mice a HFCS diet for 20 weeks, followed by an 8-week intervention with FMT or saline, continuing for a total of 28 weeks. Gut microbiota composition, serum biochemical markers, liver histopathology, and inflammatory cytokine expression were evaluated.

RESULTS: The HFCS diet induced significant changes in gut microbiota, including increased Firmicutes and decreased Bacteroidetes and Bifidobacterium. FMT partially restored microbiota composition to resemble that of control mice. Mice receiving FMT showed reduced body weight and a consistent trend toward improvement in serum alanine transaminase and total cholesterol levels, although these changes did not reach statistical significance. Liver histology showed amelioration of steatosis and inflammation, as evidenced by reduced MAFLD activity score and decreased intrahepatic expression of IL-1β and IL-17α mRNA. To further explore potential mechanisms, we analyzed a public liver transcriptomic dataset (GSE151220) involving FMT from dysbiotic donors. Differentially expressed genes were enriched in lipid metabolism and extracellular matrix-related pathways, processes known to be involved in MAFLD progression.

CONCLUSION: These results suggest that FMT is associated with modulation of the gut-liver axis and partial alleviation of HFCS-induced MAFLD features in mice. FMT may serve as a potential adjunctive strategy for managing MAFLD.},
}

@article {pmid41836406,
year = {2026},
author = {Guo, Z and Yang, J and Zang, R and Yang, Y and Wang, Q and Xu, C},
title = {The brain-gut-skin axis in inflammatory and disfiguring skin diseases: mechanistic insights, clinical correlations, and therapeutic strategies.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1737303},
doi = {10.3389/fimmu.2026.1737303},
pmid = {41836406},
issn = {1664-3224},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; *Skin Diseases/therapy/etiology/metabolism/immunology/microbiology ; *Skin/immunology/metabolism/pathology ; Animals ; *Brain-Gut Axis/immunology ; *Brain/metabolism/immunology ; Inflammation ; Dysbiosis ; },
abstract = {Emerging evidence suggests that the brain-gut-skin axis (BGSA) plays a critical role in the pathogenesis of inflammatory and disfiguring skin diseases. Conditions such as acne, atopic dermatitis, psoriasis, rosacea, vitiligo, and alopecia areata, once regarded as localized disorders driven mainly by cutaneous immune dysfunction, are now recognized as systemic conditions associated with neuroendocrine stress responses, gut microbial dysbiosis, and chronic low-grade inflammation. Mechanistic studies elucidate the intricate interorgan communication mediated by microbial metabolites (e.g., short-chain fatty acids and tryptophan derivatives), cytokine networks, neuropeptides, and hypothalamic-pituitary-adrenal (HPA) axis signaling. Building on these insights, therapeutic strategies are evolving rapidly. Microbiome-directed interventions (probiotics, postbiotics, dietary modification, and fecal microbiota transplantation), together with psychoneuroimmunological approaches, have shown potential to alleviate disease severity. Integrative therapies, including traditional herbal medicine, offer promising effects; however, we emphasize that mechanistic depth and robust clinical validation for these modalities are currently limited. This review integrates mechanistic findings, clinical correlations, and emerging therapeutic approaches, while critically distinguishing between correlation and causation. Future studies should emphasize longitudinal multi-omics analyses and standardized clinical trials to clarify causal pathways and guide precision, patient-centered management for systemic and cutaneous health.},
}

Humans
*Gastrointestinal Microbiome/immunology
*Skin Diseases/therapy/etiology/metabolism/immunology/microbiology
*Skin/immunology/metabolism/pathology
Animals
*Brain-Gut Axis/immunology
*Brain/metabolism/immunology
Inflammation
Dysbiosis

@article {pmid41839386,
year = {2026},
author = {Zhou, J and Zheng, L and Zheng, Z and Ding, K and Fu, Z and Ni, Y},
title = {The characteristic of microglia and gut-microglia-brain axis: implications for cognitive impairment and therapeutic strategies.},
journal = {The Journal of nutritional biochemistry},
volume = {},
number = {},
pages = {110351},
doi = {10.1016/j.jnutbio.2026.110351},
pmid = {41839386},
issn = {1873-4847},
abstract = {Aging-associated cognitive impairment (CI) is a core feature of neurodegenerative diseases, profoundly affecting the daily life of patients. Microglial dysfunction significantly contributes to the pathogenesis of CI. The gut-brain axis serves as a pivotal regulator of microglial functions, making it a promising target for halting the development and progression of CI. Deciphering the mechanisms of the gut-microglia-brain (GMB) axis may help devise potential therapeutic strategies to mitigate CI. This review first describes the recent progress in the development and functions of microglia, including the latest advancements in this field. Subsequently, the dynamic and complex communications between microglia and the gut microecosystem, including intestinal cells, gut microbiota, gut microbiota-derived metabolites, gut-derived exosomes, and intestinal bacteriophages, were discussed. Finally, current therapeutic strategies targeting the GMB axis to mitigate CI, such as lifestyle interventions, fecal microbiota transplantation (FMT), phages, exosomes, and pharmacological therapies, were summarized. The understanding of GMB axis-mediated cognitive function may pave the way for the identification of novel therapeutic strategies to mitigate aging-associated CI.},
}

@article {pmid41828959,
year = {2026},
author = {Liang, Y and Huang, P and Li, J and Manafu, Z and Wang, R and Chen, X and Zhang, X and Wu, Y and Malajiang, X and Yiming, A and Duishan, S and Wusiman, A},
title = {The Protective Effects and Underlying Mechanisms of Taraxacum kok-saghyz Polysaccharides Against Intestinal Dysbiosis-Induced Mastitis Were Elucidated Using a Murine Model of the "Gut-Mammary" Axis.},
journal = {Animals : an open access journal from MDPI},
volume = {16},
number = {5},
pages = {},
pmid = {41828959},
issn = {2076-2615},
support = {XJRC-2025-KJ-KJQY-002//Adelijiang Wusiman/ ; },
abstract = {The gut-mammary axis represents a promising therapeutic target for mastitis. Although plant-derived polysaccharides exhibit immunomodulatory properties, their capacity to modulate this axis-and specifically to ameliorate dysbiosis-induced mastitis-remains unexplored. Here, we investigated the therapeutic potential of Taraxacum kok-saghyz leaf-derived polysaccharides (TKP-L) against mastitis in a murine model of gut dysbiosis, with dysbiosis induced by fecal microbiota transplantation (FMT) from donor cows. Pregnant mice (n = 60) with antibiotic-depleted microbiota received FMT suspensions prepared from the feces of healthy dairy cows or cows with clinical mastitis (based on somatic cell count). Mice were randomly divided into five groups: Control (vehicle), M-FMT (mastitis-cow FMT, disease model), H-FMT (healthy-cow FMT), TKP-L (M-FMT + oral TKP-L, 500 mg/kg/day), and Ciprofloxacin (M-FMT + ciprofloxacin, positive Control). After FMT establishment, TKP-L or ciprofloxacin was administered for 14 days. We assessed histopathology, pro-inflammatory mediators (IL-6, IL-1β, TNF-α, MPO), tight junction proteins (occludin, ZO-1, Claudin-3), and bacterial translocation using GFP-E. coli, and gut/milk microbiota via 16S rRNA sequencing. Compared to the M-FMT group, TKP-L treatment significantly alleviated mammary inflammation and pathology, inhibited pro-inflammatory cytokine expression, and enhanced the expression of tight junction proteins in both intestinal and mammary tissues, correlating with reduced bacterial translocation to the mammary gland. Microbiota analysis showed that TKP-L restored microbial homeostasis in the gut and milk, concurrently increasing the relative abundance of beneficial bacteria such as Limosilactobacillus. TKP-L alleviates gut dysbiosis-induced mastitis in mice by concurrently modulating the gut-mammary axis through microbial remodeling, enhancement of epithelial barriers, and anti-inflammatory actions. These findings highlight TKP-L as a promising gut microbiota-targeting candidate for mastitis intervention.},
}

@article {pmid41831535,
year = {2026},
author = {Chen, J and Xiao, C and Cao, M and Hu, Y and Yan, Y and Tong, J and Cheng, C and Huang, J},
title = {Association between gut virome and prenatal stress-induced changes in behavior and immune responses in male offspring.},
journal = {Brain, behavior, and immunity},
volume = {},
number = {},
pages = {106532},
doi = {10.1016/j.bbi.2026.106532},
pmid = {41831535},
issn = {1090-2139},
abstract = {Maternal stress during gestation is associated with an increased risk of neurodevelopmental disorders in offspring. The gut-brain axis is considered a potential mediating pathway. As a key component of the gut microbiome, the bacteriophages can remodel bacterial community structure and function. However, whether gut viruses contribute to prenatal stress-induced behavioral alterations in offspring remains unclear. Here, we reported that prenatal stress induces anxiety-like behaviors and alters the gut virome and bacteriome specifically in male offspring. By comparing the gut virome and bacteriome between dams and their offspring, we found that the gut microbial profile of male offspring is more similar to that of their mothers than that of female offspring. To investigate whether changes in the gut virome are causally linked to stress-related behavioral or physiological outcomes, we transplanted gut viromes from control offspring into the offspring exposed to maternal prenatal stress. The results showed that transplantation of the gut virome from control offspring alleviated anxiety-like behaviors, restored the gut microbiome, and modulated immune responses in prenatally stressed offspring. Our findings highlight the critical role of gut bacteriophages in mediating prenatal stress-induced behavioral changes and demonstrate that fecal virome transplantation (FVT) can mitigate such alterations. Thus, we establish a causal link between prenatal stress, the gut virome, immune function, and behavior, pointing to FVT as a potential therapeutic strategy for certain neurodevelopment-related behavioral abnormalities.},
}

@article {pmid41832194,
year = {2026},
author = {Arshad, M and Zhang, CY and Gao, ZK and Sun, H and Xu, DQ and Fan, CY and Zhang, BW and Geng, JX and Li, Y and Kotusov, A and Liu, SL and Zhang, N and Mu, XQ},
title = {Capecitabine combined with fecal microbiota transplantation prevents colorectal cancer progression through correction of microbial dysbiosis and immune regulation.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-43626-1},
pmid = {41832194},
issn = {2045-2322},
support = {NSFC82020108022, NSFCU23A20521//National Natural Science Foundation of China/ ; NSFC81903631//National Natural Science Foundation of China/ ; UNPYSCT14 2018065//Youth Innovation Fund of University in Hei Longjiang/ ; },
}

@article {pmid41828553,
year = {2026},
author = {Alba, C and Palomino, L and Vergara, B and Rodríguez-Belvis, MV and Aragón, A and Zaghlul, MADC and Jurado, R and Martín-Fernández, C and Vázquez-Gómez, JA and González-Vicent, M and Molina-Angulo, B and Sánchez-Llorente, P and García-Hernández, P and Rodríguez, JM and Muñoz-Codoceo, RA and Herranz, C},
title = {Metataxonomic Analysis and Fatty Acid Profiling of Feces from Children Undergoing Hematopoietic Stem Cell Transplantation.},
journal = {International journal of molecular sciences},
volume = {27},
number = {5},
pages = {},
doi = {10.3390/ijms27052331},
pmid = {41828553},
issn = {1422-0067},
support = {XVIII//Mutua Madrileña/ ; PR17/24-31883//Comunidad de Madrid/ ; },
mesh = {Humans ; *Hematopoietic Stem Cell Transplantation/adverse effects ; *Feces/microbiology/chemistry ; Child ; *Graft vs Host Disease/etiology/microbiology ; Male ; Female ; *Gastrointestinal Microbiome ; *Fatty Acids, Volatile/analysis ; Child, Preschool ; Adolescent ; RNA, Ribosomal, 16S/genetics ; Infant ; Bacteria/genetics/classification ; *Fatty Acids ; },
abstract = {Allogeneic hematopoietic stem cell transplantation (HSCT) is a medical procedure to treat hematologic malignancies and restore bone marrow function. However, this approach may lead to graft-versus-host disease (GvHD), a major cause of mortality and morbidity after allogeneic HSCT. Some studies have suggested the involvement of gut microbiota in the development and prognosis of GvHD. In this context, the main objective of this study was to compare the fecal microbiome composition and short-chain profile of pediatric patients who underwent successful HSCT, developed GvHD or died. The bacterial composition was analyzed using 16S rRNA gene sequencing, while short-chain fatty acids (SCFAs) were quantified by gas chromatography. Fecal samples at engraftment were mainly characterized by a loss of bacterial diversity, a depletion of sequences belonging to the genus Blautia and significantly lower concentrations of fecal butyrate and acetate compared with those obtained before HSCT and 100 days after HSCT. Our findings confirm that children experiencing GvHD after HSCT have distinct gut microbiota and SCFA profiles, which might contribute to developing new microbiota-targeted strategies for GvHD prevention during HSCT procedures.},
}

Humans
*Hematopoietic Stem Cell Transplantation/adverse effects
*Feces/microbiology/chemistry
Child
*Graft vs Host Disease/etiology/microbiology
Male
Female
*Gastrointestinal Microbiome
*Fatty Acids, Volatile/analysis
Child, Preschool
Adolescent
RNA, Ribosomal, 16S/genetics
Infant
Bacteria/genetics/classification
*Fatty Acids

@article {pmid41828467,
year = {2026},
author = {Shen, H and Yu, X and Wang, Z and Zhou, S and Jiang, J and Guo, H and Han, Y},
title = {Gut Microbiota Remodeling Mediates the Therapeutic Effects of a Plant-Based Medicine on DSS-Induced Ulcerative Colitis in Mice via the Butyrate-SVCT1-Vitamin C Axis.},
journal = {International journal of molecular sciences},
volume = {27},
number = {5},
pages = {},
doi = {10.3390/ijms27052245},
pmid = {41828467},
issn = {1422-0067},
support = {No. 2025-I2M-KJ-016//the CAMS Innovation Fund for Medical Sciences/ ; No. 3332025150//the Fundamental Research Funds for Central Universities, Peking Union Medical College/ ; No. 2024-I2M-ZH-012//the CAMS Innovation Fund for Medical Sciences/ ; No. 20230484467//the Beijing Nova Program from Beijing Municipal Science & Technology Commission/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Colitis, Ulcerative/drug therapy/chemically induced/metabolism/microbiology ; *Ascorbic Acid/metabolism ; Mice ; Dextran Sulfate/adverse effects ; *Butyrates/metabolism ; *Sodium-Coupled Vitamin C Transporters/metabolism ; Disease Models, Animal ; Fecal Microbiota Transplantation ; Male ; Mice, Inbred C57BL ; *Drugs, Chinese Herbal/pharmacology/therapeutic use ; Fatty Acids, Volatile/metabolism ; Colon/metabolism/drug effects ; Dysbiosis ; },
abstract = {Ulcerative colitis (UC) is a chronic inflammatory bowel disease with a rising global incidence in recent years. Dengzhan shengmai (DZSM), a plant-based formulation clinically used in the management of cerebrovascular diseases, possesses documented anti-inflammatory and antioxidant properties; however, its effects on UC are unclear. In this study, we investigated the therapeutic potential and underlying mechanism of DZSM in a dextran sulfate sodium (DSS)-induced murine colitis model. Our results showed that DZSM significantly alleviated UC-related parameters. Mechanistically, DZSM remodeled gut microbiota dysbiosis, specifically enriching the abundance of short-chain fatty acid (SCFA)-producing bacteria and elevating colonic levels of SCFAs. Notably, butyrate upregulated the expression of the sodium-dependent vitamin C transporter 1 (SVCT1) in colonic epithelial cells, thereby enhancing cellular vitamin C (VitC) uptake. The accumulated VitC synergized with butyrate to exert potent antioxidant and anti-inflammatory effects, further reinforcing epithelial barrier function. Importantly, fecal microbiota transplantation (FMT) confirmed that the protective effects of DZSM on UC were achieved by modulating gut microbiota, at least partially. Collectively, our findings demonstrate for the first time that DZSM alleviates DSS-induced colitis in mice through a novel butyrate-SVCT1-VitC axis driven by gut microbiota remodeling, providing new mechanistic insights into the microbiota-dependent efficacy of plant-based medicine.},
}

Animals
*Gastrointestinal Microbiome/drug effects
*Colitis, Ulcerative/drug therapy/chemically induced/metabolism/microbiology
*Ascorbic Acid/metabolism
Mice
Dextran Sulfate/adverse effects
*Butyrates/metabolism
*Sodium-Coupled Vitamin C Transporters/metabolism
Disease Models, Animal
Fecal Microbiota Transplantation
Male
Mice, Inbred C57BL
*Drugs, Chinese Herbal/pharmacology/therapeutic use
Fatty Acids, Volatile/metabolism
Colon/metabolism/drug effects
Dysbiosis

@article {pmid41826553,
year = {2026},
author = {Garcia-Peterson, LM and Wellman, AS and Xu, X and Ji, M and Duval, C and Shats, I and Wu, X and Randall, TA and Bostan, H and Cunefare, D and Ganta, CK and Sifre, M and Xu, X and Blumberg, RS and Li, JL and Li, X},
title = {Paneth cell SIRT1 deficiency increases intestinal stress resistance by modulating the gut microbiota.},
journal = {EMBO reports},
volume = {},
number = {},
pages = {},
pmid = {41826553},
issn = {1469-3178},
support = {Z01 ES102205//HHS | NIH | National Institute of Environmental Health Sciences (DEHS)/ ; 1FI2GM143339-01//HHS | NIH | National Institute of General Medical Sciences (NIGMS)/ ; DK088199//HHS | National Institutes of Health (NIH)/ ; },
abstract = {Paneth cells, intestine-originated innate immune-like cells, are important for maintenance of the intestinal stem cell niche, gut microbiota, and gastrointestinal barrier. Dysfunctional Paneth cells under pathological conditions are a site of origin for intestinal inflammation. However, mechanisms underlying stress-induced Paneth cell dysregulation remain unclear. Here, we report that SIRT1, the most conserved mammalian NAD[+]-dependent protein deacetylase and a well-known genetic repressor of inflammation, cell-autonomously suppresses Paneth cell function and sensitizes the gut epithelium to environmental stress. Specifically, deletion of Paneth cell SIRT1 in mice elevates Wnt signaling and ATF4/endoplasmic reticulum stress pathway in Paneth cells. These molecular alterations are coupled with increased Paneth cell abundance and enhanced anti-microbial peptide production in young mice, improved protection against intestinal immune cell expansion in aged mice, and increased resistance to chemically induced colitis. Using microbiota-depleted mice with or without fecal transplantation, we further demonstrate that Paneth cell SIRT1 deficiency ameliorates colitis by interacting with the gut microbiota. Collectively, our findings uncover an unanticipated function of Paneth cell SIRT1 in conferring stress sensitivity in the gut epithelium.},
}

@article {pmid41826399,
year = {2026},
author = {Wang, L and Zhang, S and Liu, Y and Li, D and Tian, G and Li, X and Li, Y},
title = {A study on the efficacy and safety of fecal microbiota transplantation as an adjunctive therapy for treating depressive episodes.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-41801-y},
pmid = {41826399},
issn = {2045-2322},
support = {2025ZL480//Traditional Chinese Medicine Scientific Research Fund Project (A)/ ; 2022ZA150//Traditional Chinese Medicine Scientific Research Fund Project (A)/ ; },
}

@article {pmid41826284,
year = {2026},
author = {Zhang, R and Feng, R and Wang, J and Chen, Y and Liu, H and Zhu, Q and Tian, H and Qin, C and Teng, J and Tang, B and Wu, M and Zeng, J and Wu, E and Ding, X and Wang, X},
title = {Gut microbiota modulation via repeated donor fecal transplantation improves motor and gastrointestinal symptoms in drug-naïve Parkinson's disease: a randomized phase 2 trial.},
journal = {Signal transduction and targeted therapy},
volume = {11},
number = {1},
pages = {},
pmid = {41826284},
issn = {2059-3635},
support = {82201407//National Natural Science Foundation of China (National Science Foundation of China)/ ; 82122022,82471272, 82171248, 82471350, 82201407//National Natural Science Foundation of China (National Science Foundation of China)/ ; 82130035, 82371308//National Natural Science Foundation of China (National Science Foundation of China)/ ; R04017//Sun Yat-sen University (SYSU)/ ; },
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; *Parkinson Disease/therapy/microbiology/pathology ; *Gastrointestinal Microbiome ; Male ; Female ; Middle Aged ; Aged ; },
abstract = {The gut-brain axis is increasingly recognized as a critical contributor to Parkinson's disease (PD) pathogenesis, yet the therapeutic impact of microbiota modulation remains unclear due to lack of clinical trials in drug-naïve patients. We conducted a randomized, double-blind, placebo-controlled phase 2 trial to evaluate the safety, tolerability, and efficacy of repeated donor fecal microbiota transplantation (dFMT) in de novo PD. FMT was administered for seven days (200 mL on days 1-3; 50 mL on days 4-7) per 4-week cycle. Seventy-two patients were randomized 1:1 to receive dFMT or autologous FMT (aFMT), and 66 completed the trial. At 35 weeks, the dFMT group showed significant improvement in motor symptoms (mean change in Unified Parkinson's Disease Rating Scale [UPDRS] III: -3.8 vs. +0.1; p = 0.0001) and a substantially greater reduction in constipation severity (dFMT vs. aFMT: -6.5 vs. -0.7; p < 0.0001), accompanied by improved quality-of-life scores. Microbiome profiling revealed greater similarity to donor composition and a marked reduction in Escherichia-Shigella, correlating with decreased colonic α-synuclein aggregation (r = 0.3775, p = 0.0277), supporting a gut-brain mechanistic link. Biochemical analyses showed elevated fecal dopamine and 3,4-dihydroxyphenylacetic acid levels, while histological assessments demonstrated strengthened epithelial barrier integrity with increased E-cadherin expression. All adverse events were mild and self-limited; no serious treatment-related events were observed. These findings demonstrate that repeated dFMT is safe, well tolerated, and yields clinically meaningful motor and gastrointestinal improvements in drug-naïve PD, providing integrated mechanistic and clinical evidence that microbiota-targeted modulation represents a promising nonpharmacologic therapeutic strategy for neurodegenerative disease. Trial registration: Chinese Clinical Trial Registry, ChiCTR2200064151.},
}

Humans
*Fecal Microbiota Transplantation/methods
*Parkinson Disease/therapy/microbiology/pathology
*Gastrointestinal Microbiome
Male
Female
Middle Aged
Aged

@article {pmid41826266,
year = {2026},
author = {Wu, K and Yu, H and Cao, K and Dai, B and Yuan, Y and Qian, X and Zhong, H and Qu, Y and Jiang, H and Chen, T},
title = {Overconsumption of fructose aggravates acute GVHD by inducing gut dysbiosis and promoting macrophage-mediated inflammatory response.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2642459},
doi = {10.1080/19490976.2026.2642459},
pmid = {41826266},
issn = {1949-0984},
mesh = {Animals ; *Fructose/adverse effects/metabolism/administration & dosage ; *Graft vs Host Disease/microbiology/immunology/pathology ; *Dysbiosis/microbiology/immunology ; *Gastrointestinal Microbiome/drug effects ; Mice ; *Macrophages/immunology/drug effects ; Mice, Inbred C57BL ; Male ; Cytokines/metabolism ; Inflammation ; Fecal Microbiota Transplantation ; Bacterial Translocation ; Disease Models, Animal ; Bacteria/classification/genetics/isolation & purification ; Macrophage Activation ; },
abstract = {Increased fructose intake is a triggering factor in a series of inflammatory diseases. However, the pathogenic role of fructose overconsumption in acute graft-versus-host disease (aGVHD) has not yet been clarified. In this study, we found that a high-fructose diet (HFR) aggravated the severity and mortality of aGVHD in mice and enhanced gut dysbiosis and bacterial translocation with impairment of the intestinal epithelial barrier. Fecal microbiota transplantation experiments further demonstrated that the microbiota derived from HFR-fed aGVHD mice was sufficient to reproduce intestinal barrier disruption and bacterial translocation in aGVHD recipients. HFR exacerbated the severity of aGVHD after depletion of the gut microbiota by antibiotics. Given the results that in vitro cultivated T-cells do not respond to fructose stimulation, we further investigated whether fructose overexposure affects macrophage activation. In fructose-treated bone marrow-derived macrophages (BMDMs), HIF-1α was stabilized by mitochondrial reactive oxygen species production, resulting in increased glycolysis and subsequently augmented expression of the inflammatory cytokines IL-6, IL-12, TNF-α, and IL-1β. Interestingly, we found that macrophages derived from HFR-fed aGVHD mice were able to enhance T-cell proliferation and Th1/Th17 differentiation. In parallel, correlation analysis integrating 16S rRNA and metabolomics sequencing data revealed that the abundances of Akkermansiaceae and Erysipelotrichaceae were positively correlated with the levels of indole-5,6-quinone and 6,7-dimethyl-8-(D-ribityl)lumazine. After depletion of macrophages and the gut microbiota in host mice, GVHD severity was significantly reversed even after HFR treatment. Taken together, our data reveal that high fructose intake exacerbated aGVHD by inducing a gut microbiota imbalance and promoting inflammatory macrophage activation. This provides a potential therapeutic strategy to alleviate aGVHD via precise adjustment of the fructose dietary.},
}

Animals
*Fructose/adverse effects/metabolism/administration & dosage
*Graft vs Host Disease/microbiology/immunology/pathology
*Dysbiosis/microbiology/immunology
*Gastrointestinal Microbiome/drug effects
Mice
*Macrophages/immunology/drug effects
Mice, Inbred C57BL
Male
Cytokines/metabolism
Inflammation
Fecal Microbiota Transplantation
Bacterial Translocation
Disease Models, Animal
Bacteria/classification/genetics/isolation & purification
Macrophage Activation

@article {pmid41824007,
year = {2026},
author = {Zhu, S and Zou, M and Wu, Q and Zou, Y and Tan, T and Huang, Z and Gong, Z and Luo, H and Dong, X},
title = {The Gut-Liver Axis in Metabolic Dysfunction-Associated Steatotic Liver Disease: From Mechanistic Insights to Precision Therapeutics.},
journal = {FASEB journal : official publication of the Federation of American Societies for Experimental Biology},
volume = {40},
number = {6},
pages = {e71687},
doi = {10.1096/fj.202503607RR},
pmid = {41824007},
issn = {1530-6860},
support = {2024GXNSFAA010247//Guangxi Natural Science Fundation/ ; 2024GXNSFBA010227//Guangxi Youth Science Fun Project/ ; QYY-GCRC-202301//Research Foudation for Advanced Talents of The people's and Hospital of Guangxi Zhuang Autonomous Region, Guangxi Academy of Medical Science/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Liver/metabolism/pathology ; *Fatty Liver/therapy/microbiology/metabolism ; Probiotics/therapeutic use ; Fecal Microbiota Transplantation/methods ; *Precision Medicine/methods ; Dysbiosis/microbiology ; Animals ; },
abstract = {Metabolic dysfunction-associated steatotic liver disease (MASLD) has become the most prevalent chronic liver condition globally, shifting the diagnostic paradigm toward an affirmative, metabolism-focused framework. The gut-liver axis is a central pathophysiological pathway. This review aims to synthesize revolutionary advances from 2023 to 2025 in understanding and treating MASLD by focusing on the gut microbiome's role. This comprehensive review analyzes cutting-edge research published between 2023 and 2025. We examined evidence from landmark clinical trials, developments in next-generation probiotics, the integration of artificial intelligence (AI) with multiomics for diagnostics, and studies clarifying the interplay between host genetics and the microbiome in MASLD pathogenesis. Causal links between gut dysbiosis and MASLD pathology are now firmly established. Fecal microbiota transplantation (FMT) effectively prevents hepatic encephalopathy recurrence, and next-generation probiotics like Akkermansia muciniphila have entered MASLD-specific trials. AI-driven diagnostic tools have achieved regulatory qualification from the European Medicines Agency. Furthermore, host genetics, particularly PNPLA3 variants, are shown to not only predispose to MASLD but also shape specific microbial communities that functionally contribute to disease progression. The field is rapidly advancing from correlative observations to causal evidence, enabling the development of microbiome-based biomarkers and personalized therapies. The future of MASLD management lies in precision strategies, such as bacteriophage therapy and functionally defined probiotics, which integrate metabolic, microbial, and genetic factors into individualized care, heralding a new therapeutic era.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Liver/metabolism/pathology
*Fatty Liver/therapy/microbiology/metabolism
Probiotics/therapeutic use
Fecal Microbiota Transplantation/methods
*Precision Medicine/methods
Dysbiosis/microbiology
Animals

@article {pmid41823302,
year = {2026},
author = {Al, KF and Jia, S and Silverman, M and Reid, G and Burton, JP and Parvathy, S},
title = {Prebiotic Modulation of FMT Donor Microbiota Enhances MASLD-Relevant Taxa and Functions in an In Vitro Gut Model.},
journal = {Journal of applied microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1093/jambio/lxag074},
pmid = {41823302},
issn = {1365-2672},
abstract = {AIMS: Metabolic dysfunction-associated steatotic liver disease (MASLD, formerly non-alcoholic fatty liver disease) is a prevalent and progressive condition closely linked to gut microbiota composition. Fecal microbiota transplantation (FMT) may help restore a health-associated microbiome, but its efficacy is often limited by inconsistent engraftment of beneficial taxa. Prebiotics may selectively support keystone microbes associated with reduced MASLD risk. This study evaluated two prebiotics, inulin and xylooligosaccharides (XOS), for their ability to modulate the microbiota of healthy FMT donors in an in vitro gut model, focusing on enriching beneficial taxa and functions associated with MASLD resilience.

METHODS AND RESULTS: Stool from eight clinically qualified FMT donors was cultured anaerobically for 24 hours with or without prebiotics. Microbiota composition was assessed by 16S rRNA gene sequencing and short-chain fatty acid (SCFA) concentrations were measured using nuclear magnetic resonance. Functional potential was inferred using predictive metagenomic analysis. Prebiotic responses were highly donor-specific, yet both inulin and XOS consistently enriched Bifidobacterium and Bacteroides-genera associated with SCFA production and metabolic health. XOS preferentially enriched Lactobacillus and Parabacteroides, while inulin enhanced Holdemanella and Mediterraneibacter. Functional pathways relevant to MASLD pathophysiology were enriched, including carbohydrate metabolism, vitamin biosynthesis, fatty acid metabolism, and tryptophan degradation. Both prebiotics significantly increased acetate levels, while butyrate showed a donor-dependent increasing trend.

CONCLUSIONS: These findings suggest that prebiotic supplementation can selectively enrich MASLD-relevant microbial taxa and functions in donor-derived FMT material, supporting their potential as adjuvants to enhance the efficacy and disease-specificity of FMT interventions for MASLD.},
}

@article {pmid41822494,
year = {2026},
author = {Chen, H and Yu, S and Zhang, M and Tian, B and Yang, L and Lu, J},
title = {Gut microbial metabolites in inflammatory bowel disease: immunological mechanisms regulating Treg/Th17 balance and therapeutic potential.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1780865},
pmid = {41822494},
issn = {1664-3224},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; *Th17 Cells/immunology/metabolism ; *Inflammatory Bowel Diseases/immunology/metabolism/therapy/microbiology ; *T-Lymphocytes, Regulatory/immunology/metabolism ; Animals ; Dysbiosis/immunology ; Fatty Acids, Volatile/metabolism ; Epigenesis, Genetic ; },
abstract = {Inflammatory bowel disease (IBD) is a chronic inflammatory disorder resulting from a combination of genetic susceptibility, environmental factors, and an abnormal immune response of the intestinal immune system to commensal microorganisms. The gut microbiota and its metabolites play a pivotal role in maintaining intestinal immune homeostasis. Recent advances indicate that dysbiosis of the microbiota is accompanied by alterations in its metabolic functions. Abnormal levels of key metabolites, particularly short-chain fatty acids (SCFAs), tryptophan derivatives, and secondary bile acids, are closely associated with the pathogenesis of IBD. These metabolites act as G protein-coupled receptor ligands, nuclear receptor ligands, or epigenetic modifiers, deeply involved in the differentiation, function, and dynamic balance between regulatory T cells (Tregs) and T helper 17 cells (Th17). Disruption of the Treg/Th17 balance is a central driver of intestinal immune inflammation in IBD. This review systematically explores the molecular networks through which major microbial metabolites regulate the differentiation and function of Treg and Th17 cells, including their profound effects on cellular metabolic reprogramming, the epigenetic landscape, and the local immune microenvironment. Furthermore, it analyzes how the disturbance of the microbial metabolome in the pathological state of IBD leads to the attenuation of beneficial immunoregulatory signals and the generation of potential pro-inflammatory signals, thereby contributing to a vicious cycle of immune tolerance deficiency and chronic inflammation. Based on these mechanisms, this article evaluates therapeutic strategies targeting the microbiota-metabolism-immune axis, such as dietary interventions, probiotics/prebiotics, postbiotics, engineered bacterial therapies, fecal microbiota transplantation, and small-molecule receptor modulators, discussing their current status and challenges. Finally, the limitations of current research are outlined, and future directions are proposed, including the use of integrated multi-omics analyses, spatial biology technologies, and organoid models to advance the development of personalized precision medicine.},
}

Humans
*Gastrointestinal Microbiome/immunology
*Th17 Cells/immunology/metabolism
*Inflammatory Bowel Diseases/immunology/metabolism/therapy/microbiology
*T-Lymphocytes, Regulatory/immunology/metabolism
Animals
Dysbiosis/immunology
Fatty Acids, Volatile/metabolism
Epigenesis, Genetic

@article {pmid41822330,
year = {2026},
author = {Luo, L and Xue, M and Sun, L and Dai, Z},
title = {Gut microbiota in obesity management: from microbial clocks to precision microbial therapies.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1705021},
pmid = {41822330},
issn = {2235-2988},
mesh = {*Gastrointestinal Microbiome/physiology ; Humans ; *Obesity/therapy/microbiology ; Fecal Microbiota Transplantation ; Circadian Rhythm ; Precision Medicine/methods ; *Circadian Clocks ; *Obesity Management/methods ; Animals ; },
abstract = {The gut microbiota exhibits robust circadian oscillations that synchronize with host metabolic cycles. Disruption of these microbial rhythms is increasingly recognized as a factor contributing to the pathogenesis of obesity. Clinical evidence supports that chrono-modulated interventions, including chrono-nutrition, temporal fecal microbiota transplantation (FMT), and engineered microbial systems, represent promising approaches in obesity management. This review synthesizes the features of gut microbiota circadian dynamics, the intrinsic and extrinsic factors regulating microbiota oscillations, and the precise microbial intervention measures targeting temporal patterns. Through the integration of insights into the microbiota-clock-metabolism axis, this review emphasizes the necessity of time-specific strategies in translating microbial circadian biology into effective, personalized obesity therapies.},
}

*Gastrointestinal Microbiome/physiology
Humans
*Obesity/therapy/microbiology
Fecal Microbiota Transplantation
Circadian Rhythm
Precision Medicine/methods
*Circadian Clocks
*Obesity Management/methods
Animals

@article {pmid41820416,
year = {2026},
author = {Ichimura, R and Tanaka, K and Song, I and Shimizu, E and Ogawa, Y and Tsubota, K and Fukuda, S},
title = {Association between bone marrow donor origin and gut microbiota composition following fecal microbiota transplantation in mice.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-36933-0},
pmid = {41820416},
issn = {2045-2322},
support = {22H03541//JSPS KAKENHI/ ; JP23gm1010009//AMED-CREST/ ; JPMJER1902//JST ERATO/ ; },
abstract = {Fecal microbiota transplantation (FMT) has been reported as a method to directly alter the recipient's gut microbiota in order to normalize its composition and confer therapeutic benefits. It is essential to maintain a consistent gut microbiota in FMT donors. However, various environmental factors influence the maintenance of gut microbiota composition. We investigated whether bone marrow transplantation (BMT) donor origin, presumably affecting the resultant recipient immune environment, may influence FMT outcomes by conducting a study combining BMT and FMT treatments in mice. Our results show that the origin of the bone marrow donor affected the extent to which the FMT recipient microbiota resembled that of the FMT donor. However, these changes did not reduce the overall microbiota dissimilarity compared to FMT alone. Among the affected microbes, the relative abundance of a mucus-associated bacterium in the family Muribaculaceae was higher, suggesting sensitivity to the combined influence of BMT and FMT donor origins. These findings are consistent with the possibility that bacterial proximity to the intestinal epithelium could modulate persistence patterns in response to distinct post-BMT environments. Altogether, the observed trends suggest that differences associated with bone marrow donor origin may shape post-FMT microbial retention.},
}

@article {pmid41822725,
year = {2024},
author = {Mpountouridis, A and Tsigalou, C and Bezirtzoglou, I and Bezirtzoglou, E and Stavropoulou, E},
title = {Gut microbiome in non-alcoholic fatty liver disease.},
journal = {Frontiers in gastroenterology (Lausanne, Switzerland)},
volume = {3},
number = {},
pages = {1534431},
pmid = {41822725},
issn = {2813-1169},
abstract = {Non-alcoholic fatty liver disease (NAFLD) has a rapidly growing incidence worldwide, affecting approximately one-third of world population. The disturbance of gut commensal bacteria impacting host's homeostasis is referred to as gut dysbiosis. The gut microbiome contributes to the pathogenesis of NAFLD through various pathways. Gut microbiota is at constant interactions with the intestinal epithelial barrier and affects its integrity. Through gut-liver axis, gut microbiota may influence liver immune function. The release of lipopolysaccharides (LPS) from intestines to portal vein which are transported to the liver, may trigger hepatic inflammation, steatosis and even fibrosis. Moreover, the gut microbiome induces the conversion of primary bile acids (BAs) to secondary BAs, which activates intestinal receptors, such as FXR and TGR5. FXR activation decreases fat absorption and thus reduces hepatic lipid accumulation, while TGR5 activation promotes the release of glucagon-like peptide-1 (GLP-1) in blood. Furthermore, gut ethanol-producing bacteria has been implicated in NAFLD development. Additionally, in NAFLD there is a reduction in intestinal levels of short-chain fatty acids, such as butyrate, propionate and acetate. Many bacterial alterations have been observed in NAFLD, including the increased Bacteroidetes and decreased Firmicutes. Many probiotics have been tried in NAFLD prevention and management, including a plethora of strains from Lactobacilli, Bifidobacteria and Streptococcus and some of them have promising perspectives. There is also some promising data from the administration of prebiotics (such as inulin and fructo-oligosaccharides) and symbiotics (probiotics plus prebiotics). Faecal microbiota transplantation (FMT) is yet to be evaluated for its efficacy against NAFLD.},
}

@article {pmid41821822,
year = {2023},
author = {Silva, R and Dinis, L and Peris, A and Novais, L and Calhau, C and Pestana, D and Marques, C},
title = {Fecal microbiota transplantation-could stool donors' and receptors' diet be the key to future success?.},
journal = {Frontiers in gastroenterology (Lausanne, Switzerland)},
volume = {2},
number = {},
pages = {1270899},
pmid = {41821822},
issn = {2813-1169},
abstract = {Fecal microbiota transplantation (FMT) is indicated in many countries for patients with multiple recurrences of Clostridioides difficile infection (CDI) for whom appropriate antibiotic treatments have failed. Donor selection is a demanding and rigorous process in view of the implementation of FMT programs worldwide. One of the most noteworthy factors that has been shown to affect FMT outcomes is the microbial diversity of the stool donor. A detailed assessment of the donor's microbiota is crucial, as the microbiota is complex, dynamic, and resilient, and a healthy microbiota has several dimensions in addition to the absence of pathogens. Diet is one of the most important factors that modulates the composition and function of the gut microbiome (GM) and has a critical role in orchestrating the host-microbiota crosstalk throughout life. The diversity of the human GM seems to be related to variations in dietary patterns. Currently, the dietary patterns of stool donors and receptors are not taken into consideration in any way for FMT. In this study, we reflect on the importance of including this type of assessment in the stool donor screening process and knowing the impact of diet on the GM, as well as the importance of monitoring receptors' diet to ensure the engraftment of the transplanted microbiota.},
}

@article {pmid41821793,
year = {2023},
author = {Almeida, C and Gonçalves-Nobre, JG and Alpuim Costa, D and Barata, P},
title = {The potential links between human gut microbiota and cardiovascular health and disease - is there a gut-cardiovascular axis?.},
journal = {Frontiers in gastroenterology (Lausanne, Switzerland)},
volume = {2},
number = {},
pages = {1235126},
pmid = {41821793},
issn = {2813-1169},
abstract = {The gut-heart axis is an emerging concept highlighting the crucial link between gut microbiota and cardiovascular diseases (CVDs). Recent studies have demonstrated that gut microbiota is pivotal in regulating host metabolism, inflammation, and immune function, critical drivers of CVD pathophysiology. Despite a strong link between gut microbiota and CVDs, this ecosystem's complexity still needs to be fully understood. The short-chain fatty acids, trimethylamine N-oxide, bile acids, and polyamines are directly or indirectly involved in the development and prognosis of CVDs. This review explores the relationship between gut microbiota metabolites and CVDs, focusing on atherosclerosis and hypertension, and analyzes personalized microbiota-based modulation interventions, such as physical activity, diet, probiotics, prebiotics, and fecal microbiota transplantation, as a promising strategy for CVD prevention and treatment.},
}

@article {pmid41822072,
year = {2022},
author = {Masi, L and Ciuffini, C and Petito, V and Pisani, LF and Lopetuso, LR and Graziani, C and Pugliese, D and Laterza, L and Puca, P and Di Vincenzo, F and Pizzoferrato, M and Napolitano, D and Turchini, L and Amatucci, V and Schiavoni, E and Privitera, G and Minordi, LM and Mentella, MC and Papa, A and Armuzzi, A and Gasbarrini, A and Scaldaferri, F},
title = {Innovative, complementary and alternative therapy in inflammatory bowel diseases: A broad 2020s update.},
journal = {Frontiers in gastroenterology (Lausanne, Switzerland)},
volume = {1},
number = {},
pages = {1022530},
pmid = {41822072},
issn = {2813-1169},
abstract = {Inflammatory bowel diseases (IBD) are chronic disabling conditions with a complex and multifactorial etiology, which is still not completely understood. In the last 20 years, anti-TNF-α antagonists have revolutionized the treatment of IBD, but many patients still do not respond or experience adverse events. Therefore, new biological therapies and small molecules, targeting several different pathways of gut inflammation, have been developed of which some have already been introduced in clinical practice while many others are currently investigated. Moreover, therapeutic procedures such as leukocytapheresis, fecal microbiota transplant and stem cell transplantation are currently being investigated for treating IBD. Lastly, complementary and alternative medicine has become a field of interest for gastroenterologist to reduce symptom burden in IBD patients. In this comprehensive and updated review, a novel classification of current and developing drugs is provided.},
}

@article {pmid41822071,
year = {2022},
author = {Bibbò, S and Fusco, S and Ianiro, G and Settanni, CR and Ferrarese, D and Grassi, C and Cammarota, G and Gasbarrini, A},
title = {Gut microbiota in anxiety and depression: Pathogenesis and therapeutics.},
journal = {Frontiers in gastroenterology (Lausanne, Switzerland)},
volume = {1},
number = {},
pages = {1019578},
pmid = {41822071},
issn = {2813-1169},
abstract = {Depression and anxiety disorders represent a burdensome clinical issue. Considering the unsatisfactory clinical response of some patients to antidepressant therapy, new personalized approaches are being studied. In recent years, pre-clinical and clinical studies have investigated the role of intestinal microbiota demonstrating the importance of the gut-brain axis in these diseases. Indeed, gut microbes are able to interact with the brain interfering with behavior through some mechanisms such as amino acid metabolism, short-chain fatty acids, vagus nerve, endocrine signaling and immune responses. Experiments of gut microbiota transfer from subjects with major depression to animal models corroborated the causative role of intestinal microbes in mood disorders and anxiety. Furthermore, the incidence of dysbiosis in patients with anxiety and depression suggests a potential role for gut microbiota modulators in the treatment of these disorders. In particular, several probiotics and synbiotics have been shown to be effective in improving clinical symptoms, promising results have emerged also from fecal microbiota transplantation, but the evidence is still limited. These promising results switch on the use of gut microbiota modulators as an adjunctive tool to anti-depressant therapy. Developing pharmaceutical or nutraceutical strategies to modify the composition of gut microbiota may offer novel and personalized therapeutic tools against anxiety and depression.},
}

@article {pmid41820001,
year = {2026},
author = {Chen, D and Zhang, B and Zhang, X and Huang, J and Wang, O},
title = {[Effects of different feeds on intestinal microbiota and fat deposition in rats colonized with normal triglycerides individuals].},
journal = {Wei sheng yan jiu = Journal of hygiene research},
volume = {55},
number = {1},
pages = {86-91},
doi = {10.19813/j.cnki.weishengyanjiu.2026.01.015},
pmid = {41820001},
issn = {1000-8020},
abstract = {OBJECTIVE: To study the changes in intestinal microbiota, intestinal microbiota and fat deposition in rats with normal triglyceride(TG) colonization under different feed conditions.

METHODS: 10-week-old male sterile SD rats were randomly divided into 2 groups according to body weight, with 6 rats in each group, namely the high-fat diet group and the normal diet group. Rats were given fecal bacterial solution by gavage at a dose of 1 mL/100 g of body weight, every other day, for a total of 3 times, followed by 2 weeks of adaptive growth of the microbiota. After the transplantation was completed, the rats were respectively fed with high-fat diet and normal diet for 9 weeks. Their body weight was weighed every week, and feces were collected every 3 weeks. At the end of the experiment, the rats were sacrificed, and the liver, perirenal fat, subcutaneous fat and brown fat were weighed. Oil red O staining and lipid biochemical index detection were performed on the liver, and high-throughput sequencing was used to analyze the changes in intestinal microbiota of the rats.

RESULTS: After the experiment, compared with the normal feed group, the final body weight, perirenal fat and subcutaneous fat of rats in the high-fat feed group all increased significantly(P<0.05). The serum total cholesterol(TC)and the low density lipopro-tein cholesterol(LDL-C)level was extremely significantly increased(P<0.01). Obvious lipid deposition can be seen in the liver.16 S RNA sequencing analysis of the intestinal microbiota revealed that there were differences and changes in the diversity of Alpha and Beta of the intestinal microbiota, as well as the types and quantities of the microbiota in the high-fat diet group compared with the normal diet group. From the perspective of the phylum level analysis, the abundance of Bacteroidetes in the high-fat feed group decreased from 63.59% at week 0 to 30.94% at week 9, the abundance of Firmicutes decreased from 30.57% to 25.08%, and the F/B value increased from 0.48 at week 0 to 0.81 at week 9. At the genus level, after a 9-week feeding cycle, the abundance of Prevotella＿9 and Phascolarctobacterium in the intestinal tract of rats in the high-fat diet group decreased. The abundance of pathogenic bacteria such as Parabacteroides has increased.

CONCLUSION: In normal TG population rats with colonized intestinal flora, significant changes occurred in lipid metabolism and the composition of intestinal flora under different feeds.},
}

@article {pmid41819520,
year = {2026},
author = {Peng, Z and Liao, C and Liu, B and Yu, W and Huang, J and Chen, S and Li, L and Liang, H},
title = {Gut Microbiota-Derived Eicosapentaenoic Acid Alleviates Kidney Fibrosis in Diabetic Nephropathy Following Acute Kidney Injury.},
journal = {European journal of pharmacology},
volume = {},
number = {},
pages = {178741},
doi = {10.1016/j.ejphar.2026.178741},
pmid = {41819520},
issn = {1879-0712},
abstract = {Acute kidney injury (AKI) superimposed on diabetic nephropathy (DN) accelerates fibrosis progression to end-stage renal disease, but the underlying mechanisms remain poorly understood. Since gut microbiota and their metabolites are pivotal contributors to diabetic pathogenesis and fibrotic development, we examined the role of gut microbiota-derived metabolites in the regulation of fibrosis following AKI-on-DN. Using a murine model of folic acid-induced AKI in diabetic nephropathy, we revealed that folic acid injury exacerbated kidney dysfunction and fibrosis, which was associated with macrophage to myofibroblast transition (MMT). Integrative multi-omics profiling identified dysbiosis of intestinal flora as a critical pathological amplifier. Fecal microbiota transplantation blunted MMT and attenuated kidney fibrosis in diabetic kidney mice following folic acid stress. Furthermore, Metabolomic profiling identified a robust decline of gut microbiota-derived eicosapentaenoic acid (EPA) in AKI-on-DN mice, paralleled by reduced EPA levels in both serum and feces. EPA supplementation substantially impeded MMT and alleviated kidney fibrosis in AKI-on-DN mice. Notably, macrophage depletion considerably diminished MMT and collagen deposition in injured kidneys of AKI-on-DN mice. Collectively, our findings demonstrate that EPA plays a crucial role in regulating macrophage to myofibroblast transformation, thereby driving kidney fibrosis following AKI superimposed on diabetic nephropathy.},
}

@article {pmid41818727,
year = {2026},
author = {Li, G and Shen, Q and Ma, C and Wang, C and Song, B and Cao, Y},
title = {Gut microbiota and neurotransmitter metabolic profiling in a rat model simulating hypoactive sexual desire disorder.},
journal = {The journal of sexual medicine},
volume = {23},
number = {4},
pages = {},
doi = {10.1093/jsxmed/qdag067},
pmid = {41818727},
issn = {1743-6109},
support = {82201777//National Natural Science Foundation of China/ ; JK20245//Basic and the Project of MOE Key Laboratory of Population Health Across Life Cycle/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; Rats, Sprague-Dawley ; Female ; Rats ; *Neurotransmitter Agents/metabolism ; Disease Models, Animal ; *Sexual Dysfunctions, Psychological/microbiology/metabolism/therapy ; Fecal Microbiota Transplantation ; Prefrontal Cortex/metabolism ; Sexual Behavior, Animal ; },
abstract = {BACKGROUND: Hypoactive Sexual Desire Disorder (HSDD) is a highly prevalent, clinically impactful female sexual health condition whose pathogenesis is closely associated with disrupted excitation-inhibition homeostasis in the central nervous system, while the mechanistic role of gut microbiota in this pathological process via the gut-brain axis remains largely unelucidated.

AIM: To explore gut microbiota-neurotransmitter interactions in an HSDD-simulating rat model and verify their causal role via fecal microbiota transplantation (FMT).

METHODS: Female Sprague-Dawley rats were stratified into high copulatory behavior, normal copulatory behavior (NCB), and reduced copulatory behavior (RCB) groups via quantified mating behavioral assays, with the RCB phenotype used to establish a preclinical rat model simulating the core features of human HSDD. FMT was performed in four experimental groups: RCB-FMT-RCB, NCB-FMT-NCB, RCB-FMT-NCB, and NCB-FMT-RCB. Gut microbial composition was characterized by 16S rRNA gene sequencing, and prefrontal cortex (PFC) neurotransmitter levels were quantified using liquid chromatography-tandem mass spectrometry (LC-MS/MS). Sexual behavioral parameters were assessed following FMT administration.

OUTCOMES: Determined gut microbial and PFC neurotransmitter differences between RCB and normal rats, and validated FMT's regulatory effects on recipients' copulatory behavior, gut microbiota, and neurotransmitter balance.

RESULTS: Compared with NCB rats, RCB rats exhibited a distinct microbial biomarker profile, characterized by enrichment of Oscillibacter and Bacteroides and depletion of Jeotgalicoccus. In the PFC, RCB rats had elevated levels of inhibitory neurotransmitters (5-HT, GABA) and 5-HIAA, alongside reduced levels of excitatory neurotransmitters (DOPA, Glu). FMT induced phenotypic transfer: NCB-FMT-RCB rats displayed diminished sexual desire and developed RCB-like microbial and neurotransmitter profiles, while RCB-FMT-NCB rats exhibited improved copulatory behavioral endpoints and partial normalization of PFC neurotransmitter levels. Spearman's correlation analysis demonstrated that Oscillibacter and Bacteroides abundances were correlated with neurotransmitter imbalance in the PFC.

CLINICAL IMPLICATIONS: This study provides novel preclinical insights into the role of the gut-brain axis in HSDD, supporting further exploration of gut microbiota as a potential research target for HSDD.

STRENGTHS AND LIMITATIONS: Strengths include a validated RCB rat model, bidirectional FMT for causality; limitations involve the inability to assess subjective distress in rodents, rat-human physiological differences, PFC-only neurotransmitter analysis, unclear molecular pathways, and lack of long-term data.

CONCLUSIONS: Gut microbial dysbiosis contributes to RCB (simulating human HSDD) in female rats via modulating prefrontal cortex neurotransmitter excitation-inhibition homeostasis, with Oscillibacter and Bacteroides as key functional genera. These findings provide preliminary preclinical evidence for the gut-brain axis in sexual behavior regulation and human HSDD pathogenesis.},
}

Animals
*Gastrointestinal Microbiome/physiology
Rats, Sprague-Dawley
Female
Rats
*Neurotransmitter Agents/metabolism
Disease Models, Animal
*Sexual Dysfunctions, Psychological/microbiology/metabolism/therapy
Fecal Microbiota Transplantation
Prefrontal Cortex/metabolism
Sexual Behavior, Animal

@article {pmid41817170,
year = {2026},
author = {Loeven, AM and Pacheco, FA and Brown, AN and Fadool, DA},
title = {Lack of Structural Change in Olfactory Circuitry Following Fecal Microbiome Transplant From Donors Subjected to Diet-induced Obesity.},
journal = {Journal of neurochemistry},
volume = {170},
number = {3},
pages = {e70396},
doi = {10.1111/jnc.70396},
pmid = {41817170},
issn = {1471-4159},
support = {//Robinson Family and the Tallahassee Memorial Hospital/ ; F31 DC019867/NH/NIH HHS/United States ; R01 DK133464/NH/NIH HHS/United States ; T32 DC000044/NH/NIH HHS/United States ; },
mesh = {Animals ; Male ; Mice ; *Obesity/pathology/etiology/microbiology ; Female ; *Diet, High-Fat/adverse effects ; *Fecal Microbiota Transplantation/methods ; Mice, Inbred C57BL ; *Gastrointestinal Microbiome/physiology ; *Olfactory Bulb/pathology ; Olfactory Receptor Neurons/pathology ; },
abstract = {Obesity and fatty diets are known to damage the structure and function of chemosensory systems. Consumption of a moderately high-fat diet (MHF) induces loss of olfactory sensory neurons (OSNs) and reduces the density of associated axonal projections to the olfactory bulb that are central in the coding of odor information. Previous work has demonstrated reduced alpha diversity, as well as signature changes in microbiome composition when mice are challenged with a MHF diet that precipitates diet-induced obesity. Herein, we tested the hypothesis that a dysbiotic gut microbiome is sufficient to induce olfactory damage. Male and female donor mice were randomly assigned to a control-fat (CF) or MHF diet for 5 months duration, followed by baseline measurements of body weight, body composition (EchoMRI), glucose tolerance, and metabolic phenotyping via indirect calorimetry. We next performed fecal microbiome transplantation (FMT) from these donors to CF-maintained recipient mice. After 8 weeks post FMT, we observed no difference in body weight, glucose clearance, body composition, or fat pad weights as a consequence of transfer from MHF-maintained donors. Following FMT, recipient male mice exhibited increased Erysipelotrichaceae abundance and decreased Lactobacillaceae abundance, similar to MHF-fed donors. Recipient brains were processed for tissue clearing using immunolabeling-enabled three-dimensional imaging of solvent-cleared organs (iDISCO) and then imaged using high resolution light sheet microscopy. The volume of olfactory glomeruli expressing Olfr160 odor receptors could be visualized using genetic reporters; the FMT from MHF-maintained donors failed to evoke structural changes to these defined olfactory synapses. We conclude that diet-induced obesity, associated adiposity, and metabolic dysfunctions drive functional loss and structural changes to the olfactory system, but that gut microbiome dysbiosis alone is not sufficient to yield olfactory circuitry deficits.},
}

Animals
Male
Mice
*Obesity/pathology/etiology/microbiology
Female
*Diet, High-Fat/adverse effects
*Fecal Microbiota Transplantation/methods
Mice, Inbred C57BL
*Gastrointestinal Microbiome/physiology
*Olfactory Bulb/pathology
Olfactory Receptor Neurons/pathology

@article {pmid41816663,
year = {2026},
author = {Li, Y},
title = {Gut microbiota in the pathogenesis and treatment of inflammatory bowel disease: a critical review of mechanisms and therapeutic advances.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1738292},
pmid = {41816663},
issn = {2296-858X},
abstract = {Inflammatory bowel disease (IBD), comprising Crohn's disease (CD) and ulcerative colitis (UC), is a complex, recrudescent chronic gastrointestinal disease. The prevalence of IBD has increased globally year by year, and the exact pathogenesis remains incompletely understood. Evidence indicates that there is a strong correlation between dysbiosis of gut microbiota and the occurrence and progression of IBD. This review systematically describes recent advances in understanding the role of gut microbiota in IBD, with a particular focus on how dysbiosis contributes to pathogenesis. In addition, this review synthesizes the latest research progress and challenges of therapies of IBD targeting the gut microbiota, highlighting both their therapeutic potential and current limitations. Importantly, literature is based on targeted selection of high-quality sources, including clinical trials, meta-analyses, systematic reviews, and regulatory documents, to provide a balanced and up-to-date perspective. Emphasis is laid on the potential of microbiota-targeted therapies in IBD management.},
}

@article {pmid41816355,
year = {2026},
author = {Wang, X and Xu, Z and Yao, Y and Jia, H and Du, M and Wang, S and Yan, F and Li, L},
title = {Periodontitis promotes intestinal inflammation through gut microbiota-mediated suppression of GPR109A.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1761932},
pmid = {41816355},
issn = {2235-2988},
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; *Periodontitis/microbiology/complications/pathology ; Mice ; Mice, Inbred C57BL ; *Receptors, G-Protein-Coupled/metabolism/genetics ; *Inflammation/microbiology/pathology ; Fatty Acids, Volatile/analysis/metabolism ; Probiotics/administration & dosage ; Male ; Intestinal Mucosa/pathology/metabolism/microbiology ; Disease Models, Animal ; Colon/pathology/microbiology/metabolism ; Fecal Microbiota Transplantation ; Occludin/metabolism ; *Receptors, Nicotinic/metabolism/genetics ; Zonula Occludens-1 Protein/metabolism ; },
abstract = {OBJECTIVE: To determine whether periodontitis promotes intestinal inflammation through gut microbiota-mediated suppression of the GPR109A receptor.

METHODS: Periodontitis was induced by ligatures in C57BL/6J mice under normal chow or high-fructose diet. Periodontal destruction was evaluated by micro-computed tomography and hematoxylin and eosin staining. Colonic GPR109A expression, intestinal epithelial integrity, as well as intestinal and systemic inflammation were assessed by histology and immunostaining, quantitative polymerase chain reaction (qPCR) and enzyme-linked immunosorbent assay (ELISA). Short-chain fatty acids (SCFAs) in colonic contents were quantified by GC-MS/MS. Further, the probiotic strain CBM588 was supplemented to two groups of mice (CP/LP group) to alleviate periodontitis-induced inflammation, and GPR109A expression was detected. To investigate the role of periodontitis-associated gut microbiota, fecal microbiota from control (GF-CON) and ligatured (GF-LIG) mice were transplanted into germ-free recipients, and colonic GPR109A levels and inflammatory responses were analyzed. Finally, GPR109A function was modulated by administration of GSK256073 and mepenzolate bromide in ligatured mice, and corresponding changes in tight junctional integrity as well as intestinal and systemic inflammation were evaluated.

RESULTS: Periodontitis significantly downregulated the expression of colonic GPR109A and disrupted the localization of ZO-1 and Occludin. Probiotic supplementation restored GPR109A expression and rescued ZO-1 distribution. Fecal microbiota transplantation from periodontitis donors led to GPR109A suppression, tight junction impairment, and inflammatory upregulation in germ-free mice, confirming a microbiota-dependent mechanism. Activation of GPR109A reversed barrier disruption and reduced pro-inflammatory cytokine levels.

CONCLUSION: Periodontitis promotes colonic inflammation by gut microbiota-induced suppression of GPR109A receptor, leading to the destruction of the epithelial barrier. Activation of GPR109A restores barrier function and attenuates inflammation.},
}

Animals
*Gastrointestinal Microbiome/physiology
*Periodontitis/microbiology/complications/pathology
Mice
Mice, Inbred C57BL
*Receptors, G-Protein-Coupled/metabolism/genetics
*Inflammation/microbiology/pathology
Fatty Acids, Volatile/analysis/metabolism
Probiotics/administration & dosage
Male
Intestinal Mucosa/pathology/metabolism/microbiology
Disease Models, Animal
Colon/pathology/microbiology/metabolism
Fecal Microbiota Transplantation
Occludin/metabolism
*Receptors, Nicotinic/metabolism/genetics
Zonula Occludens-1 Protein/metabolism

@article {pmid41816323,
year = {2026},
author = {Huang, Z and Liu, J and Zheng, X and Geng, X and Tan, J and Ai, Y and Li, H and Zhou, D},
title = {Integrating bioinformatic prediction and the "gut microbiota-inflammation-skin axis" to decipher the mechanisms of quercetin (from Evodia rutaecarpa) in diabetic wound healing.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1755280},
pmid = {41816323},
issn = {1664-3224},
mesh = {Animals ; *Wound Healing/drug effects ; *Gastrointestinal Microbiome/drug effects ; *Quercetin/pharmacology/therapeutic use ; Humans ; Mice ; Rats ; Male ; *Diabetes Mellitus, Experimental/drug therapy/complications ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; RAW 264.7 Cells ; *Evodia/chemistry ; Computational Biology/methods ; Inflammation/drug therapy ; Human Umbilical Vein Endothelial Cells ; *Skin/drug effects/pathology/metabolism ; *Diabetic Foot/drug therapy ; Rats, Sprague-Dawley ; },
abstract = {BACKGROUND: Diabetic foot ulcer (DFU) is a serious complication of diabetes with impaired healing. This study focused on the herbal medicine Evodia rutaecarpa as a case to investigate the mechanisms of diabetic wound healing via the "gut microbiota-inflammation-skin axis". We specifically aimed to elucidate the role of its core bioactive flavonoid, quercetin (Que), whose therapeutic potential in this context remains underexplored.

METHODS: In vitro, the direct interaction between Que and HIF1α was assessed by cellular thermal shift assay, and its functional effect on the HIF1α/VEGF pathway was evaluated in a lipopolysaccharide-induced RAW264.7/HUVEC co-culture system. In vivo, a streptozotocin-induced diabetic rat model with full-thickness dorsal wounds was treated with Que. Wound healing rates, metabolic parameters, systemic inflammation, and gut microbiota composition were analyzed. The causal role of the gut microbiota was further tested using fecal microbiota transplantation from Que-treated donors to diabetic recipient rats, and the biological activity of resulting drug-containing serum was assessed in HUVEC and RAW264.7 cell cultures.

RESULTS: Que was identified as a principal active component of E. rutaecarpa with predicted binding affinity for key targets involved in inflammatory and hypoxic responses. In vitro, Que directly bound to and stabilized HIF1α protein and upregulated the expression of both HIF1α and VEGF in HUVECs under inflammatory co-culture conditions. In diabetic rats, Que treatment significantly accelerated wound closure, improved systemic glucose and lipid metabolism, reduced serum levels of TNF-α and IL-1β, and modulated the gut microbiota structure. FMT from Que-treated rats replicated the pro-healing effects, enhancing angiogenesis and collagen deposition in wounds, and reducing tissue inflammation. Consistently, serum derived from the FMT-Que group promoted HUVEC migration and tube formation, and attenuated the pro-inflammatory cytokine expression in RAW264.7 cells.

CONCLUSION: This study demonstrated that Que promoted diabetic wound healing by modulating the "gut microbiota-inflammation-skin axis", thereby reducing systemic inflammation and enhancing local angiogenesis.},
}

Animals
*Wound Healing/drug effects
*Gastrointestinal Microbiome/drug effects
*Quercetin/pharmacology/therapeutic use
Humans
Mice
Rats
Male
*Diabetes Mellitus, Experimental/drug therapy/complications
Hypoxia-Inducible Factor 1, alpha Subunit/metabolism
RAW 264.7 Cells
*Evodia/chemistry
Computational Biology/methods
Inflammation/drug therapy
Human Umbilical Vein Endothelial Cells
*Skin/drug effects/pathology/metabolism
*Diabetic Foot/drug therapy
Rats, Sprague-Dawley

@article {pmid41816239,
year = {2026},
author = {Li, M and Zhai, H and Qiao, L and Wang, Z and Yang, L and Zheng, X and Shi, H and Geng, W and Wang, J},
title = {Targeting the gut microbiota: the application and prospects of probiotics, fecal microbiota transplantation, and natural products in MASLD.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1735669},
pmid = {41816239},
issn = {2296-861X},
abstract = {Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as the most prevalent chronic liver condition globally. Studies have revealed distinct differences in the gut microbiota (GM) composition between healthy individuals and MASLD patients, suggesting a crucial role of GM in disease initiation and progression. This review summarizes characteristic gut microbial alterations in MASLD, examines the relationship between GM and their metabolites in MASLD pathogenesis, and discusses potential mechanistic pathways. Furthermore, we summarize the possible therapeutic applications of probiotics, fecal microbiota transplantation (FMT), and natural products in managing MASLD through GM modulation. Although current evidence indicates these interventions may slow or prevent MASLD progression, most research remains limited to animal experiments and small-scale clinical studies. The scarcity of high-quality clinical evidence has created a significant gap between theoretical research and clinical application. Therefore, this article aims to summarize existing findings, explore the prospects of GM-targeted strategies for MASLD treatment, and propose future research directions in this field.},
}

@article {pmid41816110,
year = {2026},
author = {Li, Z and Yan, J and Zeng, Z and Zhao, L},
title = {The role of gut microbiota and its metabolites in preventing oncogenesis.},
journal = {Frontiers in cell and developmental biology},
volume = {14},
number = {},
pages = {1790063},
pmid = {41816110},
issn = {2296-634X},
abstract = {The gut microbiota is increasingly recognized as a key determinant of cancer susceptibility, functioning as a dynamic interface between environmental exposures and host physiology. Dysbiosis disrupts immune homeostasis, epithelial integrity, and metabolic equilibrium, thereby fostering a microenvironment conducive to oncogenesis. Conversely, a balanced microbial ecosystem and its metabolites exert potent anti-tumor effects through immune modulation, maintenance of mucosal barrier function, and detoxification of carcinogens. This Review synthesizes emerging mechanistic insights into how commensal microbes and their metabolic products coordinate host defense pathways to suppress malignant transformation. We further discuss translational strategies-ranging from probiotics, prebiotics, and synbiotics to fecal microbiota transplantation and dietary interventions-that leverage microbiome modulation for cancer prevention. Despite compelling preclinical evidence, clinical translation remains constrained by inter-individual variability and incomplete mechanistic understanding. Integration of multi-omics analyses, gnotobiotic models, and precision microbial engineering offers a path toward microbiota-based interventions as a cornerstone of personalized cancer prevention and immunomodulation.},
}

@article {pmid41815180,
year = {2026},
author = {Kumar, SE and Selvarajan, S and Varghese, T and Bharadwaj, PK and Lakshmi, KS and Hanmantgad, S and Dutta, AK and Joseph, AJ and Mathews, V and George, B},
title = {Fecal Calprotectin as a biomarker for early diagnosis and prediction of steroid response in Acute Gastrointestinal Graft versus Host Disease.},
journal = {Blood cell therapy},
volume = {9},
number = {1},
pages = {31-40},
pmid = {41815180},
issn = {2432-7026},
abstract = {BACKGROUND: Acute gastrointestinal graft-versus-host disease (GI-GVHD) is a complication of allogeneic hematopoietic stem cell transplantation (HSCT) that requires early diagnosis. Fecal calprotectin (FC) is a biomarker of intestinal inflammation. We studied the role of FC in differentiating GI-GVHD from other diarrhea.

METHODS: We prospectively studied allogeneic HSCT recipients between 2017 and 2020. FC levels were measured pre-transplant, on post-transplant day 14, on day 1 of diarrhea, and post-steroid treatment (day 3-7 of steroid treatment).

RESULTS: We studied 116 patients with median age 14.5 (5-29) years; 84 were male (72.4%). Fifty-seven patients (49.1%) developed diarrhea post-HSCT, 34 (59.7%) patients had GI-GVHD, and 23 patients (40.3%) developed other diarrheal illnesses. FC level on day1 of diarrhea among GI-GVHD patients (n=33) was higher (63 μg/g [Q1-Q3:25.6-358.5]) compared to other diarrhea (27.5 μg/g [21.1-60.4], p=0.045). FC cut-off > 53.7 μg/g had sensitivity (78.6%) and specificity (57.9%) with area under the receiver operating characteristic curve of 0.67 to predict GI-GVHD on day 1 of diarrhea. FC levels in steroid non-responders (n=7) were higher (311.5 μg/g [40.5-1,291.5]) than responders (n=11) (31.2 μg/g [20.8-137.2] μg/g); p=0.03. Haplomatch, severe GI-GVHD, and coexisting skin GVHD were significant predictors of poor treatment response.

CONCLUSION: A higher FC value on day 1 of diarrhea aids in the diagnosis of acute GI-GVHD and predicts poor response to treatment.},
}

@article {pmid41814703,
year = {2025},
author = {Huang, YJ and Xie, YL and Mo, PY and Tan, ZX and Wu, XM and Wang, SL},
title = {[Anti-depressant mechanism of Bupleuri Radix in regulating hippocampal FGFR1-5-HT_(1A)R heterodimer formation via intestinal flora-short-chain fatty acids].},
journal = {Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica},
volume = {50},
number = {24},
pages = {6947-6956},
doi = {10.19540/j.cnki.cjcmm.20250825.801},
pmid = {41814703},
issn = {1001-5302},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; Mice ; *Fatty Acids, Volatile/metabolism ; *Hippocampus/metabolism/drug effects ; Male ; Humans ; *Antidepressive Agents/administration & dosage ; *Bupleurum/chemistry ; *Depression/drug therapy/metabolism/microbiology/genetics ; *Receptor, Fibroblast Growth Factor, Type 1/metabolism/genetics/chemistry ; *Drugs, Chinese Herbal/administration & dosage ; *Receptor, Serotonin, 5-HT1A/metabolism/genetics/chemistry ; Mice, Inbred C57BL ; Dimerization ; },
abstract = {Based on the "gut-brain" axis, this study investigated the molecular mechanism of the antidepressant effect of Bupleuri Radix. The effect of Bupleuri Radix on human intestinal flora cultured in vitro was analyzed by 16S rRNA sequencing. Differential bacteria were identified by real-time quantitative PCR(qPCR). Short-chain fatty acid(SCFA) content was determined by the GC-FID method. A depression-like mouse model was established using the "triple-one" compound stress method. Mice were administered the aqueous extract of Bupleuri Radix by gavage, transplanted with Bacteroides acidifaciens or spore-forming bacteria, or gavaged with SCFAs. Behavioral changes were assessed. SCFA content in feces was measured by GC-FID. Hippocampal(fibroblast growth factor 21, FGF21) protein expression was detected by Western blot. The formation of fibroblast growth factor receptor 1-5-hydroxytryptamine receptor 1A(FGFR1-5-HT_(1A)R) heterodimers was examined using the Duolink PLA method. The results showed that Bupleuri Radix significantly increased the abundance of the three spore-forming bacterial genera Ruminococcus, Dorea, and Blautia(P<0.05), as well as B. acidifaciens(P<0.001). Administration of Bupleuri Radix(P<0.001 or P<0.05) and transplantation of B. acidifaciens(P<0.01) both increased the levels of SCFAs such as acetic acid and butyric acid in bacterial metabolites. Treatment with Bupleuri Radix, transplantation of B. acidifaciens, or high doses of SCFAs significantly improved depression-like behaviors in mice, increased hippocampal FGF21 expression(P<0.05, P<0.01, or P<0.001), and promoted FGFR1-5-HT_(1A)R heterodimer formation(P<0.05 or P<0.01), whereas transplantation of spore-forming bacteria showed no obvious antidepressant effect. In conclusion, the antidepressant effect of Bupleuri Radix is mediated by intestinal bacteria such as B. acidifaciens, which regulate the synthesis and metabolism of SCFAs, thereby modulating hippocampal FGF21 expression and activating FGFR1-5-HT_(1A)R heterodimers.},
}

Animals
*Gastrointestinal Microbiome/drug effects
Mice
*Fatty Acids, Volatile/metabolism
*Hippocampus/metabolism/drug effects
Male
Humans
*Antidepressive Agents/administration & dosage
*Bupleurum/chemistry
*Depression/drug therapy/metabolism/microbiology/genetics
*Receptor, Fibroblast Growth Factor, Type 1/metabolism/genetics/chemistry
*Drugs, Chinese Herbal/administration & dosage
*Receptor, Serotonin, 5-HT1A/metabolism/genetics/chemistry
Mice, Inbred C57BL
Dimerization

@article {pmid41774188,
year = {2026},
author = {Yadav, A and Melkani, GC},
title = {Microbes, mood, and metabolism/obesity: Pharmacological insights into the gut-obesity-depression triad.},
journal = {Cellular and molecular life sciences : CMLS},
volume = {83},
number = {1},
pages = {},
pmid = {41774188},
issn = {1420-9071},
support = {AG065992//National Institute of Aging/ ; },
abstract = {The global rise in obesity and depression, two highly prevalent and often comorbid disorders has intensified interest in the gut–brain axis as a shared biological link. Mounting evidence indicates that the gut microbiota profoundly influences both metabolic and neuropsychiatric regulation, positioning it as a promising therapeutic target for these interconnected conditions. This review explores the complex interactions among microbial dysbiosis, host metabolism, and mood regulation, emphasizing pharmacological strategies that harness this triad for treatment. Gut-derived hormones such as glucagon-like peptide-1 (GLP-1) and microbiome-produced metabolites, including short-chain fatty acids (SCFAs) and bile acids, have demonstrated potential to modulate appetite, insulin sensitivity, inflammation, and brain function. GLP-1 receptor agonists like semaglutide originally developed for diabetes and obesity also exhibit antidepressant properties, highlighting their dual therapeutic promise. Emerging microbiome-based interventions, such as precision probiotics, engineered psychobiotics, and fecal microbiota transplantation (FMT), are being investigated to restore microbial balance and improve both metabolic and mood outcomes. Furthermore, combination therapies pairing microbiota-targeted agents with conventional antidepressants or anti-obesity drugs may offer synergistic benefits, enhance efficacy while minimize adverse effects. Despite this promise, significant challenges remain, including ensuring safety, understanding long-term impacts, navigating regulatory hurdles for live biotherapeutics, and addressing ethical concerns about altering the human microbiome. A deeper understanding of the gut–microbiome–brain axis may ultimately enable personalized, microbiota-guided therapies that treat both the physiological and psychological dimensions of obesity and depression, marking a major step toward holistic and precision medicine.},
}

@article {pmid41812936,
year = {2026},
author = {Lv, J and Zhang, Y and Yue, Y and Huang, S and Zhang, S and Fu, Y and Dai, C and Han, C and Hao, Z},
title = {Lianweng Formula Alleviates Colonic Inflammation through Gut Microbiota-Mediated Inactivation of the PTGS2/AKR1C3/ALOX5 Pathway and Subsequent Suppression of Arachidonic Acid Metabolism.},
journal = {Journal of ethnopharmacology},
volume = {},
number = {},
pages = {121512},
doi = {10.1016/j.jep.2026.121512},
pmid = {41812936},
issn = {1872-7573},
abstract = {BACKGROUND: Current clinical management of ulcerative colitis (UC) is often limited by inadequate efficacy and adverse effects. Our previous studies identified Lianweng formula (LW) as a promising therapeutic candidate and preliminarily elucidated its bioactive components. However, the integrated mechanism involving the interplay between gut microbiota and host metabolism remains obscure.

PURPOSE: This study aimed to elucidate the regulatory mechanism of LW on arachidonic acid (AA) metabolism in UC rats, with a specific focus on the mediating role of gut microbiota.

METHODS: The therapeutic efficacy of LW was first evaluated in a UC rat model by assessing inflammatory cytokines, histological injury, and mucosal barrier integrity. Integrated 16S rRNA sequencing and untargeted metabolomics were performed to map the alterations in gut microbiota and colonic metabolic profiles. Crucially, antibiotic cocktail (ABX) depletion and fecal microbiota transplantation (FMT) were employed to verify the causal role of gut microbiota in mediating LW's efficacy. Finally, targeted metabolomics was conducted to decipher the specific crosstalk between microbial composition and the AA metabolic pathway.

RESULTS: Oral administration of LW significantly alleviated colonic pathological damage and restored intestinal barrier integrity, while effectively suppressing the inflammatory response in UC rats. Furthermore, LW effectively restored gut microbiota homeostasis by increasing the abundance of beneficial genera, such as g_Odoribacter and g_Rikenella, and decreasing the abundance of harmful genera, including g_Desulfovibrio and g_Paludicola, among others. Untargeted metabolomics highlighted the AA metabolic pathway as a critical target of LW, exhibiting strong correlations with the altered gut microbiota. Notably, gut microbiota depletion via ABX significantly compromised the therapeutic efficacy of LW and nullified its regulation of AA metabolism, identifying gut microbes as essential mediators. This causal link was further corroborated by FMT, which demonstrated that LW-modulated microbiota successfully recapitulated the suppression of AA metabolism and the therapeutic benefits. These findings were consistently validated by quantitative targeted metabolomics profiling.

CONCLUSION: Our findings demonstrate that LW significantly mitigates colonic inflammation in UC rats, primarily by inhibiting the arachidonic acid metabolic pathway. Notably, this metabolic regulation and the consequent anti-inflammatory effects are critically dependent on LW-induced gut microbiota remodeling. This study offers novel therapeutic insights into UC treatment by highlighting the pivotal role of microbiota-metabolite crosstalk in the mechanism of action of LW.},
}

@article {pmid41809655,
year = {2026},
author = {Zhou, B and Parekh, Z and Phung, C and Rodriguez, SH and Skondra, D},
title = {The gut-retina axis in age-related macular degeneration: immune crosstalk and metabolite production.},
journal = {Experimental biology and medicine (Maywood, N.J.)},
volume = {251},
number = {},
pages = {10847},
pmid = {41809655},
issn = {1535-3699},
mesh = {Humans ; *Macular Degeneration/immunology/microbiology/metabolism ; *Gastrointestinal Microbiome/immunology/physiology ; Animals ; Dysbiosis/immunology ; *Retina/immunology/metabolism/pathology ; },
abstract = {Current therapies slow down advanced features but do not halt or reverse degeneration and neovascularization in dry and wet age-related macular degeneration (AMD). Recent research implicates the gastrointestinal microbiome as a potential critical modulator in AMD pathogenesis through the gut-retina axis. Dysbiosis, characterized by imbalanced microbial diversity, composition and function, can exacerbate systemic and retinal inflammation through microglial priming, inflammasome activation, and secretion of pro-angiogenic cytokines (IL-6, IL-1β, TNF-α, VEGF). Additionally, microbiome-derived metabolites such as short-chain fatty acids and bile acids may exert modulatory roles in host immunity and homeostasis. Their depletion in conjunction with enrichment of specific microbial taxa have been linked to progression of advanced AMD. Together, these complex systems of immune crosstalk in relation to dysbiosis highlight the gut-retina axis as a promising therapeutic target. Dietary modifications, particularly Mediterranean and high-fiber diets, enhance production of protective metabolites and are associated with decreased AMD progression risk compared to Western dietary patterns. Experimental strategies such as fecal microbiota transplantation in animal models and drug repurposing strategies show promise in modulating disease severity. This review synthesizes current mechanistic insights into microbial-immune crosstalk in AMD, emphasizing the interplay of dysbiosis, immune activation, and metabolite signaling.},
}

Humans
*Macular Degeneration/immunology/microbiology/metabolism
*Gastrointestinal Microbiome/immunology/physiology
Animals
Dysbiosis/immunology
*Retina/immunology/metabolism/pathology

@article {pmid41809597,
year = {2026},
author = {Chen, N and Ma, T and Chen, R and Zhang, Y and Tang, X and Sun, Y},
title = {Transcutaneous electrical nerve stimulation treated anterior talo-fibular ligament injured rat through the gut-joint axis and intestinal microbiota.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1770614},
pmid = {41809597},
issn = {1664-302X},
abstract = {OBJECTIVE: This study demonstrated that transcutaneous electrical nerve stimulation (TENS) and its induced fecal microbiota transplantation (FMT) could treat anterior talo-fibular ligament (ATFL) injury rat and modify the intestinal microbiota via the gut-joint axis.

METHODS: An ATFL injury model was duplicated and treated with low, medium, or high-intensity of TENS. After 1, 2, and 3 weeks of TENS treatment, the improvements and the expression levels of NOD2/IL-6/NF-κB/BMP-2/TGF-β were measured. The intestinal microbiota was analyzed via 16S rDNA sequencing. After FMT which induced by TENS, the improvement of ATFL injury rat was analyzed.

RESULTS: After TENS treatment, compared with the model control group, the bio-mechanical, gait, bone mineral density (BMD), etc. parameters were elevated in the TENS groups (p < 0.05); the expression of NOD2/IL-6 decreased and the BMP-2/TGF-β increased in the TENS groups (p < 0.05). The intestinal microbiota was altered, including increases in the abundances of Erysipelotrichaceae, Lachnospira, Eubacterium, Phascolarctobacterium, and Alloprevotella. After FMT, similar improvements were found in ATFL injury rats.

CONCLUSION: TENS ameliorated ATFL injury rat by regulating the NOD2/IL-6/NF-κB/BMP-2/TGF-β and changed the intestinal microbiota through the gut-joint axis. Dominant intestinal microbiota was associated with FMT and could improve ATFL injury rat.},
}

@article {pmid41809453,
year = {2026},
author = {Zhao, X and Zhang, W and Zhang, Y and Liu, XA},
title = {Gastrointestinal dysfunction after brain injury: Mechanisms and the role of the brain-gut axis.},
journal = {World journal of gastroenterology},
volume = {32},
number = {10},
pages = {115731},
pmid = {41809453},
issn = {2219-2840},
mesh = {Humans ; *Gastrointestinal Diseases/etiology/therapy/physiopathology ; *Brain-Gut Axis/physiology ; Dysbiosis/therapy/etiology/microbiology/physiopathology ; Probiotics/therapeutic use ; *Brain/physiopathology ; *Brain Injuries/complications/physiopathology ; Gastrointestinal Microbiome ; Enteric Nervous System/physiopathology ; Fecal Microbiota Transplantation ; Animals ; *Gastrointestinal Tract/innervation/physiopathology ; Vagus Nerve ; Gastric Emptying ; },
abstract = {Brain injury (BI) encompasses traumatic BI and stroke, and is a leading cause of mortality and morbidity worldwide. In addition to primary brain damage, BI can cause a series of sequelae, of which gastrointestinal (GI) dysfunction is one of the most important affecting patient outcomes. GI dysfunction, including delayed gastric emptying, increased intestinal permeability, and gut dysbiosis, is common among patients with BI. GI dysfunction not only impairs nutrient absorption and increases the risk for infection, but also enhances secondary BI by aggravating the systemic inflammatory response. The brain-gut axis refers to the bidirectional communication network between the central nervous system and enteric nervous system. This article provides an overview of the mechanisms underlying GI dysfunction after BI and the close relationship with the brain-gut axis. Furthermore, the potential mechanisms underlying brain-gut modulation by probiotics, fecal microbiota transplantation, and vagus nerve stimulation are discussed, which may provide new insights into the treatment of GI dysfunction in patients with BI. An in-depth understanding of the interaction between the brain and GI system is essential to develop more effective therapeutic strategies to alleviate patient suffering and improve survival and quality of life.},
}

Humans
*Gastrointestinal Diseases/etiology/therapy/physiopathology
*Brain-Gut Axis/physiology
Dysbiosis/therapy/etiology/microbiology/physiopathology
Probiotics/therapeutic use
*Brain/physiopathology
*Brain Injuries/complications/physiopathology
Gastrointestinal Microbiome
Enteric Nervous System/physiopathology
Fecal Microbiota Transplantation
Animals
*Gastrointestinal Tract/innervation/physiopathology
Vagus Nerve
Gastric Emptying

@article {pmid41809178,
year = {2026},
author = {Mundhra, SK and Kochhar, R},
title = {Methodological insights into fecal microbiota transplantation: Dissecting key approaches for success.},
journal = {World journal of methodology},
volume = {16},
number = {1},
pages = {108875},
pmid = {41809178},
issn = {2222-0682},
abstract = {Fecal microbiota transplantation (FMT) has emerged as a revolutionary treatment strategy for restoring gut microbiota in recurrent Clostridioides difficile infection and has also been explored across a broader range of dysbiosis-related diseases such as inflammatory bowel disease where it has demonstrated promising results and potential therapeutic benefits. The success of FMT largely depends on the careful implementation of best practices, which include selecting appropriate donors, preparing the stool properly, and choosing the right delivery methods. This mini-review explores the evolution of FMT methodologies, including donor screening protocols, advances in stool preparation, and innovations in administration routes. We also discuss emerging approaches, such as synthetic microbiota and microbiome engineering, alongside the challenges and future directions for standardizing FMT. These methodological advancements aim to enhance safety, efficacy, and accessibility of FMT, establishing it as a key player in microbiome-based therapies.},
}

@article {pmid41809160,
year = {2026},
author = {Mishra, A and Juneja, D},
title = {Decolonizing the gut from multidrug-resistant bacteria: Current strategies and future perspectives.},
journal = {World journal of methodology},
volume = {16},
number = {1},
pages = {108646},
pmid = {41809160},
issn = {2222-0682},
abstract = {The rise of multidrug-resistant organisms (MDROs) represents a serious global health crisis, with the gastrointestinal tract serving as a major reservoir for these pathogens. This review highlights the burden of gut colonization by MDROs, its role in spreading antimicrobial resistance, and explores current and emerging strategies for decolonization. Various non-antibiotic approaches such as probiotics, prebiotics, bacterial consortia, selective digestive decontamination, faecal microbiota transplantation, bacteriophage therapy, and Clustered Regularly Interspersed Short Palindromic Repeats-CRISPR-associated protein systems along with dietary interventions have been assessed for their potential to restore microbial balance and reduce MDRO carriage. While promising results have emerged from early studies and animal models, most interventions remain investigational. Rigorous clinical trials, standardized protocols, and safety assessments are essential before these approaches can be integrated into routine practice for MDRO management.},
}

@article {pmid41808568,
year = {2026},
author = {Sharma, S and Parashar, M and Lal, K and Naik, M and Tanwar, SS},
title = {Doxorubicin-Induced Cardiotoxicity: Comprehensive Pathway Insights and Advanced Preclinical Therapeutics.},
journal = {Journal of applied toxicology : JAT},
volume = {},
number = {},
pages = {},
doi = {10.1002/jat.70131},
pmid = {41808568},
issn = {1099-1263},
abstract = {Doxorubicin, a secondary metabolite of Streptomyces peucetius var. caesius and a member of the anthracycline family, exerts anticancer effects via DNA intercalation and topoisomerase II inhibition in tumor cells. However, its clinical application is limited by dose-dependent and cumulative cardiotoxicity. The mechanisms underlying doxorubicin-induced cardiotoxicity (DIC) include oxidative stress, lipid peroxidation, mitochondrial dysfunction, calcium dysregulation, disrupted iron homeostasis, nitric oxide release, and inflammatory mediator production. Emerging evidence highlights autophagy dysregulation, with doxorubicin upregulating cardiac autophagy by suppressing GATA4 and ribosomal protein S6 kinase beta-1(S6K1). Mitochondria-dependent ferroptosis also plays a significant role, driven by downregulation of glutathione peroxidase 4 (GPX4), lipid peroxidation via DOX-Fe[2+] complexes, and dysregulated iron metabolism. Additionally, DOX triggers pyroptosis in cardiomyocytes, involving proteins such as NLRP3 (NOD-, LRR-, and pyrin domain-containing protein 3), caspase-3, and gasdermin D (GSDMD). Epigenetic alterations, including DNA hypomethylation (via downregulation of DNMT1 (DNA (cytosine-5)-methyltransferase 1), changes in microRNA levels (e.g., upregulation of miR-520h targeting HDAC19 (histone deacetylase 1), and histone deacetylase inhibition, exacerbate cardiac damage. Recent studies also emphasize the role of gut microbiota in doxorubicin-induced cardiotoxicity. Doxorubicin induces dysbiosis, leading to cardiomyocyte apoptosis and elevated myocardial enzyme levels. Interventions such as dietary modifications, fecal microbiota transplantation, probiotics, and natural compounds like glabridin and emodin show promise. Glabridin reduces inflammation by modulating colonic macrophage polarization, while emodin inhibits ferroptosis via gut microbiota remodeling mediated by Nrf2. This review explores oxidative stress, lipid peroxidation, ferroptosis, apoptosis, inflammation, autophagy, epigenetics, and gut microbiota in DIC, alongside promising pharmacological strategies to mitigate its effects.},
}

@article {pmid37665552,
year = {2023},
author = {Liu, NH and Liu, HQ and Zheng, JY and Zhu, ML and Wu, LH and Pan, HF and He, XX},
title = {Fresh Washed Microbiota Transplantation Alters Gut Microbiota Metabolites to Ameliorate Sleeping Disorder Symptom of Autistic Children.},
journal = {Journal of microbiology (Seoul, Korea)},
volume = {61},
number = {8},
pages = {741-753},
pmid = {37665552},
issn = {1976-3794},
support = {ZYYCXTD-C-202208//Innovation Team and Talents Cultivation Program of National Administration of Traditional Chinese Medicine/ ; 2022B1212010012//Guangdong Provincial Key Laboratory of TCM Pathgenesis and Prescriptions of Heart and Spleen Diseases/ ; 2020B1111100011//Special Project for Research and Development in Key areas of Guangdong Province/ ; 2018A030313639//Natural Science Foundation of Guangdong Province/ ; 2019A1515010125//Natural Science Foundation of Guangdong Province/ ; 2023A1515010751//Natural Science Foundation of Guangdong Province/ ; 2019-GDXK-0013//Guangdong Key Discipline Research Project of Department of Education of Guangdong Province/ ; 2020KZDZX1132//COVID-19 Epidemic Prevention and Control Special Research Project of Department of Education of Guangdong Province/ ; 202201010134//Basic and Applied Basic Research Project of Guangzhou Basic Research Program/ ; 2021xk36//Discipline Collaborative Innovation Team of Guangzhou University of Traditional Chinese Medicine/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; Male ; Female ; Child ; Child, Preschool ; *Fecal Microbiota Transplantation/methods ; *Autism Spectrum Disorder/therapy/microbiology ; *Sleep Wake Disorders/therapy/microbiology ; Dysbiosis/therapy/microbiology ; Bacteria/classification/metabolism/genetics/isolation & purification ; Feces/microbiology ; *Autistic Disorder/therapy/microbiology ; },
abstract = {Accumulating studies have raised concerns about gut dysbiosis associating autism spectrum disorder (ASD) and its related symptoms. However, the effect of gut microbiota modification on the Chinese ASD population and its underlying mechanism were still elusive. Herein, we enrolled 24 ASD children to perform the first course of fresh washed microbiota transplantation (WMT), 18 patients decided to participate the second course, 13 of which stayed to participate the third course, and there were 8 patients at the fourth course. Then we evaluated the effects of fresh WMT on these patients and their related symptoms. Our results found that the sleeping disorder symptom was positively interrelated to ASD, fresh WMT significantly alleviated ASD and its sleeping disorder and constipation symptoms. In addition, WMT stably and continuously downregulated Bacteroides/Flavonifractor/Parasutterella while upregulated Prevotella_9 to decrease toxic metabolic production and improve detoxification by regulating glycolysis/myo-inositol/D-glucuronide/D-glucarate degradation, L-1,2-propanediol degradation, fatty acid β-oxidation. Thus, our results suggested that fresh WMT moderated gut microbiome to improve the behavioral and sleeping disorder symptoms of ASD via decrease toxic metabolic production and improve detoxification. Which thus provides a promising gut ecological strategy for ASD children and its related symptoms treatments.},
}

Humans
*Gastrointestinal Microbiome/physiology
Male
Female
Child
Child, Preschool
*Fecal Microbiota Transplantation/methods
*Autism Spectrum Disorder/therapy/microbiology
*Sleep Wake Disorders/therapy/microbiology
Dysbiosis/therapy/microbiology
Bacteria/classification/metabolism/genetics/isolation & purification
Feces/microbiology
*Autistic Disorder/therapy/microbiology

@article {pmid41807298,
year = {2026},
author = {Huang, J and Qin, Q and Li, X and Jiang, K and Xu, J and Mao, Y and Kang, W and Gao, R and Cheng, Y and Zhao, W and Ke, J and Mou, X},
title = {Bacteroides-associated NAD[+] depletion correlates with exacerbated radiation-induced colorectal injury and impaired mucosal proliferative capacity.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2641260},
doi = {10.1080/19490976.2026.2641260},
pmid = {41807298},
issn = {1949-0984},
abstract = {Radiation proctitis (RP) is a frequent complication of pelvic radiotherapy that compromises treatment delivery and patient quality of life, yet the factors shaping injury severity remain incompletely defined. We prospectively profiled pretreatment fecal microbiomes and metabolomes from 55 patients and stratified them by outcome into mild versus severe RP. Baseline microbial composition showed Bacteroidales enriched in severe RP and Firmicutes enriched in mild cases. Multi-omics integration highlighted nicotinate/nicotinamide pathways; severe RP was characterized by concomitant reductions in both fecal and tissue NAD[+] levels, along with an enrichment of microbial nicotinate/nicotinamide metabolism genes, primarily contributed by Bacteroides ovatus, B. xylanisolvens, and B. fragilis. In mice, fecal microbiota transplantation from severe-RP donors exacerbated radiation-induced colorectal injury and decreased colorectal NAD[+], supporting a causal role for the microbiota. Gavage with Bacteroides similarly worsened pathology and lowered NAD[+], whereas nicotinamide mononucleotide (NMN) supplementation attenuated the injury. Mechanistically, Bacteroides gavage reduced mitochondrial membrane potential, decreased the Lgr5[+] stem-cell proportion and proliferative indices, associated with Wnt pathway modulation. NMN reversed these effects in parallel with NAD[+] restoration. Together, these results identify a microbiota‒metabolite association wherein Bacteroidales enrichment is associated with NAD[+] depletion, reduced mucosal proliferative capacity, and exacerbated radiation-induced colorectal injury. The work deepens insight into RP pathogenesis and suggests a potential basis for microbiome- and metabolite-targeted approaches to attenuate severe RP.},
}

@article {pmid41804768,
year = {2026},
author = {Fan, S and Yin, G and Ren, Y and Fan, X and Liang, Y and Ma, N and Luo, Y and Deng, Y and Zhang, C and Xiang, T and Zuo, J and Tang, J and Luo, D and Fan, X},
title = {Epigallocatechin-3-gallate ameliorates LPS-induced ARDS by modulating Akkermansia-associated SCFAs metabolism and inhibiting the JAK2/STAT3 candidate signaling pathway.},
journal = {Food & function},
volume = {},
number = {},
pages = {},
doi = {10.1039/d5fo05380c},
pmid = {41804768},
issn = {2042-650X},
abstract = {Acute respiratory distress syndrome (ARDS) is a leading cause of acute respiratory failure and mortality, characterized by significant inflammation and damage to the alveolar-capillary membrane, which disrupts gas exchange. Although the triggers of ARDS vary, uncontrolled inflammation plays a central role in its progression, with current treatment options being limited. Dysbiosis of the gut microbiota fuels systemic inflammation via the gut-lung axis and acts as a key driver of ARDS onset and progression. Epigallocatechin-3-gallate (EGCG), a major polyphenolic constituent derived from green tea, with known anti-inflammatory effects, and microbiota-modulating properties, holds potential as a therapeutic intervention for ARDS. This study investigated the mechanism of EGCG's intervention in ARDS and its impact on gut microbiota using C57BL/6J mice. The mice were divided into groups receiving different doses of EGCG pretreatment, followed by intratracheal instillation of lipopolysaccharide (LPS)-induced ARDS. Various techniques, including pathological examination, ELISA, and immunohistochemistry (IHC), were employed to assess pulmonary inflammation and examine intestinal tight junction integrity. Gut microbiota composition was analyzed via 16S rRNA sequencing. To further elucidate the role of the gut microbiota, fecal microbiota transplantation (FMT) was performed following gut microbiota depletion. Feces from EGCG-treated donor mice were transplanted into recipient mice, with results compared to the EGCG-pretreated group. A more focused investigation involved the transplantation of Akkermansia muciniphila (AKK), and its effects on pulmonary inflammation and intestinal tight-junction integrity were observed. Additionally, GC-MS analysis confirmed that AKK-derived metabolites were short-chain fatty acids (SCFAs), and the effects of SCFAs were compared to those of EGCG pretreatment. Network pharmacology and transcriptomic analysis suggested that SCFAs likely exert their effects through the JAK2/STAT3 signaling pathway. The effects of SCFAs and EGCG pretreatment were further validated using specific inhibitors to assess pulmonary and intestinal conditions. In the LPS-induced ARDS model, EGCG significantly reduced the inflammatory response, decreased inflammatory cell infiltration, and inhibited pro-inflammatory cytokine production, thereby limiting lung and intestinal tissue damage. Mechanistically, EGCG enriched the gut microbiota, particularly increasing AKK abundance, which promoted SCFAs production. These SCFAs entered systemic circulation, reached the lungs, and modulated the JAK2/STAT3 candidate signaling pathway to suppress inflammation, ultimately alleviating ARDS pathology. In conclusion, EGCG mitigates ARDS-related inflammatory damage by increasing Akkermansia muciniphila abundance and enhancing SCFAs production, which inhibits the JAK2/STAT3 candidate pathway. This study introduces a novel gut microbiota-based approach for ARDS treatment and offers new insights into the role of gut-derived metabolites in ARDS pathogenesis.},
}

@article {pmid41804658,
year = {2026},
author = {Lin, H and Feng, Z and Tu, Q and Li, H and Zhang, Y and Wei, X and Yi, Q and Zhang, H and Wang, Y and Li, X and Li, Y and Huang, J and Chen, Z and Shentu, H and Wang, A and Chen, Y and He, X and Cao, X},
title = {Advance Microbiota Transplantation: A Novel Addition-Subtraction Paradigm for Optimising Faecal Microbiota Transplantation.},
journal = {Microbial biotechnology},
volume = {19},
number = {3},
pages = {e70323},
doi = {10.1111/1751-7915.70323},
pmid = {41804658},
issn = {1751-7915},
support = {2024YFA1307102//National Key Research and Development Program of China/ ; C2501011//Shenzhen Medical Research Fund/ ; ZDSYS20220606100800002//Shenzhen Key Laboratory of Gastrointestinal Microbiota and Disease, Shenzhen Science and Technology Program (Strategic Emerging Industries Special Project)/ ; LCYSSQ20220823091405012//Shenzhen Science and Technology Program (Young Scientists Project in Industrial Fields)/ ; SZSM202411029//Sanming Project of Medicine in Shenzhen/ ; },
mesh = {*Fecal Microbiota Transplantation/methods/standards ; Humans ; *Clostridium Infections/therapy ; Clostridioides difficile ; },
abstract = {Faecal microbiota transplantation (FMT) is highly effective for recurrent Clostridioides difficile infection but yields inconsistent benefits in chronic indications. As a crude whole-microbiota transplant, FMT contains numerous undefined active components, complicating efforts to ensure treatment predictability and stability. Therefore, we propose Advance Microbiota Transplantation (AMT), a comprehensive, phase-based hypothesis that employs an addition-subtraction strategy throughout the pre-, peri- and post-transplant stages. AMT comprises donor and recipient pre-treatment, procedural optimisation and post-transplant adjuvant interventions to mitigate donor variability, ecological resistance, procedural heterogeneity and unstable engraftment. Through a systematic synthesis of current evidence-based FMT research, we explored how the addition-subtraction strategy can be operationalised to shape the AMT concept and define testable, phase-specific levers, thereby providing a foundation for future clinical translation. In parallel, we appraised the reporting quality using the Preferred Reporting Items for Microbiotherapy (PRIM) and identified six persistently under-reported items that limit the interpretability, comparability, and reproducibility of FMT research. This review aims to facilitate the integration of AMT into clinical practice.},
}

*Fecal Microbiota Transplantation/methods/standards
Humans
*Clostridium Infections/therapy
Clostridioides difficile

@article {pmid41803890,
year = {2026},
author = {Liu, J and Ning, X and Yuan, J and Yu, Z and Qin, Y and Xing, Y and Zhao, J and Sun, S},
title = {Gut dysbiosis in kidney injury: therapeutic potential of fecal microbiota transplantation.},
journal = {European journal of medical research},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40001-026-04100-w},
pmid = {41803890},
issn = {2047-783X},
abstract = {Chronic kidney disease (CKD) poses a substantial global health burden. The gut-kidney axis has become a critical area of research, given the influence of gut microbiota on the kidney. CKD exhibits a distinct gut dysbiosis signature, comprising an altered microbial architecture divergent from healthy individuals and specific microbial changes that exhibit distinct associations with the degree of renal impairment. Preclinical studies lend support to the therapeutic capacity of fecal microbiota transplantation (FMT) in CKD, demonstrating its efficacy in reshaping gut dysbiosis, rehabilitating the gut barrier, rectifying immune imbalance, and reducing fibrosis. These mechanistic insights are complemented by observations of its synergistic effects when combined with standard therapeutics in other conditions, underscoring its potential to improve human kidney outcomes. This review synthesizes current knowledge on CKD-associated dysbiosis, impaired intestinal barrier, and the therapeutic potential of FMT in mitigating the progression of CKD.},
}

@article {pmid41803870,
year = {2026},
author = {Wang, Y and Tian, W and Ye, Z and Liao, Y and Huang, C and Qi, D and Wang, Y and Chen, Y and Zhou, Y},
title = {Based on the gut-heart axis: Polygonum capitatum improves atherosclerosis by modulating gut microbiota and TMAO, supporting MCPIP1/p53-associated endothelial protection.},
journal = {Chinese medicine},
volume = {21},
number = {1},
pages = {},
pmid = {41803870},
issn = {1749-8546},
support = {2024YJSKYJJ376//Guizhou Provincial Postgraduate Education Innovation Program project funding/ ; 82160099//National Natural Science Foundation of China/ ; Qian-ke-he basic talents-GCC[2023]085//Guizhou High-level Innovative Talents Project/ ; Qiankehe support [2022] generally 263//Science and Technology Plan Project of Guizhou Province/ ; },
abstract = {Polygonum capitatum (PC), known as "Tou Hua Liao" (Chinese name), is an essential source of Hmong medicinal plants, which has been used for treating various human diseases. This study examined whether PC has lipid-lowering and anti-atherosclerotic effects and explored the underlying mechanisms. We focused on PC's influence on gut microbiota-derived metabolites. First, we analyzed animal-derived serum containing PC components and the botanical compounds of PC by UPLC-MS/MS to identify potential bioactive constituents. Second, we treated high-fat diet-fed hamsters with PC to determine whether the treatment improved plasma lipids and attenuated atherosclerosis progression. We then assessed PC's effects on the gut microbiota by 16S rDNA sequencing and performed fecal microbiota transplantation in hamster models. Finally, we used human umbilical vein endothelial cells (HUVECs) to probe molecular mechanisms by which PC might inhibit oxidative stress and apoptosis. In a diet-induced atherosclerotic hamster model, PC treatment reduced atherosclerosis by decreasing lipid accumulation, oxidative stress, and apoptosis, and it restored gut microbiota balance while markedly lowering the abundance of TMAO-producing bacteria. PC also exerted antioxidant and anti-apoptotic effects and inhibited endothelial apoptosis via an MCPIP1-dependent mechanism. Together, these results indicate that PC suppresses atherosclerosis through two likely pathways: reduction of gut microbiota-derived TMAO production and inhibition of oxidative stress-driven endothelial apoptosis. Network pharmacology analysis of PC-specific blood-absorbed components supports these findings.},
}

@article {pmid41803498,
year = {2026},
author = {Zhou, H and Sun, R and Nie, X and Xia, L and Dong, H and Liu, Y and Hou, S and Dong, W and Zhu, X and Yao, Y and Zhao, GP and Lu, S and Wang, Y and Yang, C},
title = {A clinic-responder-derived defined microbial consortium enhances anti-PD-1 immunotherapy efficacy in mice.},
journal = {Nature microbiology},
volume = {},
number = {},
pages = {},
pmid = {41803498},
issn = {2058-5276},
support = {82241228//National Natural Science Foundation of China (National Science Foundation of China)/ ; 32230060//National Natural Science Foundation of China (National Science Foundation of China)/ ; 31925001//National Natural Science Foundation of China (National Science Foundation of China)/ ; 82073152//National Natural Science Foundation of China (National Science Foundation of China)/ ; 82241227//National Natural Science Foundation of China (National Science Foundation of China)/ ; 82030045//National Natural Science Foundation of China (National Science Foundation of China)/ ; 82241228//National Natural Science Foundation of China (National Science Foundation of China)/ ; },
abstract = {Targeting the gut microbiota is a promising strategy to enhance the efficiency of cancer immunotherapy; however, success has been limited. Here we combined metagenomic analysis and in silico prediction to identify bacterial species associated with immunotherapy response in patients with non-small-cell lung cancer. We constructed a defined consortium (RCom) of 15 bacterial species, most of which were isolated from responder patient faeces, associated with improved clinical response to anti-programmed cell death protein 1 (PD-1) treatment. Metabolic models and in vitro experiments revealed that RCom is a stable and cooperative community, and in vivo experiments showed that RCom engrafts and produces immunomodulatory metabolites. Oral administration of RCom improved the anti-tumour activity of anti-PD-1 by increasing the intratumoural infiltration and cytotoxic function of CD8[+] T cells in syngeneic tumour models and across mice with heterogeneity in baseline gut microbiota composition. RCom supplementation also limited anti-PD-1 resistance in mice conferred by faecal microbiota transplantation from individual non-responsive patients. These findings suggest that RCom is a potential adjuvant to improve responsiveness to anti-PD-1 therapy in cancer.},
}

@article {pmid41718556,
year = {2026},
author = {Johnson, KM and Grady, J and Kellermayer, R and Winter, HS and Tabibian, JH and Buness, CW and Fischer, R and Shah, A and Dulai, PS and Rangnekar, AS and Alrabadi, L and Shah, SB and Holtmann, G and Räisänen, L and Lewindon, P and Ali, AH},
title = {Oral vancomycin for primary sclerosing cholangitis and associated inflammatory bowel disease - paving a path forward.},
journal = {Expert review of gastroenterology & hepatology},
volume = {},
number = {},
pages = {1-14},
doi = {10.1080/17474124.2026.2635420},
pmid = {41718556},
issn = {1747-4132},
abstract = {INTRODUCTION: Primary sclerosing cholangitis (PSC) is a fibro-inflammatory cholangiopathy strongly associated with inflammatory bowel disease (PSC-IBD). With no approved PSC therapy, clinicians face uncertainty about oral vancomycin (OV) as a therapeutic option. This review synthesizes clinical effectiveness evidence alongside mechanistic data.

AREAS COVERED: We searched PubMed/Google Scholar for studies of vancomycin in PSC from 1998 through November, 2025. OV shows consistent IBD benefits and variable liver responses. In PSC-IBD, clinical and endoscopic remission occurred in 60% at 6 months and in 71% at 12 months in a pediatric cohort; in an adult single-arm study (n = 15), 80% achieved endoscopic remission at 4 weeks with universal mucosal healing, reductions in fecal calprotectin and Mayo scores, and relapse after withdrawal. For liver disease, a pediatric open-label cohort (n = 45) reported ≥50% declines in gamma-glutamyl transferase in 82%; in an adult pilot randomized controlled trial, alkaline phosphatase fell 46% at 12 weeks. Imaging/histology improved as evidenced by MRCP in 26/34 large-duct PSC and reduced portal/periportal inflammation in 11/12 small-duct PSC. No vancomycin-resistant enterococci development has been reported.

EXPERT OPINION: OV appears effective for colitis control in PSC-IBD. Differences in observed liver outcomes across studies likely reflect variation in treatment duration, dose, and endpoint selection. Liver responses may depend on higher doses. Cross-specialty guidance and pragmatic, integrated trials are needed.},
}

@article {pmid41554400,
year = {2026},
author = {Chen, N and Ai, R and Wen, Q and Wu, J and Zhang, F and Cui, B and Ji, G},
title = {Washed microbiota transplantation as salvage therapy for antibiotic-resistant Salmonella infection in two pediatric patients.},
journal = {International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases},
volume = {164},
number = {},
pages = {108408},
doi = {10.1016/j.ijid.2026.108408},
pmid = {41554400},
issn = {1878-3511},
mesh = {Humans ; *Salmonella Infections/therapy/microbiology ; *Salvage Therapy/methods ; Anti-Bacterial Agents/therapeutic use ; *Fecal Microbiota Transplantation/methods ; Male ; Female ; Child ; Treatment Outcome ; Child, Preschool ; Drug Resistance, Bacterial ; Salmonella/drug effects ; },
abstract = {OBJECTIVES: As antibiotic-resistant Salmonella infections pose a serious therapeutic challenge in children, this case report aims to introduce washed microbiota transplantation (WMT) as a novel salvage therapy.

DESIGN OR METHODS: Two pediatric patients with Salmonella infection received WMT as salvage therapy after failing antibiotic treatment.

RESULTS: Both patients achieved sustained clinical and microbiological remission.

CONCLUSION: WMT is a promising option for refractory pediatric salmonellosis.},
}

Humans
*Salmonella Infections/therapy/microbiology
*Salvage Therapy/methods
Anti-Bacterial Agents/therapeutic use
*Fecal Microbiota Transplantation/methods
Male
Female
Child
Treatment Outcome
Child, Preschool
Drug Resistance, Bacterial
Salmonella/drug effects

@article {pmid41802647,
year = {2026},
author = {Luo, J and Jin, X and Cui, M and He, H and Liao, J and Wen, W and Li, W and Cao, Y},
title = {Wulingsan Alleviates Metabolic dysfunction-associated Steatotic Liver Disease through Regulating Gut Microbiota-Bile Acid axis.},
journal = {Prostaglandins & other lipid mediators},
volume = {},
number = {},
pages = {107067},
doi = {10.1016/j.prostaglandins.2026.107067},
pmid = {41802647},
issn = {1098-8823},
abstract = {BACKGROUND: Metabolic dysfunction-associated Steatotic Liver Disease (MASLD) is closely linked to gut microbiota disorders and bile acid imbalance. Wulingsan (WLS) have shown promise in regulating these pathways, but its mechanism of action unclear. This study aimed to evaluate the therapeutic effect of WLS on the rat MASLD model from the perspectives of intestinal microbiota composition and bile acid homeostasis.

METHODS: The MASLD model was induced by a high-fat diet (HFD) and treated with different doses of WLS. Body weight and serum lipid profiles were monitored, inflammation were assessed to ELISA and RT-qPCR. H&E staining to evaluate histopathological changes. The 16S rRNA sequencing and LC-MS/MS analysis of gut microbiota composition and bile acid profiles. The fecal microbiota transplantation (FMT) experiment verified the effect of WLS on the gut microbiota.

RESULTS: WLS treatment reduces the body weight of MASLD rats, improves lipid indicators, and inhibits inflammation and liver damage. The results of the FMT experiment indicated that transplantation of fecal microbiota from WLS-treated donors regulated the gut microbial composition and restored bile acid metabolic homeostasis in recipient rats.

DISCUSSION: This study demonstrates that WLS treats MASLD by modulating multiple pathological pathways. Its effects in improving lipid metabolism and reducing hepatic inflammation align with the pathophysiological mechanisms of MASLD, indicating direct hepatoprotective actions. WLS intervention significantly restored gut microbiota diversity, increased the proportion of beneficial bacteria, suppressed potentially harmful bacterial genera, and corrected dysbiosis. FMT experiments further confirmed that gut microbes play a crucial role in mediating the therapeutic benefits of WLS. When microbiota from WLS-treated donors were transplanted into recipient rats, significant improvements were observed in metabolic markers, hepatic histopathology, and bile acid homeostasis. Collectively, the data support that WLS improves MASLD through a multi-targeted strategy centered on the gut-liver axis.

CONCLUSION: WLS has an effective therapeutic effect on MASLD by improving lipid metabolism, reducing liver inflammation, reshaping the intestinal microbiota and normalizing bile acid homeostasis.},
}

@article {pmid41802308,
year = {2026},
author = {Han, JY and Kim, MJ and Park, JW and Jeong, SY},
title = {Gut microbiome in colorectal cancer: recent advances and clinical implications.},
journal = {Annals of coloproctology},
volume = {42},
number = {1},
pages = {72-85},
doi = {10.3393/ac.2026.00010.0001},
pmid = {41802308},
issn = {2287-9714},
abstract = {The gut microbiome is not just a bystander of colorectal carcinogenesis but is an active driver of colorectal cancer (CRC). CRC-associated microbiome contributes in the tumorigenesis through chronic inflammation, formation of toxic metabolite and genotoxins, oncogenic signal activation, immune evasion, and barrier disruption-all reinforcing a tumor microenvironment. In contrast, beneficial microbiome supports the barrier-immune-metabolic axis by maintaining mucosal integrity and balanced immune tone. Despite extensive studies of microbiome-based CRC biomarkers, microbiome-based CRC biomarkers have not been yet ready for routine clinical use due to variation across populations and lack of standardization of key steps such as sampling, analysis, cutoffs, and interpretation. Microbiome-based therapies aim to change the overall intestinal ecosystem rather than simply adding or removing single strains. At present, dietary modulation and prebiotics are considered supportive measures, while probiotics or synbiotics are in preclinical stage. Fecal microbiota transplantation (FMT) still faces important challenges in effectiveness, standardization and safety. By its role in reshaping the tumor-host immune environment, FMT is viewed as a potential option for cancer therapy after further development through well-controlled clinical trials with careful safety monitoring.},
}

@article {pmid41801218,
year = {2026},
author = {Zhang, Y and Teng, M and He, W and Li, L and Zhang, Y and Wang, S and Wang, C and Wang, D},
title = {4-Hydroxybenzyl Alcohol Mitigates Hyperlipidemia-Associated Depression by Inhibiting Neuroinflammation via the NKIRAS2/NF-κB Pathway.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e17873},
doi = {10.1002/advs.202517873},
pmid = {41801218},
issn = {2198-3844},
support = {20240101212JC//Natural Science Foundation of Jilin Province/ ; },
abstract = {Epidemiological data link hyperlipidemia to increased depression susceptibility. This study investigates the potential involvement of 4-hydroxybenzyl alcohol (4-HBA), a bioactive molecule known for its neuroprotective and anti-inflammatory effects, in the pathophysiology of hyperlipidemia-associated depression. High-fat diet (HFD)-fed mice develop concurrent hyperlipidemia and depression-like behaviors, with 4-HBA identified as a key modulated brain metabolite in fecal microbiota transplantation recipients. In HFD-fed mice, 4-HBA treatment simultaneously improves lipid metabolism and significantly alleviates depression-like behaviors, accompanied by suppression of the nuclear factor κB (NF-κB) signaling pathway in the brain. In LPS-stimulated BV2 cells, 4-HBA inhibits NF-κB activation through NF-κB inhibitor interacting Ras-like 2 (NKIRAS2), thereby coordinating the downregulation of inflammatory responses. Conditioned medium from 4-HBA-treated BV2 cells enhances neuronal viability and reduces inflammatory responses in HT22 neurons in co-culture. Importantly, silencing Nkiras2 in BV2 cells and organotypic brain slice cultures negated the anti-inflammatory and neuroprotective actions of 4-HBA. These findings demonstrate that the NKIRAS2/NF-κB pathway is a molecular mediator underlying the biological effects of 4-HBA. These findings position 4-HBA as a dual-action metabolite capable of concurrently mitigating metabolic and psychiatric manifestations through neuroinflammatory regulation.},
}

@article {pmid41800260,
year = {2026},
author = {Zhang, J and Yan, S and Gao, T and Li, M and Li, Y and Li, L and Ji, D and Bian, Z and Huang, W and Hou, J and Lu, T and Su, L},
title = {Gut Microbiota-driven Tryptophan Metabolism Towards the Indole Pathway Mediates Schisandra Chinensis Polysaccharide's Alleviation of Ulcerative Colitis and Comorbid Depression via Aryl Hydrocarbon Receptor.},
journal = {International journal of biological sciences},
volume = {22},
number = {5},
pages = {2557-2580},
pmid = {41800260},
issn = {1449-2288},
mesh = {*Gastrointestinal Microbiome/drug effects ; *Tryptophan/metabolism ; *Receptors, Aryl Hydrocarbon/metabolism ; Animals ; *Colitis, Ulcerative/drug therapy/metabolism ; Mice ; *Schisandra/chemistry ; *Depression/drug therapy/metabolism ; *Polysaccharides/pharmacology/therapeutic use ; *Indoles/metabolism ; Male ; Mice, Inbred C57BL ; },
abstract = {Patients with ulcerative colitis (UC) exhibit heightened depression risk, linked to microbiota-gut-brain axis dysfunction. This study isolated a novel low-molecular-weight Schisandra chinensis polysaccharide (SCP) that ameliorated UC and comorbid depression by remodeling gut microbiota, redirecting tryptophan (Trp) metabolism toward the indole pathway, and activating aryl hydrocarbon receptor (AhR). Structurally, SCP features a →4)-α-D-Glcp backbone with O-6 branched chains. In dextran sulfate sodium-induced UC mice, SCP mitigated colonic inflammation, restored intestinal barrier integrity, and improved depression-like behaviors by repairing blood-brain barrier, reducing neuroinflammation, preserving hippocampal neurons, and modulating synaptic plasticity. Multi-omics revealed SCP enriched beneficial microbiota (e.g., Limosilactobacillus reuteri) and rebalanced Trp metabolism along the gut-brain axis. SCP suppressed the hyperactive kynurenine (Kyn) pathway (reduced Kyn/Trp ratio) while elevating indole-3-propionic acid (IPA) levels in colon, serum, and hippocampus. Functioning as a pivotal molecule, IPA exerted dual anti-inflammatory effects in both colon and hippocampus via AhR activation and NF-κB inhibition. Antibiotic depletion and fecal microbiota transplantation validated SCP's microbiota-dependent efficacy, while IPA supplementation recapitulated SCP's benefits. AhR inhibition abolished SCP's therapeutic actions, confirming AhR as the critical target. Collectively, these findings propose a novel therapeutic strategy for UC and associated depression, highlighting SCP's potential value in targeting the Trp metabolism-AhR axis.},
}

*Gastrointestinal Microbiome/drug effects
*Tryptophan/metabolism
*Receptors, Aryl Hydrocarbon/metabolism
Animals
*Colitis, Ulcerative/drug therapy/metabolism
Mice
*Schisandra/chemistry
*Depression/drug therapy/metabolism
*Polysaccharides/pharmacology/therapeutic use
*Indoles/metabolism
Male
Mice, Inbred C57BL

@article {pmid41800246,
year = {2026},
author = {Liu, Y and Wang, S and Xiang, X and Du, Y and Xue, Q and Niu, Y and Peng, W and Ye, L and Zhou, Q},
title = {Gut-Lung Microbiota Axis Shapes the Immune Microenvironment and Immunotherapeutic Response in Lung Cancer.},
journal = {International journal of biological sciences},
volume = {22},
number = {5},
pages = {2265-2284},
pmid = {41800246},
issn = {1449-2288},
mesh = {Humans ; *Lung Neoplasms/immunology/therapy/microbiology ; *Gastrointestinal Microbiome/physiology/immunology ; *Tumor Microenvironment/immunology ; *Immunotherapy/methods ; *Lung/microbiology/immunology ; Dysbiosis ; Animals ; },
abstract = {The gut-lung axis microbiota plays a pivotal role in shaping the tumor immune microenvironment (TIME) and regulating immunotherapeutic responses in lung cancer. This review highlights that pulmonary and gut microbial dysbiosis drives lung cancer development through inducing chronic inflammation, remodeling the immune microenvironment, and reprogramming metabolism. Lung cancer patients exhibit distinct microbial signatures characterized by altered microbiotal diversity and enrichment of specific taxa like Streptococcus, Veillonella, and Bacteroidetes in the airways, along with gut microbial shifts involving decreased Firmicutes/Bacteroidetes ratio. These microbial alterations promote tumor progression via activation of pro-inflammatory pathways (e.g., interleukin-17 (IL-17)/interleukin-23 (IL-23) axis) and suppression of antitumor immunity.Notably, the gut-lung microbiome exerts a profound impact on immunotherapeutic efficacy: responders are enriched with beneficial microbes like Akkermansia muciniphila and Bifidobacterium that enhance CD8[+] T cell responses, while non-responders show elevated levels of Gammaproteobacteria and Fusobacterium associated with immunosuppression. Regulatory mechanisms include systemic immune modulation by microbial metabolites such as short-chain fatty acids, as well as activation of key signaling pathways including cGAS-STING and CD40L-CD40/NF-κB. Emerging translational applications encompass lung cancer diagnosis and immunotherapeutic response prediction via microbial biomarkers, as well as therapeutic interventions including fecal microbiota transplantation (FMT) and probiotic supplementation. Future studies should clarify microbe-host interaction mechanisms and develop personalized microbiota-based strategies to overcome immunotherapy resistance, offering the potential to revolutionize precision oncology through integrating microbiota modulation with conventional therapies.},
}

Humans
*Lung Neoplasms/immunology/therapy/microbiology
*Gastrointestinal Microbiome/physiology/immunology
*Tumor Microenvironment/immunology
*Immunotherapy/methods
*Lung/microbiology/immunology
Dysbiosis
Animals

@article {pmid41800020,
year = {2026},
author = {Park, U and Heo, JY and Chun, SM and Lee, JC and Lee, SH and Lee, SW},
title = {Harnessing the Gut Microbiota to Improve Cancer Immunotherapy: Focus on Lung Cancer.},
journal = {Immune network},
volume = {26},
number = {1},
pages = {e7},
pmid = {41800020},
issn = {1598-2629},
abstract = {The gut microbiota has emerged as a key orchestrator of systemic immunity, capable of reshaping the tumor microenvironment and modulating responses to cancer immunotherapy via the gut-lung axis. While immune checkpoint blockade (ICB) has revolutionized lung cancer treatment, a significant proportion of patients fail to respond. Accumulating evidence suggests that intestinal microbial composition modulates antitumor immunity, yet clinical associations between specific microbial taxa and ICB outcomes often show inconsistencies across cohorts. In this review, we synthesize current mechanistic insights into how gut microbial metabolites and structural components modulate pulmonary immune surveillance. We critically examine the clinical landscape of microbiome signatures in non-small cell lung cancer (NSCLC), highlighting how species- and strain-level heterogeneity contributes to divergent findings. Finally, we discuss translational strategies-ranging from fecal microbiota transplantation to rationally designed bacterial consortia and engineered probiotics-and propose a roadmap for integrating multi-omics with microbiome engineering to overcome current limitations and optimize precision immunotherapy.},
}

@article {pmid41798939,
year = {2026},
author = {Le, G and Wen, R and Huang, Z and Fang, H and Zheng, J and Wang, Y and Luo, H},
title = {Integrating network pharmacology, microbiomics, and metabolomics to uncover the therapeutic effect of Liubao tea on osteoarthritis.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1746350},
pmid = {41798939},
issn = {1664-3224},
mesh = {Animals ; Mice ; *Metabolomics/methods ; *Gastrointestinal Microbiome/drug effects ; *Osteoarthritis/drug therapy/metabolism/microbiology ; *Network Pharmacology ; Male ; Disease Models, Animal ; *Tea/chemistry ; Fecal Microbiota Transplantation ; *Plant Extracts/pharmacology ; Mice, Inbred C57BL ; },
abstract = {BACKGROUND: Osteoarthritis (OA) is a debilitating joint disorder for which with no effective disease-modifying drugs are currently available. Liubao tea, a traditional Chinese post-fermented tea, exhibits diverse bioactivities, including anti-inflammatory properties and the ability to regulate gut microbiota. However, its potential therapeutic efficacy and underlying mechanism in the context of OA remain insufficiently elucidated.

METHODS: A mouse model of osteoarthritis (OA) induced by destabilization of the medial meniscus (DMM) was established, and the mice were treated with low- and high-dose Liubao tea extract. Micro-CT, histological staining (H&E, Safranin O-Fast Green), and enzyme-linked immunosorbent assay (ELISA) were performed to evaluate joint structure, cartilage damage, and inflammatory cytokine levels. 16S rRNA sequencing, fecal microbiota transplantation (FMT), and untargeted serum metabolomics were conducted to explore gut microbiota and metabolic changes. Additionally, Brequinar, a de novo pyrimidine synthesis inhibitor, was used to verify the role of pyrimidine metabolism. Ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) was used to analyze the chemical components of Liubao tea. Network pharmacology was employed to identify the active components and their potential targets in OA treatment. Molecular docking was performed to evaluate the interactions between key components and hub targets.

RESULTS: Liubao tea treatment significantly ameliorated DMM-induced OA progression, as evidenced by improved subchondral bone microarchitecture (increased bone volume/total volume [BV/TV], trabecular number [Tb.N], trabecular thickness [Tb.Th]; decreased trabecular separation [Tb.Sp]), the reduced cartilage erosion (lowered the modified Mankin and OARSI scores), and the suppressed systemic inflammation (decreased interleukin [IL]-6, IL-1β, tumor necrosis factor [TNF]-α levels). Liubao tea remodeled gut microbiota homeostasis (increased α-diversity and altered bacterial taxa), and fecal microbiota transplantation (FMT) from Liubao tea-treated mice recapitulated its anti-OA effects. Metabolomic analysis revealed that Liubao tea significantly downregulated the pyrimidine metabolism pathway, and Brequinar treatment mimicked its therapeutic benefits, confirming the role of pyrimidine metabolism suppression in OA alleviation. UPLC-MS/MS and network pharmacology analyses identified 1,989 metabolites in Liubao tea, including 273 bioactive components (e.g., flavonoids, lignans) that targeted 324 OA-related genes. The molecular docking results demonstrated that Eupatilin, 5,6,7,8-Tetramethoxyflavone, and 5-Hydroxy-6,7,3',4',5'-Pentamethoxyflavone exhibited potential interactions with the hub targets TP53, IL6, and TNF.

CONCLUSION: Liubao tea attenuates OA progression by modulating the composition of the gut microbiota and inhibiting the pyrimidine metabolism pathway, highlighting its potential as a novel natural therapeutic agent for OA.},
}

Animals
Mice
*Metabolomics/methods
*Gastrointestinal Microbiome/drug effects
*Osteoarthritis/drug therapy/metabolism/microbiology
*Network Pharmacology
Male
Disease Models, Animal
*Tea/chemistry
Fecal Microbiota Transplantation
*Plant Extracts/pharmacology
Mice, Inbred C57BL

@article {pmid41798759,
year = {2026},
author = {Huang, Z and Mei, X and Zhou, Y},
title = {The gut microbiota: an emerging therapeutic target for ICI-associated myocarditis.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1752485},
pmid = {41798759},
issn = {2235-2988},
mesh = {Humans ; *Gastrointestinal Microbiome/drug effects/immunology ; *Myocarditis/chemically induced/therapy/microbiology/prevention & control ; *Immune Checkpoint Inhibitors/adverse effects/therapeutic use ; Probiotics/therapeutic use ; Anti-Bacterial Agents/therapeutic use ; Neoplasms/drug therapy ; Animals ; Fecal Microbiota Transplantation ; },
abstract = {Gut microbiota and their metabolites are essential for a wide range of human physiological processes, including inflammation, immunity, and homeostasis. The intricate interplay between gut microbiota and the host immune system profoundly influences both the therapeutic response and the immune-related adverse events (irAEs) in cancer patients undergoing immune checkpoint inhibitors (ICIs) therapy. Prior evidence has established the rationale for modulating the gut microbiota to improve the incidence and prognosis of ICI-associated myocarditis. In the future, we may prevent or treat ICI-associated myocarditis by regulating the gut microbiota through methods such as microbiota transplantation, antibiotic regimens, or probiotic supplements. But there is still a considerable distance between research and clinical practice.},
}

Humans
*Gastrointestinal Microbiome/drug effects/immunology
*Myocarditis/chemically induced/therapy/microbiology/prevention & control
*Immune Checkpoint Inhibitors/adverse effects/therapeutic use
Probiotics/therapeutic use
Anti-Bacterial Agents/therapeutic use
Neoplasms/drug therapy
Animals
Fecal Microbiota Transplantation

@article {pmid41798257,
year = {2026},
author = {Liu, J and Wu, X},
title = {Fecal microbiota transplantation in ulcerative colitis: evidence, mechanisms, and practice considerations.},
journal = {Therapeutic advances in gastroenterology},
volume = {19},
number = {},
pages = {17562848261426284},
pmid = {41798257},
issn = {1756-283X},
abstract = {Ulcerative colitis (UC) is a chronic inflammatory bowel disease strongly associated with intestinal dysbiosis, reduced microbial diversity, and disrupted microbial metabolite profiles. Fecal microbiota transplantation (FMT) aims to restore microbial homeostasis and has shown a signal of benefit for induction of remission in some trials, but results are heterogeneous and long-term maintenance efficacy remains uncertain. In this narrative review, we synthesize randomized controlled trials (RCTs), systematic reviews/meta-analyses, and recent guideline and regulatory updates on FMT in UC, and integrate mechanistic insights from microbiome and metabolomics research. Across RCTs, intensive lower-gastrointestinal regimens using pooled, multidonor material, and/or anaerobic processing have most consistently achieved modestly higher steroid-free clinical and endoscopic remission than placebo in mild-to-moderate UC (approximately 25%-32% vs 5%-10% in representative studies), whereas upper-gastrointestinal delivery or oral lyophilized formulations and highly restrictive donor selection have yielded mixed or negative results. Mechanistically, responders commonly demonstrate engraftment of short-chain fatty acid producing taxa and restoration of secondary bile acid pathways. Safety profiles in trials are generally comparable to placebo for common mild adverse events, but rare severe transmissions (e.g., multidrug-resistant Escherichia coli and SARS-CoV-2) have driven stricter donor screening and have limited routine use outside regulated programs. Current guidelines recommend against FMT for UC outside clinical trials. Future work should prioritize standardized protocols, biomarker-guided personalization, combination strategies (diet/priming), and development of defined microbial therapeutics to improve efficacy and safety.},
}