@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.},
}

@article {pmid41797849,
year = {2026},
author = {Jalalifar, S and Bajelan, B and Mohammadi, R and Ghafoury, R and Kalhori, Z and Pooshang-Bagheri, K and Nekouian, R and Faranoush, M},
title = {The impact of gut microbiota on leukemia and prospects for novel therapies.},
journal = {Infectious medicine},
volume = {5},
number = {1},
pages = {100239},
pmid = {41797849},
issn = {2772-431X},
abstract = {The Human Microbiome Project has underscored the pivotal role of the gut microbiome in human health, revealing its potential influence on leukemia development, progression, and treatment response. This review summarizes evidence on microbiome-targeted therapies such as probiotics, fecal microbiota transplantation, antimicrobial peptides, and nanoparticles. These approaches may improve leukemia treatment outcomes through immune and metabolic modulation and reduced toxicity. Although emerging data suggest beneficial effects, most findings remain correlative and limited by small, heterogeneous studies. Further mechanistic and clinical research is required to clarify causal pathways, standardize interventions, and evaluate long-term safety. Personalized microbiome-based strategies that integrate molecular and immunologic profiling may ultimately refine leukemia management and improve survival.},
}

@article {pmid41797510,
year = {2026},
author = {Sajid, S and Huang, J and Kong, S and Lai, C and Tan, Z and Shao, Y and Guo, L},
title = {A Multi-Organ Atlas Links Gut Microbial Metabolites to Systemic Redox Changes in Aging Mice.},
journal = {Aging cell},
volume = {25},
number = {3},
pages = {e70433},
doi = {10.1111/acel.70433},
pmid = {41797510},
issn = {1474-9726},
support = {82273757//National Natural Science Foundation of China/ ; 82574226//National Natural Science Foundation of China/ ; 2023B1515020106//Natural Science Foundation of Guangdong Province/ ; 4SG25295G//Discipline Construction Project of Guangdong Medical University/ ; 4SG25239G//Discipline Construction Project of Guangdong Medical University/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; Mice ; *Aging/metabolism ; Oxidation-Reduction ; Mice, Inbred C57BL ; Male ; },
abstract = {Aging disrupts systemic metabolism, but the mechanisms by which gut microbial metabolites drive tissue-specific decline remain unclear. We conducted a multi-organ, multi-omics atlas across the gut, serum, liver, lung, and cortex in young and early-aged mice to address this. We identified a conserved aging signature marked by the microbiota-associated depletion of protective circulating metabolites, such as lysophosphatidylcholines (LPCs), concurrently with the systemic accumulation of pro-oxidative microbial catabolites, specifically trimethylamine N-oxide (TMAO) and indole-3-acetic acid (IAA). This microbial-metabolic drift disrupted systemic lipid transport and redox balance, leading to distinct organ-level vulnerabilities: hepatic lipid retention and ferroptosis susceptibility, pulmonary immune-redox activation, and cortical neurochemical dysregulation. To establish functional relevance, we conducted an integrated meta-analysis of 40 independent studies encompassing natural aging models, fecal microbiota transplantation (FMT), and probiotic interventions. This quantitative synthesis provided convergent evidence that microbial remodeling is a functionally relevant correlate associated with systemic aging phenotypes by restoring intestinal barrier integrity (upregulating ZO-1, MUC2), suppressing tissue inflammatory factors (IL-6, IL-1β, TNF-α), and mitigating oxidative stress (reducing MDA and restoring SOD/GSH). Together, our findings highlight gut-derived metabolic reprogramming as a modifiable, upstream driver of systemic aging, offering tractable targets for therapeutic intervention.},
}

Animals
*Gastrointestinal Microbiome/physiology
Mice
*Aging/metabolism
Oxidation-Reduction
Mice, Inbred C57BL
Male

@article {pmid41794466,
year = {2026},
author = {Huang, S and Ding, H and Su, Y and Chen, Z and He, W and Chen, ZY and Zhu, H},
title = {Alpha-lipoic acid improves intestinal homeostasis and ameliorates colitis through modulation of gut microbiota and production of short chain fatty acids in mice.},
journal = {Food research international (Ottawa, Ont.)},
volume = {230},
number = {},
pages = {118582},
doi = {10.1016/j.foodres.2026.118582},
pmid = {41794466},
issn = {1873-7145},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Fatty Acids, Volatile/metabolism ; *Thioctic Acid/pharmacology ; *Colitis/chemically induced/drug therapy/microbiology ; Mice, Inbred C57BL ; Male ; *Homeostasis/drug effects ; Mice ; Dextran Sulfate ; Fecal Microbiota Transplantation ; Oxidative Stress/drug effects ; NF-kappa B/metabolism ; Disease Models, Animal ; Antioxidants/pharmacology ; Cytokines/metabolism ; },
abstract = {α-Lipoic acid (ALA) is a natural antioxidant present in both plants and animal foods. It has attracted growing attention for its potential role in maintenance of intestinal homeostasis. This study was to investigate the protective effects of dietary ALA on experimental colitis, and to evaluate its modulating effect on gut microbiome in mice. Male C57BL/6 J mice with dextran sulfate sodium (DSS)-induced acute colitis were administered ALA (40 or 80 mg/kg) dissolved in corn oil. Results showed that dietary ALA ameliorated colitis severity, improved intestinal barrier integrity, and attenuated inflammation by reducing oxidative stress and suppressing NF-κB pathway activation and pro-inflammatory cytokines expression. Moreover, dietary ALA increased the microbial diversity (Shannon index), reshaped gut microbiota composition by suppressing pathogenic bacteria and promoting beneficial taxa such as Akkermansia, and elevated levels of short chain fatty acids (SCFA). Fecal microbiota transplantation (FMT) further confirmed that ALA could modulate gut microbiota and protect against colitis in mice. In conclusion, ALA could effectively maintain the intestinal homeostasis and ameliorate colitis at least in mice. Such protective effect of ALA in gut health was mediated through modulation of gut microbiota and enhancement of SCFA production.},
}

Animals
*Gastrointestinal Microbiome/drug effects
*Fatty Acids, Volatile/metabolism
*Thioctic Acid/pharmacology
*Colitis/chemically induced/drug therapy/microbiology
Mice, Inbred C57BL
Male
*Homeostasis/drug effects
Mice
Dextran Sulfate
Fecal Microbiota Transplantation
Oxidative Stress/drug effects
NF-kappa B/metabolism
Disease Models, Animal
Antioxidants/pharmacology
Cytokines/metabolism

@article {pmid41543553,
year = {2026},
author = {Strateva, T and Niyazi, D and Stoeva, T and Peykov, S},
title = {Resistome and phylogenomic analysis of trimethoprim-sulfamethoxazole-resistant Stenotrophomonas maltophilia complex isolates obtained from Bulgarian hematopoietic stem cell transplant recipients.},
journal = {Acta microbiologica et immunologica Hungarica},
volume = {73},
number = {1},
pages = {59-70},
doi = {10.1556/030.2026.02794},
pmid = {41543553},
issn = {1588-2640},
mesh = {Humans ; *Stenotrophomonas maltophilia/genetics/drug effects/isolation & purification/classification ; Phylogeny ; *Trimethoprim, Sulfamethoxazole Drug Combination/pharmacology ; *Anti-Bacterial Agents/pharmacology ; *Hematopoietic Stem Cell Transplantation/adverse effects ; *Gram-Negative Bacterial Infections/microbiology ; Bulgaria ; Whole Genome Sequencing ; Microbial Sensitivity Tests ; Genome, Bacterial ; Transplant Recipients ; Male ; Drug Resistance, Multiple, Bacterial ; Female ; Adult ; Middle Aged ; Feces/microbiology ; },
abstract = {The present study aimed to investigate the resistome of four trimethoprim-sulfamethoxazole (SXT)-resistant Stenotrophomonas maltophilia complex (Smc) isolates from Bulgarian hematopoietic stem cell transplantation (HSCT) recipients and to subject them to phylogenomic analysis involving all sul1-positive strains of the identified species with available genomes worldwide. Preliminary identification by MALDI-TOF mass spectrometry determined all four isolates as S. maltophilia. The sources of isolation were stools (SM175, SM176, and SM179) and urine (SM178). SM176 and SM178 also showed high-level levofloxacin resistance. All isolates demonstrated in vitro susceptibility to minocycline and cefiderocol. Whole-genome sequencing (WGS) assigned SM175, SM176, and SM178 as Stenotrophomonas forensis. Two types of class 1 integrons were detected in the four isolates, namely SM175 and SM179 carried empty integrons, whereas SM176 and SM178 carried a gene cassette (3,748 bp in length) consisting of aac6'-Ib-cmlB-blaOXA-9. Alignment against public databases revealed that this cassette has not been found in Stenotrophomonas species so far, but it was present in Pseudomonas aeruginosa and Enterobacterales. Phylogenomic analysis of our assembled sequences, together with all 26 sul1-positive S. maltophilia and S. forensis genomes, indicated that S. maltophilia SM179 was not part of any S. maltophilia cluster. SM175, SM176, and SM178 were closely related (differences of 35-101 SNPs). To the best of our knowledge, this is the first report of SXT-resistant Smc isolates from post-HSCT patients with hematological malignancies in Bulgaria, which presents WGS-based resistome and phylogenomic analyses. We also report on the first sul1-containing S. forensis clinical isolates. Our findings reveal high global heterogeneity of sul1-positive S. maltophilia.},
}

Humans
*Stenotrophomonas maltophilia/genetics/drug effects/isolation & purification/classification
Phylogeny
*Trimethoprim, Sulfamethoxazole Drug Combination/pharmacology
*Anti-Bacterial Agents/pharmacology
*Hematopoietic Stem Cell Transplantation/adverse effects
*Gram-Negative Bacterial Infections/microbiology
Bulgaria
Whole Genome Sequencing
Microbial Sensitivity Tests
Genome, Bacterial
Transplant Recipients
Male
Drug Resistance, Multiple, Bacterial
Female
Adult
Middle Aged
Feces/microbiology

@article {pmid41792768,
year = {2026},
author = {Zhang, S and Tang, S and Han, H and Xu, Y and Liu, D and Wang, H and Zhong, R and Chen, L and Zhang, H},
title = {Lactobacillus reuteri SKLAN202402ZF inhibited by early-life lincomycin exposure alleviate intestinal damage and inflammation sensitivity.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-025-02327-z},
pmid = {41792768},
issn = {2049-2618},
abstract = {BACKGROUND: Early-life lincomycin and related antibiotics exposure affected gut microbiota composition and intestinal health, but which microbes play a dominant role in this process remains unclear.

RESULTS: Lactobacillus reuteri was suppressed in piglets exposed to lincomycin. Meanwhile, early-life lincomycin exposure caused intestinal morphological damage and decreased the expression of Claudin-1, Occludin, and ZO-1. Mice transplanted with lincomycin-exposed piglet fecal microbiota showed more severe inflammation and weight loss after LPS infection, and decreased colon Lactobacillus abundance. Furthermore, mice supplemented with Lactobacillus reuteri SKLAN202402ZF showed reduced lincomycin-related intestinal damage and inflammation after LPS infection. Specifically, Lactobacillus reuteri SKLAN202402ZF inhibits the expression of TLR4, MyD88, and NLRP3, and thus reduced the release of inflammatory factors such as IL-1β, IL-18, IL-17.

CONCLUSIONS: Lincomycin exposure affects the composition of gut microbes and increases subsequent susceptibility to LPS, while Lactobacillus reuteri SKLAN202402ZF has protective potential against antibiotic- associated intestinal inflammation.},
}

@article {pmid41792366,
year = {2026},
author = {Ikram, S and Ullah, M and Lee, J and Hasan, N and Yoo, JW and Khan, R and Naeem, M},
title = {Fecal microbiota transplantation in inflammatory bowel disease: a systematic review and meta-analysis of randomized controlled trials (2020-2025).},
journal = {Inflammopharmacology},
volume = {},
number = {},
pages = {},
pmid = {41792366},
issn = {1568-5608},
abstract = {BACKGROUND: Fecal microbiota transplantation (FMT) has emerged as a therapeutic strategy for Inflammatory Bowel Disease (IBD) including ulcerative colitis (UC) and Crohn's disease (CD). Although multiple randomized controlled trials (RCTs) have been published in recent years, evidence remains fragmented regarding safety and efficacy. This systematic review and meta-analysis evaluated the efficacy and safety of microbiome-based interventions in Inflammatory Bowel Disease (IBD).

METHODS: A systematic search of PubMed, Cochrane CENTRAL and Embase was conducted for randomized controlled trials (RCTs) published between January 2020 and May 2025. Eligible studies compared donor FME with placebo, autologous FMT or standard therapy in adult patients with IBD. Primary outcomes were clinical remission and endoscopic improvement; secondary outcomes included maintenance of remission and adverse events. Risk of bias was assessed using the Cochrane RoB-2 tool. Meta-analyses were performed in R using the meta and meta for packages. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were estimated using common-effects and random-effects models.

RESULTS: Six RCTs involving 220-230 patients were included (majority UC patients, two trials CD). For induction of clinical remission, FMT was associated with significantly higher rates vs controls (OR = 3.24, 95% CI 1.43-7.41, p = 0.005) under a common-effect model; random-effects model showed similar point estimate but wide CI overlapping unity. Endoscopic response was strongly increased with FMT (OR = 6.80, 95% CI 2.96-15.63, p < 0.0001). Serious adverse events were more common in FMT arms but not statistically significant (common-effects OR ~ 2.05, 95% CI 0.72-5.81, p = 0.18). Evidence for maintenance of remission from two trials was limited and inconsistent.

CONCLUSION: Microbiome-based therapies, particularly FMT, significantly improved clinical and endoscopic remission in IBD (especially in UC) compared with control interventions, but safety signals and maintenance efficacy remain uncertain. Larger and strictly designed UC and CD-specific RCTs are needed to confirm long-term efficacy, clarify safety and define the role of microbiome-targeted therapies in IBD management.},
}

@article {pmid41792228,
year = {2026},
author = {Kim, DJ and Lee, YJ and Choi, JW and Lee, HS and Lee, WS and Park, HS and Choi, EJ and Park, H and Lee, JH and Lee, JH and Lee, SB and Choi, Y and Koh, SJ},
title = {Early fecal metabolomic profiling for predicting acute graft-versus-host disease following allogeneic hematopoietic stem cell transplantation.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-38818-8},
pmid = {41792228},
issn = {2045-2322},
support = {2025IP0061-1//Grants from the Asan Institute for Life Sciences, Asan Medical Center, Seoul, Korea/ ; 2025//International Congress of BMT, funded by the Korean Society of Blood and Marrow Transplantation/ ; 26-2021-0060//Seoul National University Hospital Research Fund/ ; },
}

@article {pmid41791695,
year = {2026},
author = {Chandra, QM and Clister, D and Halim, P and Dalimunthe, A and Ichwan, M and Sari, DK and Umaya, C and Aktary, N and Rani, A and Park, MN and Kim, B and Syahputra, RA},
title = {Harnessing the gut-heart axis for cardiovascular drug innovation: microbiome, metabolites, and personalized treatment strategies.},
journal = {Clinica chimica acta; international journal of clinical chemistry},
volume = {},
number = {},
pages = {120941},
doi = {10.1016/j.cca.2026.120941},
pmid = {41791695},
issn = {1873-3492},
abstract = {Cardiovascular disease (CVD) remains the leading cause of mortality worldwide despite major advances in pharmacotherapy. Emerging evidence reveals a pivotal role for the gut-heart axis, wherein gut microbiota are and their metabolites influence CV physiology, pathology, and drug responsiveness. Dysbiosis in conditions such as hypertension, atherosclerosis, and heart failure has been associated with altered production of bioactive metabolites including trimethylamine N-oxide, short-chain fatty acids, bile acids, and tryptophan derivatives. These metabolites have been shown to modulate inflammation, endothelial function, lipid metabolism, and myocardial remodeling. This review synthesizes current knowledge on microbiome-drug interactions in CV pharmacology, including how gut bacteria may metabolize drugs (e.g., digoxin, aspirin, warfarin) and how CV agents can shape microbial communities. We further explore microbiome-targeted therapeutic strategies-probiotics, prebiotics, postbiotics, fecal microbiota transplantation, and small-molecule inhibitors of harmful metabolites-highlighting their mechanisms, preclinical evidence, and translational potential. Integrating microbiome profiling with multi-omics platforms and artificial intelligence may enable personalized treatment strategies that optimize CV outcomes. While the gut-heart axis presents an exciting frontier for drug innovation, challenges remain in establishing causality, addressing inter-individual microbiome variability, managing confounding factors such as diet and medication use, and meeting regulatory requirements. Harnessing this bidirectional relationship holds promise for transforming CV pharmacotherapy from a one-size-fits-all approach to precision medicine grounded in host-microbe interactions.},
}

@article {pmid41789806,
year = {2026},
author = {Nair, AV},
title = {Friend and Foe: Microbes in Orchestrating Immunity and Shaping Infection Dynamics.},
journal = {ACS infectious diseases},
volume = {},
number = {},
pages = {},
doi = {10.1021/acsinfecdis.5c00709},
pmid = {41789806},
issn = {2373-8227},
abstract = {Microbial communities, or microbiota, are fundamental regulators of host immunity and infection outcomes across diverse body sites, including the gut, skin, respiratory tract, and vagina. Despite advances, infectious diseases remain a global challenge, exacerbated by antimicrobial resistance and emerging pathogens. This review explores the dynamic interplay between microbiota, host immune responses, and pathogens, highlighting how microbial interactions shape immune homeostasis and colonisation resistance. The review discusses therapeutic approaches leveraging probiotics, prebiotics, defined microbial consortia, and fecal microbiota transplantation to enhance resistance against bacterial, viral, fungal, and parasitic infections. These microbiome-based strategies represent promising, sustainable alternatives to conventional antibiotics, offering scalable and mechanism-driven interventions. This review further underscores the potential of microbiota-informed therapies to contribute to effective infectious disease prevention and management while addressing global health challenges.},
}

@article {pmid41789426,
year = {2026},
author = {Xiao, Y and Li, J and Xiang, L and Xiu, W},
title = {The role of gut microbiota in liver metastasis of small cell lung cancer: mechanisms and therapeutic implications.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1767998},
pmid = {41789426},
issn = {2235-2988},
abstract = {Small cell lung cancer (SCLC) with liver metastases (LM), represents a highly aggressive clinical challenge characterized by significant morbidity, poor durable responses to chemoimmunotherapy, and limited therapeutic options. While most research has focused on tumor-intrinsic driver mutations and the local liver microenvironment, the remote influence of the gut microbiota on LM-SCLC pathogenesis remains a largely unexplored area. Emerging evidence from other cancer types suggests that the gut microbiota composition and its derived metabolites can modulate systemic immune tolerance, influence hepatic immune surveillance, and affect the efficacy and toxicity of anticancer therapies. This review synthesizes current knowledge on the gut-liver axis in cancer metastasis, with a specific focus on its pathogenesis. We discuss the molecular and immunological pathways through which gut microbial dysbiosis may promote an immunosuppressive liver microenvironment, facilitate the formation of a pro-metastatic niche, and impair anti-tumor responses. Specifically, we detail how translocated microbial products, such as lipopolysaccharide (LPS), and pro-tumorigenic secondary bile acids (SBAs) activate key hepatic immune cells (Kupffer cells, KCs) and stromal cells (hepatic stellate cells, HSCs). This activation modulates key signaling cascades and promotes the survival and outgrowth of circulating SCLC cells. Furthermore, we explore promising microbiota-based therapeutic strategies-including probiotics, prebiotics, fecal microbiota transplantation (FMT), and next-generation microbial therapeutics (NGMTs)-as novel approaches to augment standard-of-care treatments. A deeper understanding of the interplay between the gut microbiota and LM-SCLC is essential for opening new avenues for personalized combination therapies and improving outcomes for this high-risk patient population.},
}

@article {pmid41787060,
year = {2026},
author = {Li, X and Tian, X and Liu, P and Yuan, J and Liu, P and Ying, X and Guo, H and Ma, C and Zhao, D and Xuan, R and Zhao, Q and Li, B and Qiu, Y and Yan, X},
title = {Gut Microbiota Remodeling after Fecal Microbiota Transplantation Is Associated with Reduced Inflammation and Cardiac Injury in Fluoride-Arsenic Co-Exposed Rats.},
journal = {Biological trace element research},
volume = {},
number = {},
pages = {},
pmid = {41787060},
issn = {1559-0720},
support = {SD2417//Shanxi Medical University Provincial Doctoral Research Fund/ ; XD2312//Shanxi Medical University Doctoral Start-up Fund/ ; 202403021212261//the Shanxi Province Basic Research Program/ ; No.82103961//National Natural Science Foundation of China/ ; No.82173644//National Natural Science Foundation of China/ ; YDZJSX2024D064//Shanxi Province Central-Guided Local Science and Technology Development Fund Project/ ; },
abstract = {Groundwater co-contamination with arsenic and fluoride (AsF) has emerged as a widespread environmental and public health concern. Although the individual toxicities of arsenic and fluoride have been extensively studied, the mechanisms responsible for their combined cardiotoxic effects are still unclear. To address this gap, we first conducted an integrated network toxicology analysis to predict the potential molecular pathways involved in AsF-induced cardiotoxicity. The analysis identified inflammatory signaling, particularly the TLR4/NF-κB pathway, as a potential key mediator. Based on these findings, we established an animal model with fecal microbiota transplantation (FMT) intervention to investigate the interactive effects of AsF exposure and the microbiota-mediated molecular mechanisms involoved. The results clearly show that FMT in AsF-exposed rats is associated with improvements in cardiac parameters, reductions in LPS and cytokine levels, and significant changes in gut microbial composition. The TLR4/NF-κB pathway is implicated as a plausible mediating mechanism in this process. Concurrently, shifts in the abundance of Bacteroidetes were associated with changes in blood pressure. Collectively, these findings provide a new perspective for understanding the cardiotoxicity of environmental co-contaminants and offer experimental support for therapeutic strategies targeting the gut-heart axis.},
}

@article {pmid41786065,
year = {2026},
author = {Wang, X and Liu, R and Liu, J and Lin, Y and Zhou, M},
title = {Gut microbiota-derived indole metabolites in depression: mechanisms and therapeutic potential.},
journal = {European journal of pharmacology},
volume = {},
number = {},
pages = {178720},
doi = {10.1016/j.ejphar.2026.178720},
pmid = {41786065},
issn = {1879-0712},
abstract = {Depression, a prevalent neuropsychiatric disorder with complex pathophysiology and often insufficient treatment efficacy, is increasingly associated with disruptions in the gut-brain axis. This review focuses on the underappreciated role of the microbial indole pathway, a key route in tryptophan metabolism orchestrated by the gut microbiota. We synthesize recent evidence demonstrating that gut microbiota-derived indole metabolites, such as indole-3-propionic acid (IPA) and indole-3-aldehyde (IAld), are significantly reduced in depression. These metabolites exert multifaceted antidepressant effects by enhancing intestinal and blood-brain barrier integrity, suppressing neuroinflammation, and promoting neuroplasticity. Furthermore, we explore the therapeutic potential of targeting this axis through interventions like specific probiotics, prebiotics, dietary modifications, and fecal microbiota transplantation to restore microbial ecology and indole metabolite levels. By highlighting the microbiota-indole-brain pathway as a critical mechanistic and therapeutic frontier, this review provides a novel perspective on the pathogenesis and treatment of depression, moving beyond conventional monoaminergic theories.},
}

@article {pmid41785672,
year = {2026},
author = {Chen, Q and Feng, X and Wang, J and Zhu, H and Bo, Z and Wang, B and Zhao, Z},
title = {Impact of gut microbiota on hepatocellular carcinoma: Pathogenesis, diagnosis, prognosis, and therapeutic prospective.},
journal = {European journal of cancer (Oxford, England : 1990)},
volume = {237},
number = {},
pages = {116581},
doi = {10.1016/j.ejca.2026.116581},
pmid = {41785672},
issn = {1879-0852},
abstract = {Advances in sequencing technology have elucidated the complex role of the gut microbiota in hepatocellular carcinoma (HCC). Communication between the gut and the liver occurs via the gut-liver axis, and dysbiosis of the gut microbiota has been implicated in both the promotion and suppression of HCC. Furthermore, through interactions with host metabolism and immune system, the gut microbiota significantly influences treatment responses and prognostic outcomes of HCC. Despite progress in therapeutic strategies, clinical efficacy remains suboptimal, underscoring the need for a deeper understanding of the gut microbiota's role. This review highlights the potential of gut microbiota as novel biomarkers for the diagnosis and prognostic prediction of HCC, and explores its therapeutic implications. We summarize current insights into the molecular mechanisms underlying the gut microbiota-HCC interplay, and emphasize the relationship between gut microbiota and the efficacy of various treatments, including surgery, chemotherapy, radiotherapy, immunotherapy, and targeted agents. Microbiome-targeting interventions like probiotics, fecal microbiota transplantation (FMT), and dietary changes as emerging adjuvant strategies are also discussed in detail to provide potential resources for advancing translational hepatology. Although challenges remain, this review aims to provide valuable perspectives for developing individualized therapeutic strategies in HCC management.},
}

@article {pmid41785480,
year = {2026},
author = {Shekarriz, S and Vigod, SN and Bianco, T and Bala, A and Hao, C and Allard, JP and Hota, S and Poutanen, S and Surette, MG and Taylor, VH},
title = {The Safety, Efficacy, and Feasibility of Fecal Microbiota Transplantation in a Population With Bipolar Disorder During Depressive Episodes: A Pilot Parallel Arm Randomized Controlled Trial: Sécurité, efficacité et faisabilité de la transplantation de microbiote fécal chez une population atteinte de troubles bipolaires, au cours d'épisodes dépressifs : essai pilote contrôlé à répartition aléatoire et à groupes parallèles.},
journal = {Canadian journal of psychiatry. Revue canadienne de psychiatrie},
volume = {},
number = {},
pages = {7067437261420877},
doi = {10.1177/07067437261420877},
pmid = {41785480},
issn = {1497-0015},
abstract = {BackgroundThe gut microbiome has been proposed as a potential modifiable target to treat mental illness. This double-blind randomized control trial investigated fecal microbiota transplant (FMT) in bipolar disorder (BD) to assess efficacy, safety, and feasibility. The primary outcome evaluated the effectiveness of standard approved therapy for BD depression + FMT in individuals not responding to standard treatment, measured by change in the Montgomery-Åsberg Depression Rating Scale (MADRS) score from baseline to week 24. Secondary outcomes included FMT's impact on anxiety, global function, side-effects, and safety. The feasibility of this novel intervention was also assessed. Microbial analysis utilized whole-genome shotgun metagenomic sequencing, comparing outcomes between allogenic (donor) and autologous (participants own) FMT.MethodsA total of 35 participants (28 women and 7 men) with at least moderate depressive-phase BD (MADRS) were randomized to receive either allogenic FMT (n = 17) or autologous FMT (n = 18) via colonoscopy and were followed for 24 weeks.ResultsMADRS scores significantly improved from baseline to the last visit in both treatment arms. There was no significant difference between allogenic FMT (16.74-point improvement) and autologous FMT (15.4-point improvement) regarding clinical efficacy (t = -0.47, p-value = .64, 95% confidence interval [CI] = -7.3-4.6). Microbiota analysis showed that allogenic FMT let to a bacterial profile similar to the healthy donor and increased bacterial diversity at the 6-month mark, whereas those receiving autologous FMT did not. The intervention was well tolerated with no significant adverse events. Recruitment, randomization, and retention metrics support feasibility of a larger trial.ConclusionFeasibility and tolerability data indicate further investigation into microbial manipulation in BD is warranted. The absence of efficacy differences between the two types of FMT, despite microbial change, highlights the importance of a true placebo in future studies, as well as the importance of understanding exactly what bacteria are linked to improvements. ClinicalTrials.gov, NCT0327922.},
}

@article {pmid41785475,
year = {2026},
author = {Dinan, TG and Cryan, JF},
title = {Faecal Transplants for Bipolar Depression: Moving out of the Periphery?.},
journal = {Canadian journal of psychiatry. Revue canadienne de psychiatrie},
volume = {},
number = {},
pages = {7067437261428007},
doi = {10.1177/07067437261428007},
pmid = {41785475},
issn = {1497-0015},
}

@article {pmid41778019,
year = {2026},
author = {Huang, J and Zhang, Y and Zheng, W and Li, G},
title = {Gut microbiota contributes to gestational diabetes mellitus by interfering with bile acid metabolism and resistin.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1675560},
pmid = {41778019},
issn = {2235-2988},
mesh = {Animals ; *Bile Acids and Salts/metabolism ; *Diabetes, Gestational/microbiology/metabolism/etiology ; Female ; *Gastrointestinal Microbiome/physiology ; Pregnancy ; Mice, Inbred C57BL ; Mice ; Humans ; RNA, Ribosomal, 16S/genetics ; *Resistin/metabolism ; Metabolomics ; Disease Models, Animal ; Fecal Microbiota Transplantation ; Adult ; Lipopolysaccharides/blood ; },
abstract = {INTRODUCTION: Gestational diabetes mellitus (GDM) affects 6% to 15% of pregnancies globally, as a severe metabolic disorder that impairs offspring health. Mounting evidence highlights the critical role of gut microbiota in metabolic regulation, yet the causal relationship between gut microbiota and GDM pathogenesis remains unclear. This study aimed to clarify this causal link and explore the underlying mechanisms.

METHODS: An innovative human microbiota transplantation approach was adopted. Gut microbiota from GDM patients was transplanted into antibiotic-treated C57BL/6J mice. 16S rRNA sequencing was used to analyze the structural changes of gut microbiota in recipient mice, and metabolomics was employed to detect changes in circulating bile acid levels. For mechanism exploration, Luminex assay was used to detect multiple inflammatory factors, enzyme-linked immunosorbent assay (ELISA) was applied to measure lipopolysaccharide (LPS) levels, and Western blot (WB) was utilized to determine the expression of intestinal barrier protein.

RESULTS: Transplantation of gut microbiota from GDM patients directly induced glucose intolerance in pregnant antibiotic-treated C57BL/6J mice. 16S rRNA sequencing showed significant structural reorganization of the gut microbiota in GDM microbiota recipients, characterized by decreased abundance of Lachnospiraceae_FCS020_group and increased abundance of Akkermansia, Faecalibaculum, and Bilophila. These microbiota dysregulations led to reduced expression of the intestinal barrier protein Claudin-1, elevated serum lipopolysaccharide (LPS) levels, and increased resistin and matrix metalloproteinase 9 (MMP-9) levels. Metabolomic analysis revealed decreased circulating primary bile acids (cholic acid [CA] and chenodeoxycholic acid [CDCA]) and secondary bile acid deoxycholic acid (DCA). Correlation analysis indicated a positive correlation between Faecalibaculum and DCA, CDCA, as well as resistin. DCA and CDCA were significantly negatively correlated with HOMA-IR, while resistin was significantly positively correlated with GTT-AUC, FINS, and HOMA-β%.

CONCLUSION: These findings suggest that the imbalance in bile acid metabolism and mild inflammatory response caused by dysregulated gut microbiota is an adjustable environmental driving factor in the pathophysiological process of GDM.},
}

Animals
*Bile Acids and Salts/metabolism
*Diabetes, Gestational/microbiology/metabolism/etiology
Female
*Gastrointestinal Microbiome/physiology
Pregnancy
Mice, Inbred C57BL
Mice
Humans
RNA, Ribosomal, 16S/genetics
*Resistin/metabolism
Metabolomics
Disease Models, Animal
Fecal Microbiota Transplantation
Adult
Lipopolysaccharides/blood

@article {pmid41757237,
year = {2026},
author = {Wu, Q and Wang, M and Yang, J and Wang, J and Feng, S and Lu, S and Qin, Z and He, X and Wu, L},
title = {The influence of washed microbiota transplantation on menstruation in female patients of childbearing age.},
journal = {Frontiers in endocrinology},
volume = {17},
number = {},
pages = {1715020},
pmid = {41757237},
issn = {1664-2392},
mesh = {Humans ; Female ; Adult ; *Gastrointestinal Microbiome/physiology ; Quality of Life ; *Menstruation/physiology ; *Fecal Microbiota Transplantation/methods ; Young Adult ; *Menstruation Disturbances/therapy/microbiology ; },
abstract = {BACKGROUND AND AIMS: Menstrual disorders are closely related to the disorder of gut microbiota. This study aims to explore the impact of Washed microbiota transplantation (WMT) on the quality of life, depression and anxiety scale scores, and menstrual conditions of female patients of childbearing age.

METHODS: The data of female patients of childbearing age who received WMT at the First Affiliated Hospital of Guangdong Pharmaceutical University from February 2023 to February 2025 were collected. A comparative analysis was conducted on the effects of SF-36, SDS, SAS and menstrual conditions in female patients of childbearing age before and after WMT treatment. The changes of gut microbiota before and after WMT were analyzed by 16S rRNA gene sequencing.

RESULTS: A total of 23 female patients of childbearing age were included in this study. WMT significantly improved the scores of GH, SF, MH, RE and VT in SF-36 of female patients of childbearing age and significantly reduced the scores of SDS and SAS (P < 0.05). The MDQ score was negatively correlated with the PF, BP, GH, VT, RE and MH scores in SF-36, and positively correlated with the SDS and SAS scores (P < 0.05). WMT enhanced the α diversity of gut microbiota in female patients of childbearing age, and the Chao1 and Shannon indices were statistically significant (P < 0.05). At the same time, the relative abundance of Dialister, Bifidobacterium, Faecalibacterium, Roseburia and Fusobacterium increases. The relative abundances of Bacteroides, Agathobacter, Prevotella, Escherichia-Shigella and Ruminococcus decreased.

CONCLUSIONS: WMT treatment can effectively improve the quality of life score of female patients of childbearing age and reduce the scores of depression and anxiety scales. WMT can increase the diversity and abundance of gut microbiota in female patients of childbearing age and improve menstrual conditions, which provides new ideas for future clinical treatment.},
}

Humans
Female
Adult
*Gastrointestinal Microbiome/physiology
Quality of Life
*Menstruation/physiology
*Fecal Microbiota Transplantation/methods
Young Adult
*Menstruation Disturbances/therapy/microbiology

@article {pmid41653982,
year = {2026},
author = {McCafferty, CE and Townsend, JO and Bacchi, SD and Jensen, SO},
title = {Protocols for decolonisation of carbapenem-resistant Enterobacterales and vancomycin-resistant enterococci: a systematic review and meta-analysis.},
journal = {The Journal of hospital infection},
volume = {170},
number = {},
pages = {184-196},
doi = {10.1016/j.jhin.2026.01.017},
pmid = {41653982},
issn = {1532-2939},
abstract = {BACKGROUND: Rises in the prevalence of multi-drug-resistant organisms threaten patient safety globally. Vancomycin-resistant enterococci (VREs) and carbapenem-resistant Enterobacterales (CRE) are linked with prolonged hospitalisation, treatment failure, and increased mortality. Decolonisation strategies could reduce transmission and improve outcomes, but their efficacy and safety remain uncertain. This study systematically evaluates decolonisation protocols for VRE and CRE through a meta-analysis.

METHODS: Following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, a systematic review and meta-analysis were performed on studies using PubMed, ScienceDirect, Web of Science, and Scopus. Studies evaluating decolonisation protocols for VRE and CRE were included. Papers were assessed for risk of bias using the Risk of Bias 2 tool and Newcastle-Ottawa Scale. Meta-analyses were performed using RevMan, Cochrane, London, United Kingdom.

RESULTS: Sixteen studies with a total of 872 participants were included for meta-analysis. Faecal microbiota transplantation (FMT) significantly improved clearance of CRE (risk ratio [RR]: 2.01; 95% confidence interval [CI]: 1.27-3.18) and VRE (RR: 2.96, 95% CI: 1.60-5.47) compared with controls, with low to moderate heterogeneity. Selective digestive decontamination (SDD) significantly increased clearance of CRE (RR: 2.47, 95% CI: 1.32-4.63), but not VRE (RR: 1.52, 95% CI: 0.70-3.30). Adverse events were generally mild, but SDD was associated with increased antimicrobial resistance in several studies.

CONCLUSIONS: FMT and SDD are promising interventions for CRE decolonisation, with FMT also showing benefit in VRE. The durability of SDD effects appears limited, with significant risk of promoting resistance. Future studies should standardise endpoints, evaluate combination approaches, and explore bacteriophage therapy. We suggest implementing uniform terminology with 'provisional clearance' as a descriptor for eradication at 1 month post intervention and 'enduring clearance' following continuous eradication for 6 months.},
}

@article {pmid41783924,
year = {2026},
author = {Luo, S and Lou, F and Yang, P and Zhang, Y and Yan, L and Dong, Y and Yang, B and Wang, H and Liu, Y and Pu, J and Cannon, RD and Xie, P and Ji, P and Jin, X},
title = {Dysregulation of Oral Microbial Eicosapentaenoic Acid Induced by Chronic Restraint Stress Exacerbates Periodontitis via M1 Macrophage Polarization.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e21346},
doi = {10.1002/advs.202521346},
pmid = {41783924},
issn = {2198-3844},
support = {82370968//National Natural Science Foundation of China/ ; 2026MSXM055//Chongqing medical scientific research project (Joint project of the Chongqing Health Commission and the Science and Technology Bureau)/ ; CSTB2022NSCQ-MSX1148//Natural Science Foundation of Chongqing/ ; 2025JYJ099//Project of Luzhou Science and Technology Bureau/ ; },
abstract = {The intricate interplay between chronic psychological stress and periodontitis, mediated by oral microbiota and macrophage polarization, remains largely enigmatic. Here, we demonstrate that chronic restraint stress (CRS) exacerbates periodontitis by inducing oral microbial dysbiosis and a consequential shift in host metabolism. Clinical observations reveal a significant correlation between depressive symptoms and the severity of periodontitis, which is underpinned by a distinct oral microbiome. Crucially, fecal microbiota transplantation from CRS-exposed mice into germ-free mice was sufficient to transmit the heightened periodontitis phenotype, establishing a causal role for the stress-altered microbiota. Metabolomic profiling identified a depletion of eicosapentaenoic acid (EPA) in stressed, ligature-induced periodontitis mice. Mechanistically, supplementation with EPA ameliorates periodontitis by suppressing the NF-κB signaling pathway, thereby inhibiting the pro-inflammatory M1 polarization of macrophages. Our findings unveil a novel gut-oral axis mediated by microbiota and metabolites under stress, and position the omega-3 fatty acid EPA as a promising therapeutic agent for mitigating stress-aggravated inflammatory disorders.},
}

@article {pmid41782495,
year = {2026},
author = {Loublier, C and Taminiau, B and Seidel, L and Moula, N and Tano, C and Cesarini, C and Costa, M and Lecoq, L and Daube, G and Amory, H},
title = {Survey on Faecal Microbiota Transplantation and Probiotic Use in Equine Practice in France and Belgium.},
journal = {Veterinary medicine and science},
volume = {12},
number = {2},
pages = {e70854},
doi = {10.1002/vms3.70854},
pmid = {41782495},
issn = {2053-1095},
support = {40005849//Fonds De La Recherche Scientifique - FNRS/ ; },
abstract = {BACKGROUND: Faecal microbiota transplantation (FMT) and probiotics are used in equine practice. Understanding veterinarians' perceptions and practices is crucial for effective implementation.

OBJECTIVE: (1) Evaluate the prevalence, usage patterns and perceived effectiveness of probiotics and FMT among equine veterinarians in France and Belgium. (2) Assess their knowledge, practices and influencing factors across demographics and settings. (3) Explore links between FMT protocols and treatment satisfaction.

STUDY DESIGN: Cross-sectional survey.

METHODS: An online survey collected demographic data and responses on the use of probiotics and FMT. Analyses included descriptive statistics, chi-square tests and logistic regression models.

RESULTS: Ninety-six equine veterinarians participated, practicing in Belgium (52.1%), France (39.6%) or both (8.3%). Probiotic use was reported by 82.1%, more frequent in field than clinical practice (odds ratio [OR] = 3.61, 95% CI [1.09, 12.02], p = 0.036) and in France than Belgium (OR = 5.08, 95% CI [1.44, 17.94], p = 0.012). Probiotics were used for chronic diarrhoea (88.0%), acute diarrhoea (67.6%) and inflammatory bowel diseases (45.9%). Most veterinarians (83.3%) defined probiotics well, but 16.7% misidentified non-probiotic products. FMT was used by 76.0%, mainly occasionally and therapeutically, more in clinical than field practice (OR = 4.79, 95% CI [1.03, 22.27], p = 0.046). In theory, 58.3% prioritized infection-free donors, but only 22.5% tested donors before FMT, mostly using coprology (93.8%). Those who tested donors reported higher perceived efficacy (p = 0.0029).

MAIN LIMITATIONS: Potential selection bias, as participation was voluntary. Generalizability might be limited by focus on France and Belgium. Sample size, while informative, should be expanded.

CONCLUSION: Probiotics and FMT were commonly used therapeutically by equine veterinarians in France and Belgium. Although probiotic use was widespread, some misunderstandings remained. FMT protocols varied, with donor faeces often untested. Treatment satisfaction was generally positive but estimated success rates varied. Standardized FMT protocols are needed to improve outcomes and consistency.},
}

@article {pmid41780918,
year = {2026},
author = {Patel, RK and Teja, R and Hermann, K and Franz, R and Wong, K and Kao, D},
title = {Engaging Patient and Caregiver Partners in Codeveloping a Patient Educational Video for Improving Clostridioides difficile Infection Education: Participatory Co-Design Study.},
journal = {JMIR formative research},
volume = {10},
number = {},
pages = {e81643},
doi = {10.2196/81643},
pmid = {41780918},
issn = {2561-326X},
abstract = {BACKGROUND: Patients with recurrent Clostridioides difficile infection (rCDI) and their caregivers often face considerable uncertainty regarding medical management, including the use of fecal microbiota transplantation (FMT), largely due to the scarcity of accessible and credible educational resources. Codeveloping educational materials with patients and caregivers offers a structured way to address these gaps and ensure that resources reflect the informational, psychological, and emotional needs of patients.

OBJECTIVE: The study team sought to cocreate an educational resource through an iterative process including patient and caregiver partners with lived experience of rCDI to improve C difficile infection education.

METHODS: This study examined the cocreation process of a patient-centered educational resource between the study team and patient or caregiver participants through a series of focus group (FG) sessions. Five participants took part in 3 serial FG sessions (3-5 participants each) over 13 months. Each FG session was audio recorded, transcribed, and analyzed using the NVivo (version 14) quantitative analysis software. A semantic thematic analysis framework was applied to interpret the results. Key areas of concern and preferred formats were identified following the first FG session. The first version of the educational resource was developed by the study team to address areas of concern and was iteratively refined following feedback from subsequent FG sessions with the study participants.

RESULTS: Participants expressed concerns about the lack of credible information on treatment options and their associated risks, especially with regard to FMT. They noted inadequate coverage of C difficile infection recurrence and its physical, psychological, and emotional impacts. Participants expressed a preference for educational resources in video format. On the basis of further feedback, refinements were made to improve pacing, consistency of animation, and narration, incorporating emotional and mental health considerations. The codeveloped video was well received and valued for its clear language, messaging, step-by-step guidance, and overall accessibility and clarity.

CONCLUSIONS: Our study demonstrated the feasibility and utility of patient and caregiver involvement in cocreating an educational resource on the management of rCDI, with FMT being a treatment option. Despite efforts to address knowledge gaps and preferences expressed for a video format, uncertainties remain regarding the most effective educational resource format. The integration of patient, caregiver, and study team perspectives contributed to a codeveloped video that addresses unmet needs and is patient centered. However, diverse patient experiences remain underrepresented. Future research should consider including more diverse participants as well as evaluating the effectiveness of knowledge improvement through various educational resource formats and patient health care experiences and levels of satisfaction.},
}

@article {pmid41780589,
year = {2026},
author = {Sowulewski, O and Leszkowicz, J and Sakowska, M and Spychalski, P and Szlagatys-Sidorkiewicz, A},
title = {Definitive surgery for Hirschsprung Disease between 3 and 12 months achieves best outcomes: A Systematic Review with Meta-Analysis.},
journal = {Journal of pediatric surgery},
volume = {},
number = {},
pages = {163039},
doi = {10.1016/j.jpedsurg.2026.163039},
pmid = {41780589},
issn = {1531-5037},
abstract = {INTRODUCTION: Optimal age for definitive pull-through in Hirschsprung disease (HD) is debated. Both early and delayed interventions may influence short- and long-term outcomes, but current guidelines do not provide a clear recommendation.

METHODS: A systematic review was conducted following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Nineteen studies published between 1998 and 2025, including 3,980 pediatric patients with HD undergoing definitive pull-through surgery, were included. Age at surgery was stratified using predefined thresholds (neonatal, <3 months, <6 months, <12 months, <4 years, and above). Short- and long-term outcomes were extracted and synthesized. Risk of bias was assessed using the Newcastle-Ottawa Scale.

RESULTS: Short-term outcomes were reported in 15 studies. Hirschsprung-associated enterocolitis (HAEC) was the most frequently reported complication (0-69.1%), occurring more often in neonates than in non-neonates (22.4%, 78/348 vs. 15.5%, 125/808) and in patients operated before 3 months of age compared with those operated later (20.7%, 68/328 vs. 13.6%, 60/442). Neonatal surgery was also associated with higher rates of anastomotic leakage (7.1%, 10/140 vs. 1.5%, 6/412). Long-term outcomes were assessed in 14 studies. Patients operated during the neonatal period had higher rates of fecal incontinence (30.0%, 55/183 vs. 17.8%, 56/314) and constipation (25.2%, 39/155 vs. 12.8%, 43/336). Similarly, surgery performed before 3 months of age was associated with increased rates of fecal incontinence (18.0%, 36/200 vs. 8.6%, 20/232) and constipation (23.5%, 47/200 vs. 13.8%, 32/232) at long-term follow-up.

CONCLUSIONS: Timing of definitive surgery in Hirschsprung disease is associated with differences in postoperative outcomes. Neonatal surgery and surgery performed during early infancy (<3 months) were more often associated with higher complication rates, whereas procedures performed during infancy showed more balanced results.},
}

@article {pmid41780914,
year = {2026},
author = {Cheng, M and Zhi, S and Zheng, M and Zhang, S and Hong, J},
title = {Gut Microbiota-Induced CTLA4 Expression on CD8[+] T Cells Impairs Antitumor Immunity and Promotes Colorectal Cancer Progression.},
journal = {Immunology},
volume = {},
number = {},
pages = {},
doi = {10.1111/imm.70128},
pmid = {41780914},
issn = {1365-2567},
support = {25A180025//The Key Scientific Research Project Plan of Higher Education Institutions in Henan Province/ ; 252300423545//The Youth Fund of Natural Science Foundation of Henan Province/ ; },
abstract = {This study reveals a novel gut microbiota-CD8[+] T cell axis driving immunosuppression in colorectal cancer. Analysis of 16S rRNA sequencing identified significant gut dysbiosis in CRC patients, with marked enrichment of Phocaeicola and Bacteroides. Single-cell transcriptomics uncovered substantial T cell depletion and elevated CTLA4[+]PD1[+] immune cells within the tumour microenvironment. Critically, spatial transcriptomics demonstrated co-localization of CTLA4[+]CD8[+] T cells with tumour cells, indicating direct immunosuppressive interactions. Functional validation confirmed CTLA4 overexpression impairs CD8[+] T cell effector capacity, accelerating CRC cell proliferation and invasion. In vivo models demonstrated that faecal microbiota transplantation (FMT) promoted CTL activation, reduced Bacteroides abundance, decreased the formation of CD8[+]CTLA4[+] T cells and ameliorated CRC symptoms. Additionally, CTLA4 knockdown inhibited tumour growth and metastasis. These findings establish a mechanistic pathway: gut dysbiosis induces chronic inflammation, triggering CTLA4 upregulation on CD8[+] T cells to promote T cell exhaustion and tumour immune evasion. The study provides immunological evidence for targeting the microbiota-CTLA4 axis in CRC immunotherapy.},
}

@article {pmid41780895,
year = {2026},
author = {Ma, X and Xu, Y and Nian, Y and Luo, R and Chen, T and Su, K and Li, T and Shen, C and Xie, B and Dai, H and Zhao, J and Ma, Y},
title = {Dietary carboxymethylcellulose metabolite promotes heart allograft rejection through induction of pro-inflammatory macrophages via lysophosphatidic acid.},
journal = {American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ajt.2026.02.030},
pmid = {41780895},
issn = {1600-6143},
abstract = {Carboxymethylcellulose (CMC), a common food emulsifier, induces microbiota dysbiosis and systemic inflammation; however, its impact on transplant immunity remains unclear. Allogenic heart rejection was observed in CMC-fed recipient mice, with increased abundance of lysophosphatidic acid (LPA)-producing bacteria and increased serum LPA concentration. CMC-induced transplant rejection was caused by the gut microbiota, as confirmed by fecal microbiota transplantation and gut microbiota depletion. Furthermore, LPA-treated macrophages demonstrated a pro-inflammatory ability to accelerate allograft rejection in cytotoxic T lymphocyte-associated protein 4 immunoglobulin-induced allograft survival by upregulating glycolysis. Conversely, the administrated of a glycolysis inhibitor resulted in allograft survival and abrogated the detrimental effect of LPA. Mass spectrometry and single-cell RNA sequencing confirmed that human transplant rejection patients showed significantly elevated serum LPA levels and LPAR6 expression in graft-infiltrate macrophages. Mechanistically, LPA preferentially promoted LPAR6 expression, which interacted with Rho-associated protein kinase 2 to activate the mTOR/HIF-1α pathway, thereby enhancing glycolysis and inducing pro-inflammatory macrophage polarization. Treatment with Ki16425, an LPAR antagonist, prolonged allograft survival in CMC-fed recipients. Our findings reveal a major detrimental effect of CMC on macrophage physiology and suggest that controlling LPAR6 expression or glycolysis in macrophage may improve allograft survival in transplant recipients.},
}

@article {pmid41778780,
year = {2026},
author = {Mambuque, E and Del Amo-de Palacios, A and Huete, SG and Marsh, CC and Theron, G and García-Basteiro, AL and Serrano-Villar, S},
title = {Beyond bacilli: integrating the microbiome into the TB research agenda.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2638004},
doi = {10.1080/19490976.2026.2638004},
pmid = {41778780},
issn = {1949-0984},
abstract = {Tuberculosis (TB) remains a leading infectious killer, with growing evidence that the human microbiome-particularly in the gut and lungs-shapes susceptibility, progression, and treatment outcomes. Over the past decade, studies have reported that TB-associated dysbiosis, which is more common in the gut than in the lung, is often marked by the loss of short-chain fatty acid-producing taxa and the expansion of opportunistic microbes. However, findings are frequently confounded by diet, antibiotic exposure, comorbidities, geography, and methodological variability. Most research has relied on compositional profiling, offering limited insight into functional mechanisms. This narrative review synthesizes recent evidence, emphasizing the need to integrate multiomics approaches-metagenomics, metatranscriptomics, and metabolomics-and experimental validation to uncover causal links between microbiome alterations and TB pathogenesis or therapy response. We discuss potential clinical applications, including microbiome-based diagnostics (such as stool-based microbial or metabolite signatures for TB risk stratification), prognostic indicators (such as gut microbiome recovery predicting immune normalization during therapy), and adjunctive interventions (including microbiome-derived products to reduce drug-induced liver injury or fecal microbiota transplantation, which has been shown to be safe in people with HIV on stable ART) to mitigate drug toxicity or enhance immune recovery. Key priorities include methodological standardization, confounder control, mechanistic studies, and the inclusion of high-burden settings. By moving beyond descriptive surveys toward functional, translational research, integrating insights from different microbiome methods into TB prevention, diagnosis, and treatment could redefine the clinical research agenda and open new avenues for precision medicine in this global disease.},
}

@article {pmid41778620,
year = {2026},
author = {Wang, Y and OuYang, J and Zhang, H and Shen, Y and Guo, Z and Lv, W},
title = {The Efficacy of Gut Microbiome-Modulating Therapies on Liver Cirrhosis: A Systematic Review and Network Meta-Analysis.},
journal = {Clinical and translational gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.14309/ctg.0000000000001010},
pmid = {41778620},
issn = {2155-384X},
abstract = {OBJECTIVE: Gut microbiome-modulating therapies are potential strategies for managing liver cirrhosis (LC), yet head-to-head comparisons to determine the optimal intervention are lacking. This study aimed to evaluate and rank the therapeutic efficacy of these therapies on liver function and disease progression in patients with LC.

METHODS: We searched major databases (PubMed, Web of Science, Embase, Cochrane Library) for randomized controlled trials (RCTs) published from January 1, 2000, to December 30, 2024. Interventions included probiotics, prebiotics, synbiotics, and fecal microbiota transplantation (FMT) versus placebo or standard care. Primary outcomes were hepatic function indicators; secondary outcomes included inflammatory markers. Data were analyzed using random-effects frequentist network meta-analyses. The study was registered on PROSPERO (CRD420251000506).

RESULTS: Seventeen studies comprising 1051 individuals were included. Synbiotics demonstrated the most significant efficacy among all interventions, showing superior reduction in blood ammonia levels compared to placebo (Mean Difference (MD): -5.57), probiotics, and prebiotics. Prebiotics showed significant differences in lowering endotoxin levels compared to placebo (MD: -3.29) and probiotics. Furthermore, relative to placebo, prebiotics significantly reduced tumor necrosis factor-alpha (MD: -2.30) and interleukin-6 levels (MD: -4.60).

CONCLUSIONS: This network meta-analysis advances current knowledge by establishing an evidence-based hierarchy of efficacy. Synbiotics are most effective for reducing blood ammonia, whereas prebiotics demonstrate superior efficacy in lowering endotoxin and inflammatory markers. These results support a personalized therapeutic approach: prioritizing synbiotics for patients with hyperammonemia, and prebiotics for those characterized by systemic inflammation. Future high-quality RCTs are needed to standardize specific strain combinations.},
}

@article {pmid41778022,
year = {2026},
author = {Tan, Z and Young, E and Rajagopalan, A},
title = {Push Enteroscopic Jejunal and Ileoscopic Delivery of Fecomicrobiota Transplantation (FMT) for Treatment of Clostridioides difficile Enteritis in a Patient With a Total Colectomy and Ileal Pouch-Anal Anastomosis (IPAA): A Case Report.},
journal = {JGH open : an open access journal of gastroenterology and hepatology},
volume = {10},
number = {3},
pages = {e70381},
pmid = {41778022},
issn = {2397-9070},
abstract = {Clostridioides difficile infection (CDI) is recognized as the leading cause of antibiotic-associated diarrhea. There are several case reports of C. difficile enteritis in patients who have undergone colectomy and end ileostomy or ileal pouch-anal anastomosis. This case report describes a unique case of recurrent C. difficile enteritis following proctocolectomy and ileoanal pouch, treated successfully with faecal microbiota transplantation (FMT) via anterograde and retrograde delivery into the small bowel.},
}

@article {pmid41777702,
year = {2026},
author = {Zhang, YW and Li, RY and Wu, Y and Wang, P and Zhou, QR and Su, JC},
title = {Gut microbiota and bone aging: Focusing on the gut-X axis modes.},
journal = {Journal of orthopaedic translation},
volume = {57},
number = {},
pages = {101064},
pmid = {41777702},
issn = {2214-031X},
abstract = {UNLABELLED: As studies have continuously advanced, cross-linking interplay between various organs in aging individuals have continuously emerged as research hotspots. The role of gut microbiota in bone aging-related diseases, including osteoporosis, osteoarthritis, and intervertebral disc degeneration, has been extensively probed. This review first summarized the inseparable association between gut microbiota and osteoporosis, osteoarthritis, and intervertebral disc degeneration, which then explored potential mechanisms of gut-X axis through neuromodulation (microbiota-gut-brain-bone axis), immunomodulation (Th17 and Treg balance), endocrine regulation (gut-derived hormones and 5-HT), metabolite-mediated regulation (SCFAs), bacterial extracellular vesicles, and changes in microbial niche and gut microbiome-associated biomarkers. Moreover, potential intervention strategies including diet, probiotics, fecal microbiota transplantation, and physical activity were summarized to enhance clinical translation applicability. This review creatively exhibited integrated concept of "gut-X axis" to explore common, patterned mechanisms underlying "gut-bone axis", "gut-joint axis", and "gut-disc axis". Furthermore, it delves into potential mechanisms by which this shared pattern regulates bone aging-related diseases and prospectively outlines therapeutic strategies for bone aging based on this axis.

This review presents crucial role and regulatory significance of gut-X axis modes in common bone-aging related diseases. By anchoring the gut-X axis as intervention targets, the thinking of gut microbiota and its related metabolites in basic studies and clinical prevention and treatment of bone aging-related diseases might be expanded, and its clinical application transformation and development could be innovated.},
}

@article {pmid41776845,
year = {2026},
author = {Cai, Y and Sun, J and Chen, S and Wang, D and Jing, Y and Jin, X and Li, Z and Li, C and Ban, X},
title = {Agarotriose Alleviates Colitis by Promoting Akkermansia muciniphila-Derived Spermidine Production to Suppress PI3K/AKT/NF-κB Signaling.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c16297},
pmid = {41776845},
issn = {1520-5118},
abstract = {Agarotriose (A3), a marine-derived oligosaccharide from agar, has shown anti-inflammatory potential, yet the involvement of gut microbiota remains incompletely understood. Using a dextran sulfate sodium-induced colitis mouse model combined with antibiotic depletion and fecal microbiota transplantation, we found that the protective effects of A3 were largely dependent on the gut microbiota. Integrated multiomics analyses indicated that A3 preferentially enriched Akkermansia muciniphila and was associated with increased intraluminal spermidine levels. Spermidine abundance correlated with A. muciniphila enrichment and improvement of colitis-related phenotypes. In vitro, A3 promoted the growth of A. muciniphila and enhanced spermidine production. Transcriptomic and cellular analyses further suggested that spermidine attenuated inflammatory responses, at least in part, through modulation of the PI3K/AKT/NF-κB signaling pathway. Collectively, these results support a potential "A3-A. muciniphila-spermidine-host signaling" axis and suggest that A3 may serve as a promising marine-derived prebiotic for intestinal health.},
}

@article {pmid41677988,
year = {2026},
author = {Feng, R and Yang, Z and Zhou, Y and Zhao, H},
title = {The Gut-Brain-Immune Axis in Glioma: Emerging Mechanisms and Therapeutic Opportunities.},
journal = {Cellular and molecular neurobiology},
volume = {46},
number = {1},
pages = {},
pmid = {41677988},
issn = {1573-6830},
support = {ZR2022QH372//Science and Technology Development Plan of Shandong Province/ ; },
abstract = {Gliomas, particularly glioblastomas, represent some of the most treatment-resistant cancers due to their profoundly immunosuppressive tumor microenvironment (TME) and the restrictive nature of the blood–brain barrier. While recent advances in immunotherapy have transformed the treatment landscape for peripheral tumors, success in gliomas remains limited. Emerging evidence suggests that the gut microbiota—through the gut-brain-immune axis—may play a significant role in shaping systemic and central immune responses. Gut-derived microbial metabolites, immune cell modulation, and neuro-immune signaling pathways have been shown to influence microglial activation, T cell infiltration, and even response to immune checkpoint inhibitors (ICIs) such as PD-1 and emerging targets like TIM-3, LAG-3, and TIGIT. Furthermore, the efficacy and persistence of CAR-T and CAR-NK therapies may also be impacted by microbial composition, offering a novel avenue for therapeutic optimization. This review explores the biological underpinnings of the gut-brain-immune axis in glioma, summarizes key preclinical and clinical findings, and highlights the potential of gut microbiota modulation—via probiotics, engineered microbes, or fecal microbiota transplantation (FMT)—as an adjunct to immunotherapy. We also discuss technical and translational challenges, including interindividual variability and mechanistic uncertainty. Understanding the dynamic crosstalk between the gut and the glioma immune microenvironment may unlock new therapeutic strategies and improve outcomes in this highly lethal disease.},
}

@article {pmid41776699,
year = {2026},
author = {Song, Y and Wen, S and Guan, LL},
title = {Unraveling the dynamic changes in the intestinal microbiome: impacts on pre-weaning calf health and productivity.},
journal = {Journal of animal science and biotechnology},
volume = {17},
number = {1},
pages = {},
pmid = {41776699},
issn = {1674-9782},
abstract = {The early life gut microbial colonization in pre-weaning calves plays a pivotal role in shaping their health, growth, and productivity. This review delves into the dynamic changes of intestinal microbiota during early life, emphasizing key factors such as colostrum management, feeding strategies, roughage supplementation, and microbial interventions including probiotics, prebiotics, and fecal microbiota transplantation (FMT), and non-nutritional stressors that can shape the early life microbial colonization. We highlight the microbiota's critical functions in nutrient metabolism, immune development, gut barrier integrity, and gut-brain axis regulation. Additionally, the consequences of microbial dysbiosis on calf health and its long-term effects on production performance in beef and dairy cattle are discussed. While current research has provided valuable insights, understanding causal mechanisms remains a challenge. This review aims to guide practical strategies for targeted microbial management, offering a pathway to optimize early-life interventions for improved calf health and productivity.},
}

@article {pmid41776310,
year = {2026},
author = {Kim, M and Wang, J and Pilley, SE and Lu, RJ and Xu, A and Kim, Y and Liu, M and Fu, X and Booth, SL and Mullen, PJ and Benayoun, BA},
title = {Estropausal gut microbiota transplant improves measures of ovarian function in adult mice.},
journal = {Nature aging},
volume = {},
number = {},
pages = {},
pmid = {41776310},
issn = {2662-8465},
support = {#00034120//Pew Charitable Trusts/ ; T32 AG052374/AG/NIA NIH HHS/United States ; No. 58-1950-7-707//United States Department of Agriculture | Agricultural Research Service (USDA Agricultural Research Service)/ ; },
abstract = {The decline in ovarian function with age affects fertility and is associated with increased risk of age-related diseases, including osteoporosis and dementia. Notably, earlier menopause is linked to shorter lifespan, yet the molecular mechanisms underlying ovarian aging remain poorly understood. Recent evidence suggests the gut microbiota may influence ovarian health. Here we show that ovarian aging is associated with distinct gut microbial profiles in female mice and that the gut microbiome can directly influence ovarian health. Using fecal microbiota transplantation from young or estropausal female mice, we demonstrate that heterochronic microbiota transfer remodels the ovarian transcriptome, reduces inflammation-related gene expression and induces transcriptional features consistent with ovarian rejuvenation. These molecular changes are accompanied by enhanced ovarian health and increased fertility. Integrating metagenomics-based causal mediation analyses with serum untargeted metabolomics, we identify candidate microbial species and metabolites that may contribute to the observed effects. Our findings reveal a direct link between the gut microbiota and ovarian health.},
}

@article {pmid41776098,
year = {2026},
author = {Xiang, X and Zhu, J and Jiang, J and Ding, P and Zhu, Y and Cheng, K and Ming, Y},
title = {Unique gut microbiota and metabolomic profiling as biomarker of post-transplant recovery in acute-on-chronic liver failure after liver transplantation.},
journal = {Applied microbiology and biotechnology},
volume = {},
number = {},
pages = {},
doi = {10.1007/s00253-026-13774-5},
pmid = {41776098},
issn = {1432-0614},
support = {81771722 and 82570782//National Natural Science Foundation of China/ ; },
abstract = {Acute-on-chronic liver failure (ACLF) is a severe condition arising from chronic liver disease, characterized by acute decompensation, organ failure, and high short-term mortality. Poor outcomes have also been observed in patients with ACLF after liver transplantation (LT). Emerging evidence, including a study from our center, suggests that gut microbiota plays an important role in ACLF. Patients who underwent LT at our center between October 2022 and June 2024 were included. Fecal samples were collected within 1 month post-LT for 16S rRNA and untargeted metabolomic sequencing. In this study, 144 samples from 69 patients with ACLF, cirrhosis, or hepatocellular carcinoma (HCC) were analyzed. Distinct microbiota and metabolic profiles were observed among the groups. ACLF patients exhibited significantly altered beta diversity, with notable depletion of g__Anaerostipes. Metabolomic analysis revealed substantial differences, including enrichment of tangeritin and depletion of candesartan in the ACLF group. Network analysis identified g__Anaerostipes as a key node linking differential taxa and metabolites. A random forest model based on these features effectively distinguished patient groups, with the highest classification accuracy observed in HCC. Multi-omic signatures were also associated with early allograft dysfunction (EAD), particularly g__Lachnoclostridium. Several microbial and metabolic features, including g__Lachnoclostridium, showed significant correlations with clinical indicators. The gut microbiome after LT is closely associated with ACLF. This study offers valuable insights for further investigation into the pathogenesis and post-LT prognosis. KEY POINTS: • ACLF patients have a unique gut microbiota and metabolic profile after LT • g__Anaerostipes is the prominent biomarker of ACLF's multi-omics signature • g__Lachnoclostridium is a promising indicator of recovery after LT.},
}

@article {pmid41774771,
year = {2026},
author = {Han, X and Yu, H and Gao, Q and Wang, X and Zhang, L and Zhao, Q and Yu, L and Zhang, Y and Sui, M and Li, Y},
title = {Gut Microbiota Dysbiosis Promotes CKD-associated Atrial Fibrillation Through Activation of the NLRP3 Inflammasome.},
journal = {Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology},
volume = {},
number = {},
pages = {},
doi = {10.1093/europace/euag037},
pmid = {41774771},
issn = {1532-2092},
abstract = {BACKGROUND: Chronic kidney disease (CKD) significantly increases the risk of atrial fibrillation (AF). Although alterations in the gut microbiota have been linked to CKD progression, its exact involvement in CKD-associated AF remians unclear. We amis to investigate the role of gut microbiota in the development of CKD-associated AF, and to uncover potential mechanisms that could serve as effective targets for prevention and treatment.

METHODS AND RESULTS: A rat model of CKD was induced by an adenine-enriched diet. 16S rRNA sequencing and fecal microbiota transplantation (FMT) were utilized to study the involvement of gut microbiota. AST-120, gut barrier protectants and mono-colonization experiments were performed to investigate potential mechanism. CKD rats exhibited gut microbiota dysbiosis and a significantly increased susceptibility to AF. FMT from CKD rats transferred this heightened AF susceptibility to healthy recipient rats, linked to the activation of the NLRP3 inflammasome. Mechanistically, gut dysbiosis in CKD patients leads to elevated IS levels, causing gut barrier dysfunction and increased circulating lipopolysaccharide (LPS). Elevated LPS activates atrial TLR4 receptors, triggering NLRP3 inflammasome activation, which contributes to AF pathogenesis. Treatment with the IS scavenger AST-120 or gut barrier protectants successfully prevented CKD-associated AF. Furthermore, supplementation with Lactobacillus gasseri reduced circulating IS levels and mitigated AF susceptibility in CKD rats.

CONCLUSION: This study demonstrates that gut dysbiosis-driven elevation of IS and subsequent activation of the atrial NLRP3 inflammasome are key mechanisms in CKD-associated AF. Modulating the gut microbiota could provide a new therapeutic strategy for CKD-associated AF.},
}

@article {pmid41772743,
year = {2026},
author = {He, J and Wang, MN and Chen, HJ and Zuo, GY and Li, JL and Yin, WF and Pan, XG and Cheng, YC and Xia, CY and Xu, JK and Zhang, WK},
title = {Muribaculum intestinale alleviates depressive-like behaviors by inhibiting Th17 cell differentiation and M1 microglia polarization.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-026-02354-4},
pmid = {41772743},
issn = {2049-2618},
support = {ZRZC2025-KCC03//National High Level & Elite Medical Professionals Project of China-Japan Friendship Hospital/ ; 2025-NHLHCRF-JBGS-A-WZ-10; ZRJY2024-BJ01//National High Level & Elite Medical Professionals Project of China-Japan Friendship Hospital/ ; 82474100//National Natural Science Foundation of China/ ; 82474100, 82273815, 82273809, 82073731//National Natural Science Foundation of China/ ; },
abstract = {BACKGROUND: Gut microbiota dysbiosis has been implicated in the pathogenesis of depression. Our previous studies identified loganin as a potential antidepressant agent; however, its oral bioavailability is low. Whether loganin alleviates depression via modulation of the gut microbiota remains unclear.

METHODS: Chronic unpredictable stress mice model was used to evaluate the antidepressant-like effects of loganin. To determine the role of gut microbiota, mice were treated with an antibiotic cocktail (ABX) to deplete microbiota. Fecal microbiota transplantation (FMT) from loganin-treated donors and Muribaculum intestinale (M. intestinale) were performed to assess microbial contributions.

RESULTS: Loganin exerted antidepressant-like effects by modulating gut microbiota, as evidenced by reduced efficacy in ABX-treated mice and behavioral improvements in recipients of FMT from loganin-treated donors. Loganin modulated gut microbiota composition particularly increasing the abundance of Muribaculum, and increased short-chain fatty acids (SCFAs). M. intestinale alleviated depressive-like behaviors, prompted the butyrylation of RORγt, inhibited Th17 cells differentiation, and suppressed M1 microglia polarization. Importantly, overexpression of RORγt attenuated the behavioral benefits of M. intestinale.

CONCLUSION: Loganin exerts antidepressant-like effects by enriching Muribaculum and SCFAs, thereby inhibiting Th17 cell differentiation and M1 microglia polarization. M. intestinale may represent a promising microbial-based therapeutic strategy for depression.},
}

@article {pmid41771438,
year = {2026},
author = {Lynch, SV and Nagler, CR and Rachid, R},
title = {Microbial Therapeutics for the Prevention and Treatment of Food Allergy.},
journal = {The journal of allergy and clinical immunology. In practice},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jaip.2026.02.024},
pmid = {41771438},
issn = {2213-2201},
abstract = {Food allergy affects approximately 8% of children and 11% of adults in the United States. Available treatment including oral immunotherapy and anti-IgE are not known to lead to remission. There is now increasing evidence implicating the gut microbiome as a key regulator of allergic inflammation. Distinct microbial and metabolomic alterations characterize food-allergic individuals, and gnotobiotic mouse models show that fecal microbiota from food-allergic donors transfers allergic sensitization, whereas microbiota from healthy donors protects from anaphylaxis through induction of tolerogenic Foxp3[+]RORγt[+] regulatory T cells. Goblet cell-derived resistin-like molecule beta (RELM β) induces food allergy through modulation of the gut microbiome and depletion of indole-producing species. These findings have inspired the development of five microbial therapeutics approaches: probiotics, rationally defined bacterial consortia, fecal microbiota transplantation, metabolite-based approaches, and biologics targeting dysbiosis-associated pathways. Early-phase clinical studies support feasibility, yet long-term safety, durability, and reproducibility remain uncertain. Major challenges include inter-individual variability, ecological complexity, and regulatory standardization. Microbiome-directed therapeutics hold promise to transform food allergy management from temporary desensitization toward remission and durable immune tolerance. The application of systems biology approaches integrating metabolomics, transcriptomics, and immune phenotyping will be essential to unravel the complex host-microbial interactions that underlie the efficacy of these approaches.},
}

@article {pmid41769611,
year = {2026},
author = {Li, X and Xu, S and Li, Y and Wang, R and Qin, C and Wang, X},
title = {Research Progress on the Mechanisms of Gut Microbiota Dysbiosis Associated With Idiopathic Pulmonary Fibrosis: A Review.},
journal = {Cureus},
volume = {18},
number = {1},
pages = {e102429},
pmid = {41769611},
issn = {2168-8184},
abstract = {Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive fibrotic interstitial lung disease with an incompletely understood pathogenesis. In recent years, growing evidence has highlighted the critical role of gut microbiota dysbiosis in the onset and progression of IPF. This review comprehensively summarizes the characteristics of gut microbiota alterations associated with IPF, explores the underlying mechanisms driving these changes, and examines their impact on disease development. Particular emphasis is placed on the emerging concept of the "gut-lung axis," which elucidates the bidirectional communication between the intestinal microbiome and pulmonary health. The review further discusses microbial metabolites and immune modulation as key mediators linking gut dysbiosis to pulmonary fibrosis. Additionally, current advances in microbiota-targeted therapeutic strategies, including probiotics, prebiotics, and fecal microbiota transplantation, are analyzed for their potential in IPF management. By systematically integrating recent findings, this article aims to deepen the understanding of IPF pathophysiology and provide a theoretical foundation for novel treatment targets centered on gut microbiota regulation.},
}

@article {pmid41769404,
year = {2026},
author = {Zhao, Y and Chen, D and Qi, K},
title = {The role of gut microbiota in Hirschsprung's disease: from pathogenic mechanisms to microbiota-targeted therapies.},
journal = {PeerJ},
volume = {14},
number = {},
pages = {e20854},
pmid = {41769404},
issn = {2167-8359},
abstract = {Hirschsprung's disease (HSCR) is a common congenital disorder characterized by abnormal enteric nervous system development. Recent studies have demonstrated that gut microbiota and their metabolites play a significant role in the pathogenesis of HSCR. This review systematically examines the interplay between gut dysbiosis and pathophysiological alterations in HSCR, including disruptions in microbial composition, aberrant metabolite profiles, impaired intestinal barrier function, and dysregulated neuro-immune modulation. Research indicates that HSCR patients exhibit a characteristic gut microbial imbalance, which may influence the development and function of the enteric nervous system by altering the intestinal microenvironment, including metabolic profiles and immune status. Furthermore, this review explores the potential therapeutic value of microbiota-targeted interventions, such as probiotics and fecal microbiota transplantation (FMT), in HSCR treatment, providing a theoretical foundation for novel therapeutic strategies. These findings not only enhance the understanding of HSCR pathogenesis but also offer new perspectives for clinical prevention and treatment.},
}

@article {pmid41762317,
year = {2026},
author = {Altan, ZB and Ihlamur, M},
title = {The relationship between gut microbiota and neurodegenerative diseases: a genetic and epigenetic perspective.},
journal = {Metabolic brain disease},
volume = {41},
number = {1},
pages = {},
pmid = {41762317},
issn = {1573-7365},
abstract = {UNLABELLED: Gut microbiota (GM) is a complex and dynamic structure that can have a wide range of effects on human health. Studies in recent years have shown that microbiota is not only related to the gastrointestinal tract (GIT) but also to the immune and endocrine systems. It causes various effects on host physiology, especially through genetic and epigenetic mechanisms. It shows that microbiota-derived metabolites can play a role in the development of neurological diseases by changing gene expression. In this review article, the relationship between GM and neurodegenerative diseases (NDs) is explained in terms of genetics and epigenetics. In terms of the gut–brain axis (GBA); the role of systems such as short-chain fatty acids (SCFA), vagus nerve, inflammatory responses and intestinal permeability in the pathogenesis of NDs such as Alzheimer's (AD), Parkinson's (PD), Huntington's (HD) and Multiple Sclerosis (MS) is discussed. In addition, experimental studies have drawn attention to the effects of changes in microbiota on neuroinflammation and cognitive impairment. In terms of treatment strategies; Probiotics, prebiotics, synbiotics, fecal microbiota transplantation (FMT) and nutritional interventions targeting microbiota seem to be promising strategies. However, the fact that microbiota structure varies between individuals indicates that studies in this area should be conducted in a more personalized manner. This article aims to provide a basis for future research by approaching the relationship between microbiota and NDs in a holistic manner.

GRAPHICAL ABSTRACT: [Image: see text]},
}

@article {pmid41764851,
year = {2026},
author = {Guo, Q and He, Y and Cao, T and Lin, C and Deng, M and Wu, R and Cai, H},
title = {Tryptophan-kynurenine metabolism: A link between the gut microbiota dysbiosis and cognitive impairment.},
journal = {Microbiological research},
volume = {307},
number = {},
pages = {128481},
doi = {10.1016/j.micres.2026.128481},
pmid = {41764851},
issn = {1618-0623},
abstract = {Cognitive impairment is a central feature of neuropsychiatric and neurodegenerative disorders, significantly diminishing patients' quality of life. Emerging evidence underscores the role of gut microbiota dysbiosis in the progression of cognitive decline. The gut microbiota influences brain function through various mechanisms, with the kynurenine pathway standing out as a key biochemical route linking peripheral metabolism to central nervous system function, thereby impacting cognitive performance. Dysregulation of the kynurenine pathway has been closely associated with neurotransmitter imbalances, exacerbated neuroinflammation, and metabolic dysfunction, all of which contribute to the onset and progression of cognitive impairment. Recent studies suggest that interventions targeting the gut microbiota, such as probiotics, antibiotics, and fecal microbiota transplantation, may improve cognitive function by modulating the kynurenine pathway. This review examines the complex relationship between gut microbiota, the kynurenine pathway, and cognition, highlighting the potential of targeting kynurenine pathway-related enzymes and microbiota modulation as therapeutic strategies. Despite promising findings, the precise mechanisms and therapeutic potential of these interventions remain under investigation, offering new avenues for the treatment of cognitive disorders.},
}

@article {pmid41764528,
year = {2026},
author = {Zhang, W and Su, Q and Shi, H and Sun, Y and Li, X and Li, M and Wang, H and Yu, J and Wong, N and Chan, FKL and Zhang, J and Ng, SC},
title = {Discovery and characterization of Christensenella hongkongensis as a novel bacterium in the adenoma-carcinoma progression.},
journal = {Journal of translational medicine},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12967-026-07886-9},
pmid = {41764528},
issn = {1479-5876},
}

@article {pmid41763794,
year = {2026},
author = {Wei, K and Peng, L and Wei, Q and Wei, Y and Wang, L and Zhu, Y and Wei, Y and Wei, X},
title = {Amelioration of colitis by donor microbiota modulated with tea active ingredients: A fecal microbiota transplantation study.},
journal = {Food research international (Ottawa, Ont.)},
volume = {229},
number = {},
pages = {118473},
doi = {10.1016/j.foodres.2026.118473},
pmid = {41763794},
issn = {1873-7145},
abstract = {Fecal microbiota transplantation (FMT) using donor microbiota modulated by tea represents an emerging approach to ameliorate ulcerative colitis (UC). This study aims to demonstrate the amelioration of dextran sulfate sodium (DSS)-induced colitis by donor microbiota modulated with tea-derived bioactive ingredients-tea polyphenols (TPP), tea polysaccharides (TPS), or theabrownin (TB). Following transplantation of fecal microbiota modulated by TPP, TPS, or TB from donors into colitis mice, significant reductions in Disease Activity Index (DAI) were observed, alongside attenuated intestinal histopathological damage. Additionally, gut barrier integrity was enhanced, as indicated by upregulated expression of occludin and Muc2. Fecal microbiota modulated by TPP and TPS showed superior efficacy in alleviating colitis compared with TB-modulated microbiota. The mechanism involved that marked enrichment of beneficial genera, including Akkermansia (TPP-enriched) and Allobaculum/Lactobacillus (TPS-enriched), which promoted the biosynthesis of short-chain fatty acids (SCFAs) and secondary bile acids, while reducing primary bile acids levels. These metabolic changes enhanced intestinal barrier function and suppressed suppressing pro-inflammatory cytokines through the modulation of TLR4/NF-κB p65 and Nrf2/ARE signaling pathways. This study not only elucidates the mechanism of tea bioactive ingredients-modulated donor microbiota alleviates colitis through regulation of the gut-microbiota-metabolite axis, but also provides a foundation for FMT-based strategies in colitis intervention.},
}

@article {pmid41763137,
year = {2026},
author = {Zhou, S and Su, F and Gao, Q and Wang, M and Duan, J and Li, J},
title = {Cordyceps cicadae polysaccharides ameliorate ulcerative colitis by modulating the gut microbiota and regulating the bile acid/FXR/NF-κB signaling pathway.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {153},
number = {},
pages = {158007},
doi = {10.1016/j.phymed.2026.158007},
pmid = {41763137},
issn = {1618-095X},
abstract = {BACKGROUND: Ulcerative colitis (UC) is a chronic, relapsing inflammatory bowel disease, closely linked to dysbiosis of the intestinal microbiota and abnormal bile acid homeostasis. Polysaccharides derived from Paecilomyces cicadae (CCP) exhibit immunomodulatory and anti-inflammatory effects. However, their therapeutic potential and underlying mechanisms in UC remain poorly elucidated.

PURPOSE: This research seeks to evaluate the therapeutic efficacy of CCP in the treatment of UC and utilizing the "microbiota-bile acid metabolism-immunity" axis, elucidates the mechanisms by which CCP enhances intestinal barrier integrity and ameliorates inflammation via modulation of the gut microbiota-mediated farnesoid X receptor (FXR)/NF-κB signaling pathway.

METHODS: The physicochemical properties of CCP were characterized by FTIR spectroscopy, HPLC, and SEM analyses. A dextran sulfate sodium (DSS)-induced colitis mouse model was used to evaluate the ameliorative effects of CCP. Gut microbial alterations were profiled by 16S rDNA sequencing, while targeted metabolomics enabled comprehensive quantification of bile acid profiles in serum and fecal samples. Fecal microbiota transplantation (FMT) was conducted to validate the microbiota-mediated actions of CCP. Downstream molecular mechanisms were examined using Western blotting and immunofluorescence assays to assess modulation along the microbiota-bile acid axis.

RESULTS: CCP is primarily composed of glucose, mannose, and galactose, exhibiting a characteristic polysaccharide structure with a uniform molecular weight distribution. Treatment with CCP significantly ameliorated DSS-induced colitis in mice, as evidenced by reduced weight loss, preserved colon length, and decreased histopathological damage. 16S rDNA analysis demonstrated CCP-driven restoration of intestinal microbial diversity and a marked increase in Clostridium Kas107-2 (cluster XIVa). Metabolomics revealed normalization of bile acid metabolism, with elevated synthesis of secondary bile acids (deoxycholic acid, lithocholic acid, 12-keto LCA) and reduced levels of primary bile acids (α/β-MCA). Mechanistically, CCP activated FXR signaling, suppressed IκBα phosphorylation, downregulated NF-κB signaling, and reduced production of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6). Enhanced expression of tight junction proteins (ZO-1, Occludin, Claudin-1) indicated improved epithelial barrier function. Notably, FMT from CCP-treated donors replicated these protective effects, confirming colitis attenuation, bile acid restoration, and inhibition of FXR/NF-κB signaling.

CONCLUSIONS: CCP ameliorate experimental UC by promoting the proliferation of Clostridium cluster XIVa, modulating bile acid metabolism to facilitate secondary bile acid biosynthesis, activating FXR pathways, and suppressing NF-κB-driven inflammatory responses, thereby reinforcing intestinal epithelial barrier integrity.},
}

@article {pmid41763136,
year = {2026},
author = {Guo, Y and Xu, X and Han, A and Song, F and Zhang, Y and Jiang, X and Yu, W},
title = {Isorhamnetin alleviates diet induced MASLD in mice by modulating gut microbiota and bile acid metabolism.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {153},
number = {},
pages = {157987},
doi = {10.1016/j.phymed.2026.157987},
pmid = {41763136},
issn = {1618-095X},
abstract = {BACKGROUND: With the increasing prevalence of sedentary lifestyles and high-fat, high-sugar diets, the incidence of metabolic dysfunction-associated steatotic liver disease (MASLD) has continued to rise. Although the natural flavonoid compound isorhamnetin (ISO) has been shown to improve dyslipidemia in MASLD mice, its mechanism of action in regulating lipid metabolism via the gut microbiota and its metabolites remains unclear.

OBJECTIVE: This study investigates whether ISO can ameliorate high-fat diet-induced MASLD in mice in a dose-dependent manner and explores the mediating role of the gut microbiota in this process.

METHODS: Physiological monitoring, biochemical markers assessment, tissue section analysis, 16S rRNA sequencing, bile acid (BA) targeted metabolomics, and molecular analysis were performed on mouse tissues. In addition, fecal microbiota transplantation (FMT) from mice fed a high-dose of ISO further validated the regulatory role of the gut microbiota in MASLD mice. Molecular dynamics simulations and in vitro assays were performed to evaluate the interaction between ISO and FXR.

RESULTS: ISO dose-dependently reduced body weight and hepatic lipid content, inhibited lipid synthesis and promoted lipid oxidation. ISO reshaped the gut microbiota, increasing the relative abundance of Lachnospiraceae, Oscillospiraceae, and Ruminococcaceae. These changes altered the BA pool composition by increasing the proportion of primary and conjugated BAs, activated the hepatic-ileal Farnesoid X Receptor (FXR) signaling axis, accelerated enterohepatic BA circulation, and reduced dietary fat absorption. Concurrently, ISO enhanced intestinal barrier integrity and alleviated hepatic inflammation. Fecal microbiota transplantation from ISO-treated mice partially reproduced these metabolic benefits. Molecular dynamics simulations and in vitro experiments further verified that ISO interacts with FXR and consequently enhances FXR signaling.

CONCLUSION: ISO alleviates MASLD by synergistically regulating gut microbiota and FXR signaling, highlighting its potential as a mild, multi-target natural therapeutic candidate for MASLD therapy.},
}

@article {pmid41762381,
year = {2026},
author = {Sasidharan Pillai, S and Ashraf, AP},
title = {Gut Microbiota and Metabolic Health: From Dysbiosis to Therapeutics.},
journal = {Diabetes therapy : research, treatment and education of diabetes and related disorders},
volume = {},
number = {},
pages = {},
pmid = {41762381},
issn = {1869-6953},
abstract = {The gut microbiota (GM) is a pivotal regulator of host metabolism and a contributor to the pathophysiology of obesity, type 2 diabetes (T2D), and metabolic syndrome (MS). Disruptions in GM composition and function are collectively termed dysbiosis. This review synthesizes current evidence on GM dysbiosis, moving beyond simple taxonomic associations, to examine functional drivers of metabolic dysfunction. Dysbiosis impairs metabolic health through several interconnected pathways: enhanced dietary energy extraction, compromised intestinal barrier integrity leading to metabolic endotoxemia, chronic low-grade "meta-inflammation," and the disruption of circadian rhythms and neuro-immune signaling. Beyond bacteria, dysbiosis of the gut virome and mycobiota may further modulate metabolic risk. Animal and emerging human studies indicate that reduced virome diversity and altered phage-bacteria interactions can amplify dysbiosis, promote inflammatory signaling, and impair metabolic homeostasis. Recognition of GM dysbiosis as a contributor to metabolic disease has prompted development of therapeutic strategies aimed at restoring microbial balance and function. These interventions span a spectrum from established clinical approaches with indirect microbiota effects to experimental therapies designed to directly manipulate microbial composition or activity. We evaluate the clinical readiness of GM-targeted therapies, including dietary patterns, prebiotics, probiotics, and fecal microbiota transplantation. While established metabolic treatments such as glucagon-like peptide-1 (GLP-1) receptor agonists and bariatric surgery significantly reshape the GM, direct microbial manipulations often yield variable results in human trials. We conclude that the future of metabolic management lies in personalized microbiomics, utilizing artificial intelligence and precision-based interventions to restore specific functional microbial deficits tailored to the individual host profile.},
}

@article {pmid41761979,
year = {2026},
author = {Guo, Z and Gao, Z and Zhao, Y and Ni, X and Zhang, W and Li, L and Ren, S and Li, Q and Guo, D and Yue, L and Liu, Y and Lin, L and Fan, S and Hai, X},
title = {Administering Bifidobacterium pseudolongum With Arsenic Trioxide Attenuates Acute Promyelocytic Leukemia in Mice by Restoring Immune Microenvironment and Intestinal Homeostasis.},
journal = {Frontiers in bioscience (Landmark edition)},
volume = {31},
number = {2},
pages = {48584},
doi = {10.31083/FBL48584},
pmid = {41761979},
issn = {2768-6698},
support = {82274028//National Natural Science Foundation of China/ ; 2022ZX02C09//Heilongjiang Key R&D Program/ ; //Fundamental Research Funds for the Provincial Universities in Heilongjiang Province (2025)/ ; JJ2025PL0189//Natural Science Foundation of Heilongjiang Province/ ; 2024M10//Innovation Fund of the First Affiliated Hospital of Harbin Medical University/ ; 2024M25//Innovation Fund of the First Affiliated Hospital of Harbin Medical University/ ; 230000253533210000086//2025 Central Government Fiscal Subsidy Fund for Medical Care Compliance and Capacity Enhancement (Traditional Chinese Medicine Undertakings and Inheritance and Development Component)/ ; },
abstract = {OBJECTIVE: Arsenic trioxide (ATO) is a cornerstone of acute promyelocytic leukemia (APL) therapy but induces severe gut microbiota dysbiosis, limiting its efficacy and safety. This study investigated whether adjunctive Bifidobacterium pseudolongum (BP) could mitigate these adverse effects and enhance therapeutic outcomes.

METHODS: 16S rRNA gene sequencing data of gut microbiota were obtained from a cohort of 22 APL patients treated with ATO-based regimens (20 of 22 data were obtained and analysis further), accessible under BioProject ID PRJNA935705. To evaluate the within-sample microbial community richness and evenness, alpha and beta diversity indices were calculated. Using a murine APL model, we compared ATO monotherapy with ATO+BP co-treatment. Analyses included fecal metagenomic sequencing, single-cell RNA sequencing (sc-RNA-seq), flow cytometric immune profiling, and assessment of intestinal tight junction proteins (claudin-1, occludin, and ZO-1) via immunofluorescence.

RESULTS: ATO treatment significantly reduced gut microbial diversity and depleted beneficial taxa. Sc-RNA-seq data showed that ATO could orchestrate the APL immune microenvironment mainly through functional activation of CD8+ T cells and monocytes. BP supplementation restored microbial homeostasis and synergistically enhanced ATO's antileukemic effect, reducing the leukemic burden in peripheral blood by 72% and in bone marrow by 64% compared to ATO alone. Mechanistically, BP preserved intestinal barrier integrity by upregulating tight junction protein expression and modulated anti-tumor immunity, notably increasing bone marrow CD8+ T cells by 2.21-fold.

CONCLUSIONS: BP is an effective adjunct to ATO therapy, counteracting gut dysbiosis, intestinal damage, and the immune microenvironment while synergistically improving antileukemic efficacy. Targeting the gut-leukemia axis with BP represents a promising strategy for improving the precision and safety of APL treatment.},
}

@article {pmid41761700,
year = {2026},
author = {Pepke, ML and Hansen, SB and Limborg, MT},
title = {The ageing holobiont: crosstalk between telomere dynamics, oxidative stress and the gut microbiome.},
journal = {Biological reviews of the Cambridge Philosophical Society},
volume = {},
number = {},
pages = {},
doi = {10.1002/brv.70152},
pmid = {41761700},
issn = {1469-185X},
support = {DNRF143//Danmarks Grundforskningsfond/ ; CF21-0356//Carlsbergfondet/ ; },
abstract = {The gut tissue is at the frontline of early onset of ageing. It exhibits high cell turnover rates and rapid telomere shortening, which can have systemic effects on the developing or senescing organism. We conducted a literature review of studies on the crosstalk between telomere length dynamics, telomerase activity, oxidative stress, and gut microbiota composition and activity in animals. Studies mainly on humans and animal models include correlations between telomere dynamics and gut microbiome components, particularly under pathogenic conditions, but also manipulations of either the gut microbiome through faecal microbiota transplantations or of telomere dynamics using telomerase knockout models. This synthesis reveals that components of the gut microbiome including microbial metabolites and pathogenic bacteria can affect telomere dynamics through oxidative-stress-inducing processes, and that telomere maintenance is critical in maintaining gut barrier and tissue integrity, which link inflammation and gut dysbiosis. Some of the interactions between the gut microbiome and host telomere dynamics are bidirectional and important in maintaining intestinal homeostasis. However, many of the causal molecular or cellular mechanisms - and how they translate into organismal senescence - remain to be identified. Furthermore, we highlight how recent advances in whole genome sequencing capacities and bioinformatic tools represent an often-unexploited resource for measuring telomere lengths and may be particularly valuable tools within the hologenomic framework outlined here. Investigating the role of telomere dynamics in mediating gut microbiota-host interactions in different species will improve our understanding of how crosstalk between these hallmarks of ageing shape holobiont physiology in general and the ageing phenotype in particular.},
}

@article {pmid41761646,
year = {2026},
author = {Chen, Y and Jie, W and Xu, Y and Chen, X and Zhu, S and Ma, Y and Hu, L and Chen, C and Liu, B and Xu, D and Cai, D and Liu, Z},
title = {Correlation study between gut microbiota and intestinal permeability in cerebral small vessel disease.},
journal = {Journal of Alzheimer's disease : JAD},
volume = {},
number = {},
pages = {13872877261418554},
doi = {10.1177/13872877261418554},
pmid = {41761646},
issn = {1875-8908},
abstract = {BackgroundDysbiosis of gut microbiota and increased intestinal permeability are associated with various diseases, and their relationship with cognitive dysfunction such as cerebral small vessel disease (CSVD) and Alzheimer's disease remains to be elucidated.ObjectiveThis study investigates the role of gut microbiota dysbiosis and its relationship with intestinal permeability in patients with cognitive impairment associated with CSVD (CSVD-CI).MethodsIntestinal permeability was detected in 21 patients with CSVD-CI and 20 healthy controls by testing urine lactulose/mannitol, and correlation analysis was performed between the test results and cognitive function assessment. 16S rRNA sequencing was used to analyze the different combination of gut microbiota. Feces of the patients or controls were gavaged into C57 mice, and gut barrier function, behavior, and metabolites were assessed.ResultsPatients with CSVD-CI have a higher incidence of hypertension, higher homocysteine levels, higher scores for white matter hyperintensities, and worse cognitive function. Their urinary mannitol recovery rate is higher, which is correlated with lower scores of cognitive function assessment. Alterations in the gut microbiota involve a reduction in Prevotella-9 alongside increases in Proteobacteria and Fusobacteria. Fecal microbiota transplantation (FMT) from patients with CSVD-CI increases intestinal permeability in mice, but does not change their cognitive function; meanwhile, fecal metabolomics analysis has identified alterations in bile acids and vitamins, which are associated with shifts in the gut microbiota.ConclusionsPatients with CSVD-CI have gut microbiota imbalance and increased intestinal permeability, which are associated with cognitive decline. FMT from these patients can cause intestinal leakage and the production of harmful metabolites in mice.},
}

@article {pmid41761296,
year = {2026},
author = {Ye, H and Yang, X and Zheng, M and Dong, W and Chen, X and Chen, J and Hu, M and Zhou, M and Zheng, P and Shen, L and Wu, Y and Zheng, K and Huang, XF and Yu, Y},
title = {Early risperidone exposure impairs cognitive function by perturbation of the gut microbiome and bile acids/tyrosine-PTP1B axis.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-026-02358-0},
pmid = {41761296},
issn = {2049-2618},
abstract = {BACKGROUND: Second-generation antipsychotics (SGAs) are increasingly being utilized in children and adolescents. Risperidone, one of the most commonly prescribed SGAs in this population, has been found to adversely affect cognitive function; however, limited knowledge exists regarding the impact of risperidone on the gut microbiome-brain axis. We hypothesized that the cognitive impairment induced by risperidone is mediated by alterations in the gut microbiome and its metabolites.

RESULTS: In this study, we found that early-life risperidone exposure impaired cognition in mice, including deficits in behavior tests and hippocampal dendritic architecture. The risperidone-exposed mice also exhibited gut microbiota dysbiosis along with damage to the intestinal barrier. Fecal microbiota transplantation (FMT) from treated donors to recipients demonstrated the causal role of the gut microbiome in risperidone-induced cognitive deficits. Of note, risperidone increased the abundance of species Escherichia coli, Eggerthella lenta, Ruminococcus gnavus, Clostridium perfringens, Clostridium difficile, and Blautia hydrogenotrophica. These altered species are identified to encode 7α-HSDH, 3β/α-HSDH, TyrB, and porA, the key enzymes in secondary bile acid metabolism and tyrosine metabolism. Furthermore, a significant reduction in tauroursodeoxycholic acid (TUDCA, the metabolite of bile acid metabolism) and accumulation of p-cresol (the metabolite of tyrosine metabolism) were observed in the brains of mice exposed to risperidone. Mechanically, TUDCA prevented cognitive impairment and endoplasmic reticulum (ER) stress in the hippocampus induced by risperidone, while p-cresol induced neuronal ER stress. Knockout of protein tyrosine phosphatase 1B (PTP1B, ER stress-associated protein) in neurons ameliorated cognitive impairment and neurological damage induced by risperidone.

CONCLUSIONS: This study, for the first time, reveals that early risperidone exposure induces gut microbiome dysbiosis and disturbs the bile acids/tyrosine-PTP1B axis to impair cognitive function. These findings alert the risk of gut and neurological side effects of SGAs treatment and highlight that it is crucial to maintain gut homeostasis during the brain developmental phases of children and adolescents with SGAs exposure. Video Abstract.},
}

@article {pmid41761083,
year = {2026},
author = {Mo, C and Shao, R and Shi, Z and Lou, X and Xue, J and Ning, D and Liu, Y and Jiang, W and Wei, X and Xiao, J and Wang, F and Chen, G},
title = {Fecal microbiota transplantation reduces susceptibility to post-antibiotic CLP-induced sepsis by modulating the gut microbiota and its metabolites.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-026-04858-3},
pmid = {41761083},
issn = {1471-2180},
support = {202401AS070017//Yunnan Provincial Basic Research Program/ ; 202302AA310042//The Yunnan Provincial Major Program in Biomedicine/ ; 8256080235//National Natural Science Foundation of China/ ; },
abstract = {Sepsis remains a leading cause of mortality in intensive care units, and antibiotics continue to serve as the cornerstone of treatment. However, their potentially detrimental effects on gut health are often overlooked. Although antibiotic exposure may increase susceptibility to disease, its contribution to the progression of sepsis has not been fully elucidated. In this study, we investigated the effects of antibiotics on the gut microbiota, microbial metabolites, and intestinal barrier integrity in healthy mice, and further evaluated their impact on subsequent sepsis outcomes. Using a cecal ligation and puncture (CLP)-induced sepsis model, we demonstrated that antibiotic-induced gut dysbiosis exacerbated intestinal barrier damage and significantly increased mortality. In contrast, fecal microbiota transplantation (FMT) markedly improved survival and restored intestinal barrier function. Mechanistically, the protective effects of FMT were associated with modulation of the Hippo signaling pathway, which was accompanied by reduced intestinal permeability. Collectively, these findings highlight the critical role of antibiotic-induced gut dysbiosis in the pathogenesis of sepsis and support FMT as a potential therapeutic strategy to alleviate intestinal barrier damage and improve survival in sepsis.},
}

@article {pmid41760447,
year = {2026},
author = {Martin, M and Nguyen, VM and Puyade, M and Broca, F and Roblot, P},
title = {Faecal incontinence in systemic sclerosis: A narrative review.},
journal = {La Revue de medecine interne},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.revmed.2026.02.001},
pmid = {41760447},
issn = {1768-3122},
abstract = {Although associated with impaired health-related quality of life, faecal incontinence (FI) is underscreened in cases of systemic sclerosis (SSc). Its pathophysiology is complex and multifactorial, encompassing vasculopathy, fibrosis and probably (autoimmune) neuropathy. FI prevalence in SSc seems to be 5-6-fold higher than in the age- and sex-matched general population and is severe in nearly 15% of cases. FI is associated with diarrhoea, small intestinal bacterial overgrowth, constipation, urinary incontinence, anticentromere positivity and some features of vasculopathy. FI should be regularly screened in all SSc patients. Simple self-questionnaires are useful tools, completed by meticulous digital rectal exam for anal and puborectalis tone and by neurological examination. In case of unexplained chronic constipation or diarrhoea, endoscopic explorations are mandatory first to search for organic cause. Anorectal manometry is recommended in case of suspected anorectal dysfunction. Management should be multidisciplinary and, in general, follows the recommendations applied to the general population. It consists mainly in diet and lifestyle modifications and biofeedback therapy. Loperamide or laxative/transanal irrigation could be proposed as options in case of chronic diarrhoea or terminal constipation respectively. Nerve stimulation and faecal microbiota transplantation require further studies before conclusions can be drawn.},
}

@article {pmid41759744,
year = {2026},
author = {Waghmare, PV and Kolekar, KA and Bashir, B and Kumbhar, PS and Patil, KS and Gupta, G and Prasher, P and Jha, SK and Disouza, J and Gurav, SS and Dua, K and Singh, SK},
title = {Advocating gut-retina connection and microbiota mediated pathways in management of age-related macular degeneration: Preclinical to clinical perspective.},
journal = {Ageing research reviews},
volume = {117},
number = {},
pages = {103071},
doi = {10.1016/j.arr.2026.103071},
pmid = {41759744},
issn = {1872-9649},
abstract = {Age-related macular degeneration (ARMD) is the primary manifestation of permanent vision loss internationally. Different factors that contribute to ARMD involve ageing, genetic predisposition, oxidative stress, immunological imbalances, aberrations in the breakdown of lipids, and persistent inflammation. Gut microbiota has emerged as the significant cause of ARMD by disrupting systemic immune and inflammatory responses and metabolic homeostasis. Age-related changes in gut microbiota (dysbiosis) cause lowered microbial diversity, enhanced gut permeability, and pro-inflammatory species, leading to macular damage. The healthy gut microbiota containing Lactobacillus casei, Lactobacillus plantarum, Lactobacillus rhamnosus, Bifidobacterium bifidum, Bifidobacterium breve, Bifidobacterium longum, and Faecalibacterium prausnitzii, are responsible for maintaining gut homeostasis, protecting the retina, and preventing ARMD progression. In contrast, the elevated population of pathogenic species such as Escherichia coli, Prevotella, Desulfovibrio, Enterococcus faecalis, and Streptococcus salivarius in gut dysbiosis is involved in ARMD progression. This review explores gut microbiota and their dynamics in ageing. The age-dependent gut microbiota variations and potential biological implications for the progression of ARMD are discussed. The review also discusses observations from experimental animals and explores potential microbiome-centered treatment avenues, covering probiotics, synbiotics, dietary remedies, metabolite-based treatment, and fecal microbiota transplantation for managing ARMD. Furthermore, various challenges in the management of gut microbiota-driven ARMD are also briefed with future directions. Thus, a gut microbiota-focused paradigm can offer novel choices for ARMD prevention and treatment.},
}

@article {pmid41759374,
year = {2026},
author = {Zhou, H and Huang, Y and Chen, C and Song, M and Hylemon, PB},
title = {Gut microbiome and bile acid metabolism in liver disease: Mechanisms, clinical implications, and therapeutic opportunities.},
journal = {Pharmacological reviews},
volume = {78},
number = {2},
pages = {100120},
doi = {10.1016/j.pharmr.2026.100120},
pmid = {41759374},
issn = {1521-0081},
abstract = {The intricate interplay between the gut microbiome and bile acid metabolism via the gut-liver axis is fundamental to hepatic homeostasis. Perturbations in this axis are increasingly implicated in the pathogenesis of diverse liver diseases, including metabolic dysfunction-associated steatotic liver disease, alcohol-associated liver disease, cholestatic liver diseases, and hepatocellular carcinoma. This review integrates current understanding of hepatic bile acid synthesis, enterohepatic circulation, and gut microbial bile acid transformations, detailing how bile acids function as signaling molecules through nuclear receptors including farnesoid X receptor, pregnane X receptor, vitamin D receptor, constitutive androstane receptor, and G-protein-coupled receptors; G protein-coupled bile acid receptor 1 (also known as Takeda G protein-coupled receptor 5), and sphingosine-1-phosphate receptor 2. We explore disease-specific alterations in gut microbiota composition and bile acid profiles in metabolic dysfunction-associated steatotic liver disease, alcohol-associated liver disease, cholestatic liver diseases, and liver cancers, focusing on mechanisms linking gut dysbiosis, impaired intestinal barrier function, altered bile acid signaling, inflammation, and immune modulation to liver injury and progression. Furthermore, we discuss the clinical implications, highlighting the potential of microbiome signatures and bile acid profiles as diagnostic and prognostic biomarkers. Therapeutic strategies targeting the gut-liver axis, including probiotics, fecal microbiota transplantation, farnesoid X receptor agonists, and fibroblast growth factor 19 analogs, are reviewed. Finally, we address current challenges and future directions, emphasizing the need for multiomics integration, functional studies, and personalized medicine approaches to leverage the gut-liver axis for improved liver disease management. SIGNIFICANCE STATEMENT: Disruption of the gut microbiome-bile acid-liver axis is now recognized as a unifying mechanism driving multiple liver diseases, including metabolic dysfunction-associated steatotic liver disease, alcohol-associated liver disease, cholestatic liver diseases, and hepatocellular carcinoma. Unraveling the molecular and microbial interactions within this axis offers fundamental insights into disease pathogenesis and reveals novel therapeutic opportunities. Integrating multiomics technologies with artificial intelligence-based analytics will accelerate the discovery of predictive biomarkers and personalized interventions, advancing the field toward precision-based liver disease treatment protocols.},
}

@article {pmid41759265,
year = {2026},
author = {Qu, Y and Wang, P and Wang, D and Li, B and Yang, F},
title = {Intermittent fasting protects MPTP-induced Parkinson's disease mouse model through regulating gut microbiota dysbiosis.},
journal = {International immunopharmacology},
volume = {175},
number = {},
pages = {116447},
doi = {10.1016/j.intimp.2026.116447},
pmid = {41759265},
issn = {1878-1705},
abstract = {Parkinson's disease (PD) is a neurodegenerative disorder characterized by gut microbiota dysbiosis and excessive inflammatory responses. Intermittent fasting (IF) exerts neuroprotective effects on neurodegenerative diseases. However, the impact of IF on PD and its mechanisms still need to be elucidated. In the present study, we found that 13-week IF regimen (designed as alternate-day fasting) mitigated motor impairment, α-synuclein aggregation, and loss of dopaminergic neurons in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice. Meanwhile, IF attenuated intestinal dysfunctions, intestinal pro-inflammatory cytokines (tumor necrosis factor-αlphα (TNF-α) and interleukin-1 beta (IL-1β)) levels, and gut barrier destruction. Furthermore, IF alleviated brain barrier impairment and suppressed the activation of astrocytes and microglia. Mechanistic studies revealed that IF suppressed the toll-like receptor 4 (TLR4)/NF-κB signaling pathway both in the colon and substantia nigra. 16S rRNA sequencing demonstrated that IF alleviated MPTP-induced microbiota dysbiosis, decreasing harmful bacteria abundances (Proteobacteria, Burkholderiales, Sutterellaceae, Parasutterella, Burkholderiales_bacterium, and Desulfovibrio_fairfieldensis) while increasing probiotic bacteria abundances (Oscillospirales, Rikenellaceae, and Lactobacillus_murinus), which were significantly correlated with the anti-inflammatory effects of IF. Gas chromatography-mass spectrometry (GC-MS) revealed that IF induced the levels of fecal short chain fatty acids (SCFAs). Antibiotics intervention abolished the beneficial effects of IF, suggesting that gut microbiota contributed to the neuroprotection of IF for PD. These findings suggest that IF regimen may serve as a novel therapeutic strategy for PD, likely linked to its regulation of gut microbiota to inhibit gut-brain axis inflammation.},
}

@article {pmid41757041,
year = {2026},
author = {Tschang, MA and Vuong, RD and Eilers, B and Chac, D and Waalkes, A and Penewit, K and Easton, A and Schuessler, B and Daniels, R and Weil, AA and Salipante, SJ and Gibbons, SM and Schindler, AG},
title = {If you give a mouse a poopsicle: a novel fecal microbiota transplant method for exploring the role of the gut microbiome in stress-related outcomes in mice.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.02.16.705192},
pmid = {41757041},
issn = {2692-8205},
abstract = {The microbiome-gut-brain axis is a mediator of stress-related disorders. The number of preclinical studies exploring the potential causal mechanism of this connection using fecal microbiota transplantation (FMT) is growing. However, the most common method for delivering fecal transplants in rodent models is still oral gavage, which creates an adverse experience that may confound stress-related outcomes. Here, we establish an alternative methodology for FMT that decreases stress induced by traditional experimental procedures. We first used preference and anxiety behavior assays to identify antibiotic therapies having maximal tolerability and minimal anxiolytic properties. We then collected feces from donor mice and homogenized them with a microbe-stabilizing buffer to create a slurry, which was frozen into pellets ("poopsicles") for subsequent FMT. Recipient mice voluntarily consumed the pellets, and blood was collected to compare corticosterone levels relative to traditional gavage FMT. Plasma corticosterone levels were found to be significantly lower in mice receiving FMT via pellets compared to oral gavage. Furthermore, relative to gavage FMT, microbial signatures of mice receiving FMT via pellets were more similar to those of the donor pellets at one week following final FMT and were sustained for up to six weeks, as assessed by comparing Bray-Curtis beta-diversity distances. Together, these results establish effective antibiotic and FMT methods that minimize treatment-induced stress, while effectively transplanting fecal microbes between murine conspecifics.},
}

@article {pmid41754939,
year = {2026},
author = {Cosimato, I and Brescia, A and Franci, G and Casolaro, V and Folliero, V},
title = {Emerging Therapeutic Approaches for Modulating the Intestinal Microbiota.},
journal = {Pharmaceutics},
volume = {18},
number = {2},
pages = {},
pmid = {41754939},
issn = {1999-4923},
abstract = {Background/Objectives: The gut microbiota is increasingly recognized as a key determinant of human health, playing a vital role in metabolism, immunity, and disease susceptibility. Dysbiosis, or microbial imbalance, is associated with gastrointestinal disorders such as irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), and Clostridioides difficile infection (CDI), as well as extraintestinal conditions, including obesity, cardiovascular disease, and neuropsychiatric disorders. This review aims to provide an updated overview of emerging therapeutic strategies to modulate the gut microbiota to restore eubiosis and improve health outcomes. Methods: A narrative review of recent literature was conducted, focusing on preclinical and clinical studies investigating microbiota-targeted therapies. The review primarily covers innovative interventional approaches, including fecal microbiota transplantation (FMT), bacterial consortium transplantation (BCT), bacteriophage therapy and outer membrane vesicles (OMVs). Results: Evidence supports the role of probiotics, prebiotics, and synbiotics in remodeling microbial communities and improving host health, although their effects may be strain- and context-dependent. FMT has demonstrated high efficacy in the treatment of recurrent Clostridium difficile infections and is being studied for IBD, IBS and extraintestinal diseases, following the recent Food and Drug Administration approval of the first commercial FMT products. BCT offers a standardized alternative to donor-derived material, with early clinical successes such as FDA-approved SER-109. Phage therapy and OMVs represent promising frontiers, offering targeted microbial modulation and interactions with the immune system, although clinical data remain limited. Conclusions: Emerging gut microbiota modulation strategies offer new perspectives for precision medicine and could transform the prevention and treatment of many diseases, but further studies are needed to ensure their safety, standardization, and clinical application.},
}

@article {pmid41754110,
year = {2026},
author = {Singh, N and Hosein, E and Virkud, YV and Keet, C and Kulis, M},
title = {The Gut Microbiome in the IgE-Mediated Food-Allergic Patient-A Narrative Review.},
journal = {Nutrients},
volume = {18},
number = {4},
pages = {},
pmid = {41754110},
issn = {2072-6643},
abstract = {Food allergies (FA) are a major public health concern in both children and adults. Immunoglobulin E (IgE)-mediated FA is characterized by allergic reactions driven by allergen-specific IgE and the subsequent degranulation of mast cells and basophils. Current FA management primarily involves avoidance of allergen-containing food, and more recently, therapies such as oral immunotherapy (OIT), sublingual immunotherapy (SLIT), and the anti-IgE biologic omalizumab. However, these interventions are not curative. The gut microbiome has been implicated in the development and regulation of oral tolerance to food antigens. This narrative review explores the role of probiotics, fecal microbiota transplantation (FMT), dietary interventions, and the interaction between the microbiome and OIT as potential strategies to manage established FA. We also explore barriers to their proliferation as part of regular clinical care. We conclude that future research should (1) address how the microbiome interacts with immunotherapies other than OIT, (2) explore the role of novel microbiome-based treatments like FMT as potential adjuvants to existing food allergy therapeutics, and (3) focus on developing standardized protocols and endpoints for microbiome-based therapeutics.},
}

@article {pmid41754077,
year = {2026},
author = {Ashkanani, G and Rob, M and Yousef, M and Ashkanani, A and Al-Najjar, YA and Laws, S and Chaari, A},
title = {The Effects of Microbiome Modulating Therapies on Inflammatory Markers in Autoimmune Disease: A Systematic Review and Meta-Analysis.},
journal = {Nutrients},
volume = {18},
number = {4},
pages = {},
pmid = {41754077},
issn = {2072-6643},
abstract = {BACKGROUND: Autoimmune diseases (ADs) are a growing global health burden, driven by chronic inflammation and immune dysregulation. The gut-immune axis plays a central role in their pathogenesis, with dysbiosis linked to several conditions. This has prompted investigation into nutraceuticals such as probiotics, prebiotics, synbiotics, and fecal microbiota transplantation as adjunctive therapies.

METHODS: We conducted a systematic review and meta-analysis following PRISMA guidelines, searching PubMed, Embase, and Web of Science for randomized controlled trials evaluating these interventions in autoimmune diseases.

RESULTS: Twenty-eight randomized control trials (RCTs) involving 2002 patients across 11 countries met inclusion criteria. Across the included RCTs, pooled analyses demonstrated significant reductions in c-reactive protein (CRP) (SMD -0.67, 95% CI -1.00 to -0.33; I[2] = 80.8%) and Tumor necrosis factor-alpha (TNF-α) (SMD -1.81, 95% CI -2.67 to -0.94; I[2] = 96%), a significant increase in Interleukin-10 (IL-10) (SMD 2.65, 95% CI 0.64 to 4.66; I[2] = 98%), and no overall significant effect on Interleukin-6 (IL-6) (SMD -0.89, 95% CI -1.99 to 0.22; p = 0.12). The strongest evidence of benefit was observed in rheumatoid arthritis, multiple sclerosis, and inflammatory bowel disease. Pooled effects are limited by extreme between-study heterogeneity (I[2] 80-98%), leaving interpretation as exploratory rather than definitive. More limited or inconsistent findings were reported for systemic lupus erythematosus, hypothyroidism, axial spondylarthritis, and juvenile idiopathic arthritis. Heterogeneity in study design, probiotic strain selection, dosage, and treatment duration limited comparability across trials.

CONCLUSIONS: Overall, microbiome-targeted nutraceuticals appear promising for attenuating systemic inflammation in select autoimmune conditions, but results remain mixed. Larger, rigorously designed RCTs with standardized endpoints are needed to clarify efficacy, identify optimal formulations, and define patient populations most likely to benefit.},
}

@article {pmid41753607,
year = {2026},
author = {Yuan, H and Yi, L and Jia, H and Song, G and Cheng, W and Xie, Y and Zhu, J and Zhao, S},
title = {Gut Microbiota-Derived Metabolites to Regulate Intramuscular Fat Deposition in Pigs.},
journal = {Microorganisms},
volume = {14},
number = {2},
pages = {},
pmid = {41753607},
issn = {2076-2607},
support = {2024YFD1800404//National Key Research and Development Program of China/ ; 32360808//National Natural Science Foundation of China/ ; 31760645//National Natural Science Foundation of China/ ; 31260592//National Natural Science Foundation of China/ ; 31060331//National Natural Science Foundation of China/ ; 32560790//National Natural Science Foundation of China/ ; 202202AE090032//Major Science and Technology Project of Yunnan Province/ ; 202501AS070086//Major Science and Technology Projects of Yunnan Province/ ; },
abstract = {Intramuscular fat (IMF) is a crucial determinant of pork quality, influencing tenderness, flavor, and consumer preferences, yet selective breeding has reduced its levels in modern pigs. This review explores the molecular and cellular mechanisms of IMF deposition, including progenitor cell differentiation via pathways like Wnt/β-catenin and PPARγ, and advances in non-invasive detection methods such as hyperspectral imaging and Raman spectroscopy. It highlights correlations and causal links between the gut microbiota composition and IMF, established through omics analyses, fecal microbiota transplantation, and germ-free models. Key microbial metabolites, including short-chain fatty acids (SCFAs) and bile acids, modulate lipid metabolism bidirectionally via signaling receptors like GPR43, FXR, and TGR5. Future research should integrate multi-omics and develop probiotics to enhance IMF efficiency for sustainable pork production.},
}

@article {pmid41752141,
year = {2026},
author = {Wu, Y and Wong, OWH and Chen, S and Wang, Y and Zhang, G and Gao, Y and Chan, FKL and Ng, SC and Su, Q},
title = {Gut Microbiome Mediates the Causal Link Between Autism Spectrum Disorder and Dietary Preferences: A Mendelian Randomization Study.},
journal = {International journal of molecular sciences},
volume = {27},
number = {4},
pages = {},
pmid = {41752141},
issn = {1422-0067},
abstract = {Autism spectrum disorder (ASD) frequently co-occurs with malnutrition and gut dysbiosis, yet the underlying mechanisms remain poorly understood. Herein, this cross-sectional study first profiles dietary intake differences using dietary records from 210,874 participants (ASD = 232; non-ASD = 210,642; median age = 56.18) from the UK Biobank (UKB). Second, a bi-directional Mendelian Randomization (MR) approach serves to dissect relationships between ASD genetic susceptibility and dietary preferences by leveraging genome-wide association metadata from the iPSYCH-PGC (ASD) and UKB (dietary intake/food-liking traits). The same strategy is implemented to identify ASD-associated gut microbial species. Mediation analyses further assess the role of gut microbiota in the association between ASD and dietary preferences. Subjects with ASD exhibit higher consumption of cheese, processed meat, and oily fish, alongside lower intake of fruits, and demonstrate a preference for high-fat/salt and energy-dense foods. Additionally, the depletion of Turicibacter, Streptococcus, and Lachnospiraceae NK4A136 was causally related with ASD (all false discovery rate < 0.05; β = -0.15, β = -0.10, β = -0.093, respectively), which significantly mediates the ASD-associated elevated preference for high-fat/salt foods. In conclusion, ASD is associated with specific dietary preferences, likely mediated via gut microbiota, highlighting the future potential of gut microbiome-based therapeutics to modify eating disorders for ASD.},
}

@article {pmid41752122,
year = {2026},
author = {Wang, SJ and Nian, HY and Chen, ZH and Cui, L},
title = {Human Microbiota-Associated Pig Models for Translational Microbiome Research: A Scoping Review.},
journal = {International journal of molecular sciences},
volume = {27},
number = {4},
pages = {},
pmid = {41752122},
issn = {1422-0067},
support = {23141900100//Science and Technology Commission of Shanghai Municipality/ ; },
abstract = {The human microbiota-associated (HMA) pig model provides a physiologically relevant platform that bridges preclinical and translational research. However, its use remains limited, with existing studies showing considerable variation in establishment methods. This scoping review systematically evaluates methodological frameworks, engraftment outcomes, and research applications of HMA pig models. Additionally, it highlights their strengths, limitations, and implications for future studies. We conducted a comprehensive literature search in PubMed, Web of Science, Scopus, and Directory of Open Access Journals, following PRISMA guidelines for Scoping Reviews. The review examines the methodological foundations of HMA pig model generation and proposes a minimal reporting framework to promote standardization. It synthesizes studies on human microbiota engraftment in pigs, identifying factors that influence colonization efficiency. Finally, it summarizes current applications, discusses persistent limitations and translational challenges, and outlines opportunities for future research. Overall, these integrated insights aim to foster standardized, reproducible protocols for HMA pig model preparation and guide advancements in the field.},
}

@article {pmid41752118,
year = {2026},
author = {Kurdi, MA and Alotaibi, H and Alkhuraymi, AT and Aldahery, LN and Alhawaj, AF and Aldali, HJ},
title = {Amyotrophic Lateral Sclerosis (ALS) Genetics and Microbiota: A Comprehensive Review.},
journal = {International journal of molecular sciences},
volume = {27},
number = {4},
pages = {},
pmid = {41752118},
issn = {1422-0067},
abstract = {Amyotrophic Lateral Sclerosis (ALS) is a severe, progressive neurodegenerative disorder characterized by the loss of upper and lower motor neurons, affecting 0.5 to 2.6 per 100,000 people, with a median survival of 2 to 5 years. It is increasingly seen as a multisystem disorder, sharing essential clinicopathological features with Frontotemporal Dementia (FTD). This convergence arises from overlapping molecular processes, including severe oxidative stress, glutamate-mediated excitotoxicity, mitochondrial dysfunction, and widespread aggregated TDP-43 proteinopathy in both sporadic and familial cases. Several key genetic factors have been identified, particularly mutations in C9orf72, SOD1, TARDBP, and FUS, which serve as important targets for novel treatments, such as Tofersen, a recently approved SOD1-specific antisense oligonucleotide (ASO) gene therapy. Additionally, there is increasing evidence of the gut-brain connection. Dysbiosis, involving species such as Akkermansia muciniphila, and lower levels of neuroprotective metabolites, such as nicotinamide, may affect the course of the disease. As a result, treatment strategies are shifting toward a personalized approach. This includes using gene therapy, ranging from ASOs and RNA interference (RNAi) to new CRISPR-based genome editing. It also involves exploring microbiome-modulating treatments, such as specific probiotics and Fecal Microbiota Transplantation (FMT). While microbiome and gene therapies remain largely experimental, their potential is promising, as highlighted by the recent approval of Tofersen. These novel approaches could be further enhanced and guided by more robust diagnostic criteria and by investigating early multimodal treatment strategies to slow the progression of this complex disease.},
}

@article {pmid41751793,
year = {2026},
author = {Ptáček, O and Musil, Z and Guarnieri, G and Vrbacká, A and Moudrá, P and Zlámalová, A and Röszlerová, P and Tonhajzer, M and Musil, V and Morelli, A and Zach, P},
title = {Amyotrophic Lateral Sclerosis: The State of the Art on Treatments and the Therapeutic Role of the Intestinal Microbiome in Human Studies.},
journal = {International journal of molecular sciences},
volume = {27},
number = {4},
pages = {},
pmid = {41751793},
issn = {1422-0067},
support = {Cooperatio 39 - Oncology and Haematology//Charles University/ ; Cooperatio 33-Intensive Care Medicine//Charles University/ ; Cooperatio 36-Medical Diagnostics and Basic Medical Sciences//Charles University/ ; #NEXTGENERATIONEU//European Commission/ ; MNESYS (PE0000006) - A Multiscale integrated approach to the study of the nervous system in health and disease (DR. 1553 11.10.2022)//Ministry of University and Research (MUR), National Recovery and Resilience Plan (NRRP)/ ; },
abstract = {Amyotrophic lateral sclerosis (ALS) is a common neurodegenerative disorder; to date, there is no long-term effective treatment. Recently, a relationship has been discovered between the human intestinal microbiome and the pathogenesis of ALS, on which basis faecal microbiota transplantation (FMT) has been proposed as a potential treatment for ALS. In this review, we compare three existing case studies examining the effect of FMT on the course of ALS, highlighting differences in methodology and results. In two of the studies, a halt in the progression of ALS symptoms was observed following FMT, accompanied by improvement in patient health. However, in the third and largest study, no significant effect of FMT was observed. The possible explanation for this discrepancy may be the intentional depletion of intestinal microorganisms using antibiotics prior to FMT in the third study. Future studies and/or completion of the ongoing clinical studies will help clarify the therapeutic effectiveness of FMT in ALS patients.},
}

@article {pmid41749649,
year = {2026},
author = {Pawłowski, P and Zaj, N and Iwaniszczuk, K and Grzelka, I and Makuch, W and Samardakiewicz-Kirol, E and Kościołek, A and Samardakiewicz, M},
title = {Personalizing Nutritional Therapy in Pediatric Oncology: The Role of Gut Microbiome Profiling and Metabolomics in Mitigating Mucositis and Enhancing Immune Response to Chemotherapy.},
journal = {Children (Basel, Switzerland)},
volume = {13},
number = {2},
pages = {},
pmid = {41749649},
issn = {2227-9067},
abstract = {INTRODUCTION: Intensive chemotherapy protocols and hematopoietic stem cell transplantation (HSCT) in children with cancer frequently lead to severe complications, such as mucositis and immune dysfunction. A growing body of evidence indicates that these complications are closely associated with the patient's nutritional status and the composition of the gut microbiome, which becomes profoundly destabilized as a result of cytotoxic therapy and antibiotic use.

BACKGROUND: The aim of this review is to critically evaluate the current state of knowledge on the interplay between gut dysbiosis, metabolomic profiles-with particular emphasis on short-chain fatty acids (SCFAs)-and treatment-related toxicity in pediatric patients, as well as to delineate pathways toward personalized nutritional therapy.

METHODS: A narrative review was conducted, including clinical and preclinical studies published between January 2015 and October 2025. PubMed/MEDLINE, Embase, Cochrane Library, and other databases were searched, focusing on changes in microbiome composition, correlations between gut-derived metabolites and the severity of complications (sepsis, graft-versus-host disease [GvHD], mucositis), and the effects of targeted nutritional interventions (probiotics, prebiotics, postbiotics, and fecal microbiota transplantation [FMT]) on microbiome modulation during anticancer therapy.

RESULTS: The analysis demonstrates that pediatric oncologic treatment leads to a marked reduction in microbial diversity, including the loss of protective Clostridiales taxa (e.g., Faecalibacterium), accompanied by an overgrowth of Proteobacteria pathobionts. Metabolomic profiling indicates that low SCFA levels (e.g., butyrate < 20-50 µmol/g) are a strong predictor of severe mucositis, prolonged neutropenia, and an increased risk of sepsis. Interventions aimed at restoring eubiosis and enhancing SCFA production show potential in strengthening the intestinal barrier, modulating immune responses, and enabling maintenance of the planned relative dose intensity (RDI) of chemotherapy by reducing treatment-related toxicity.

CONCLUSIONS: Gut microbiome profiling and fecal metabolomics represent promising prognostic tools in pediatric oncology. There is an urgent need for further research employing "omics"-based approaches to develop precise, individually tailored nutritional protocols. Such strategies, including postbiotics and FMT, may minimize treatment-related adverse effects and improve long-term clinical outcomes in pediatric patients.},
}

@article {pmid41749264,
year = {2026},
author = {Li, L and Cai, F and Liu, Z and Mo, W and Zhang, J and Qin, J and Liang, C and Xu, H and Liu, S and Tang, S and Peng, P and Liang, J and Ruan, H and Qin, R and Luo, F and Xiong, G and Yang, C and Zou, J and Liu, S and Geng, Y and Huang, J},
title = {Cross-kingdom microbial interactions in the gut during inflammatory bowel disease.},
journal = {Journal of translational medicine},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12967-026-07692-3},
pmid = {41749264},
issn = {1479-5876},
abstract = {BACKGROUND: Inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), is characterized by chronic, relapsing inflammation of the gastrointestinal tract. Recent studies emphasize the importance of gut microbiome dysbiosis in IBD pathogenesis, where interactions among bacteria, fungi, protozoa, and viruses contribute to inflammation, immune modulation, and epithelial barrier disruption.

METHODS: A comprehensive narrative literature review was conducted, focusing on human data and preclinical studies. Biomedical databases were searched for research related to microbial communities and their role in IBD development, specifically targeting microbial metabolites, gut fungi, protozoa, and viruses. Relevant studies were analyzed to assess their impact on immune pathways and microbial interactions.

RESULTS: The review reveals how different microbial kingdoms collaborate through bacteria-fungi, bacteria-protozoa, and phage-bacteria interactions, influencing metabolite production and immune system function. Specific microbial metabolites like short-chain fatty acids (SCFAs), indoles, bile acids, and others play significant roles in regulating mucosal immunity and barrier function. Disruptions in these interactions lead to chronic inflammation and contribute to disease progression. Multi-kingdom therapies, including probiotics, yeast-based treatments, and fecal microbiota transplantation (FMT), show promise but face challenges due to clinical variability.

CONCLUSION: Understanding IBD as a disruption of microbial ecosystems enables the development of personalized treatment strategies. Multi-omics studies and microbiome-based interventions targeting specific microbial interactions hold potential for more effective, individualized therapies in IBD management. However, further research and larger clinical trials are necessary for translating these findings into routine clinical practice.},
}

@article {pmid41747917,
year = {2026},
author = {Liu, X and Wang, Y and Medina, AA and Liu, D and Liu, J and Tang, W and Wang, M and Chen, X and Huang, K and Liu, M and Wang, C and Liu, Y},
title = {Probiotic-derived extracellular vesicles attenuate cholestatic liver damage via gut-liver axis.},
journal = {Pharmacological research},
volume = {},
number = {},
pages = {108152},
doi = {10.1016/j.phrs.2026.108152},
pmid = {41747917},
issn = {1096-1186},
abstract = {Gut-liver axis disturbance is the unifying pathogenesis of cholestatic liver diseases. The purpose of this study was to explore the underlying mechanisms of the probiotic Lactobacillus amylovorus (LA) and its secreted extracellular vesicles (EVs) on liver damage and fibrosis in 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC)-fed and multidrug resistance protein 2 knockout (Mdr2[-/-]) mice. Direct replenishment of LA is sufficient to correct the DDC-fed and Mdr2[-/-]-induced liver damage and fibrosis. Mechanistic studies show that the secretion of EVs is required for the LA-induced liver protective effects. RNA sequencing results demonstrated that the enrichment of differentially expressed genes was associated with glutathione metabolism, microbial metabolism in diverse environments and inflammatory mediator regulation of TRP channels in DDC-fed mice. Our findings revealed that LAEVs reshaped the gut microbiota, which was associated with increased bile acids (BAs) deconjugation and fecal BAs excretion, repaired gut barrier function, activated intestinal Farnesoid X receptor/Fibroblast growth factor 15 (FXR/FGF-15) axis, reduced liver BAs and oxidative stress level, which ultimately mitigated liver damage and fibrosis in both DDC-fed and Mdr2[-/-] mice. Notably, LAEVs did not ameliorate DDC-induced liver damage or fibrosis in antibiotic-treated mice. Furthermore, LAEVs provided protection against DDC-induced liver injury and fibrosis in fecal microbiota transplantation mice. LAEVs did not ameliorate DDC-induced liver damage or fibrosis in BSH inhibitor (CAPE)-treated mice. LAEVs also failed to improve liver damage and fibrosis in DDC-induced intestinal epithelial cell-specific FXR knockout (Fxr[△IE]) mice. This study revealed that LAEVs mitigated cholestatic liver fibrosis via regulating gut microbiota-bile acid-ROS axis in mice.},
}

@article {pmid41747877,
year = {2026},
author = {Waghmare, A and Rahangadale, S and Khare, K and Taksande, B and Umekar, M and Mangrulkar, S},
title = {Interweaving microglial senescence and gut microbiome dynamics in Alzheimer's disease - Mechanisms and therapeutic frontiers.},
journal = {Molecular and cellular neurosciences},
volume = {},
number = {},
pages = {104075},
doi = {10.1016/j.mcn.2026.104075},
pmid = {41747877},
issn = {1095-9327},
abstract = {Alzheimer's disease (AD), a prevalent neurodegenerative disorder characterized by cognitive impairment and neuronal degeneration, is increasingly recognized as being driven not only by the traditional amyloid-beta and tau pathologies but also by persistent neuroinflammation and systemic immune dysregulation. Emerging evidence implicates microglia senescence and gut microbiota dysbiosis is critical contributors to the neuroinflammatory landscape. Senescent microglia marked by reduced phagocytic ability and a pro-inflammatory secretory profile, are unable to clear pathogenic stimuli, thereby intensifying neuronal damage. Simultaneously, gut dysbiosis, characterized by a reduction in beneficial bacteria and an increase in endotoxin-producing species, elevates systemic inflammation and compromises the intestinal and blood brain barrier. Microbial metabolites, such as short-chain fatty acids (SCFAs) and lipopolysaccharides (LPS), affect microglial activation through the gut-brain axis, primarily via the TLR4/NF-κB and NLRP3 inflammasome pathways, thus promoting microglial senescence and exacerbating AD pathology. Therapeutic approaches that target these interacting pathways are rejuvenation of microglia with senolytics and stimulation of TREM2; regulation of gut microbiota with probiotics, prebiotics, lifestyle modification, dietary intervention; and fecal microbiota transplantation. Precision medicine approaches incorporating microbiome profiling and immunogenetic analysis will enhance these treatments. This review combines mechanistic insight into microglial aging and gut-brain interaction, emphasizes their synergistic role in AD pathogenesis, and delineates integrated therapeutic strategies. Dissection of the gut-microglia axis can reveal novel targets for early intervention to counteract neuroinflammation, improve cognitive function, and slow disease progression in AD.},
}

@article {pmid41747725,
year = {2026},
author = {Chen, K and Liu, Y and Rong, J and Dai, N and Xu, C and Li, H and Zhong, L and Wang, B and Ji, Z and Xie, S and Xu, Y and Yang, F and Wang, J and Li, D and Gu, Y and Zhou, X and Li, Y and Chen, M and Chen, Y and Li, W and Tang, Z and Cai, J and Xu, J and Xia, S and Zhan, Q and Zhou, Z},
title = {Strain-level genetic heterogeneity and colonization dynamics drive microbiome therapeutic efficacy.},
journal = {Cell host & microbe},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.chom.2026.02.002},
pmid = {41747725},
issn = {1934-6069},
abstract = {Fecal microbiota transplantation (FMT) has shown immunotherapeutic promise, yet its efficacy in non-small-cell lung cancer (NSCLC) remains unclear. We demonstrate that FMT improves anti-PD-1 efficacy and progression-free survival in a single-arm trial of advanced PD-L1-negative NSCLC. Analyzing over 2,000 metagenomes from diverse disease cohorts and healthy controls via a high-resolution strain-tracking framework, we reveal that phylogenetically distinct strains within identical species exert opposing therapeutic effects, resolving prior inconsistencies. We identify conserved ecological principles where engraftment relies on species-intrinsic metabolic and immune evasion traits. Crucially, successful colonization by specific beneficial strain variants correlates with positive clinical outcomes. Finally, we identify 38 priority species with robust engraftment potential and significant heterogeneity as candidates for precision therapeutics. These findings establish a strain-function-efficacy paradigm, elucidating the mechanistic basis of variable outcomes and guiding next-generation microbiome drug development.},
}

@article {pmid41746975,
year = {2026},
author = {Wang, G and Liu, L and Zhang, H and Mao, P and Lu, S and Zhang, X and Li, X and Song, C},
title = {Effects of tacrolimus treatment on the gut microbiota and metabolites in liver transplant recipients.},
journal = {PloS one},
volume = {21},
number = {2},
pages = {e0343817},
pmid = {41746975},
issn = {1932-6203},
abstract = {BACKGROUND: Liver transplantation (LT) is an effective treatment for patients with end-stage liver disease. In recent years, more and more evidence has supported the association between gut microbiota dysbiosis and the pathogenesis and progression of liver diseases.

METHODS: The study included 36 patients who received tacrolimus treatment after liver transplantation. Patients were stratified into subgroups according to three key variables: tacrolimus treatment duration, whole-blood tacrolimus concentration, and tacrolimus concentration-to-dose (C/D) ratio. Fecal samples and whole-blood specimens were collected from all participants. The Illumina HiSeq X platform was used to detect the gut metagenome, analyzing the composition and characteristics of the gut microbiota. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) technology was employed to detect metabolites of the gut microbiota, revealing their metabolic profiles.

RESULTS: As the duration of tacrolimus use increased, the diversity of the gut microbiota also increased, and the abundance of Escherichia coli_D and Bacteroides stercoris rose. Additionally, the abundance of Brunovirus and Uetakevirus tended to decrease. The abundance of gene functions related to chemical carcinogenesis and bacterial invasion of epithelial cells significantly decreased. In the gut microbiota metabolites, 16 substances like Astragaloside A and Acetyl-L-carnitine significantly increased, while 108 substances like Capsaicin and TLK significantly decreased. Within a certain range, as the concentration of tacrolimus in whole blood increased, the diversity of the gut microbiota increased. The abundance of Phocaeicola and Klebsiella increased, and the abundance of Peduovirus among viruses also rose. However, excessively high concentrations may lead to a decrease in the diversity of the gut microbiota and a decrease in the abundance of Phocaeicola. With respect to the C/D ratio, increased ratios were linked to significantly higher levels of 57 fecal metabolites (e.g., PC 34:2, 5-Methyl-2'-deoxycytidine), whereas 13 metabolites (e.g., FAHFA 2:0/16:0) showed substantial declines.

CONCLUSIONS: Tacrolimus treatment is associated with distinct alterations in gut microbiota and metabolites among LT recipients. These findings provide a preliminary framework for future investigations aimed at optimizing immunosuppressive regimens, although their clinical translational potential requires validation in larger-scale, prospective cohort studies.},
}

@article {pmid41745976,
year = {2026},
author = {Németh, K and Tóth, I and Lányi, K and Schilling-Tóth, BM and Csorba, S and Žura Žaja, I and Sterczer, Á},
title = {The Collaborative Collapse: Bile Acid Dysmetabolism as a Central Pathogenic Driver in Canine and Feline Multi-Systemic Disorders-From Mechanisms to Precision Therapeutics.},
journal = {Veterinary sciences},
volume = {13},
number = {2},
pages = {},
pmid = {41745976},
issn = {2306-7381},
support = {SRF-003//University of Veterinary Medicine Budapest/ ; 2025-2.1.1-EKÖP-2025-00022//Ministry of Culture and Innovation of Hungary from the National Research, Development and Innovation Fund/ ; },
abstract = {Veterinary metabolomics has redefined bile acids (BAs) from simple digestive surfactants to systemic endocrine signals within a microbial-host metabolic axis. This review aims to evaluate how BA dysmetabolism acts as a central pathogenic factor in canine and feline disease. We analyze the BA pool's integrity, which depends on a specialized functional guild, primarily Peptacetobacter hiranonis, responsible for 7α-dehydroxylation. We delineate two principal pathological profiles: (1) microbial collapse, characterized by secondary bile acid (SBA) depletion and compromised farnesoid X receptor (FXR) and Takeda G protein-coupled receptor 5 (TGR5) signaling, which exacerbates inflammation in chronic enteropathy (CE), protein-losing enteropathy (PLE), and exocrine pancreatic insufficiency (EPI); and (2) hepato-biliary spillover, wherein host-induced dysfunction results in primary bile acid (PBA) excess. Recent data have linked these disruptions to skeletal health, feline renal fibrosis, cardiac remodeling in myxomatous mitral valve disease (MMVD), and neuroinflammation in epilepsy and hepatic encephalopathy. The discovery of microbially conjugated bile acids (MCBAs) and microbial extracellular vesicles (MEVs) reveals highly specific, vesicle-mediated communication pathways impacting systemic health. Diagnostic protocols should prioritize functional profiling, including the dysbiosis index (DI), serum conjugated BA analysis, and SBA/PBA ratios. Clinical management is moving beyond empirical fecal microbiota transplantation (FMT), towards precision synthetic microbial consortia (SynComs), neuroprotective BAs like tauroursodeoxycholic acid (TUDCA), and molecular postbiotics to restore the collaborative metabolome.},
}

@article {pmid41745910,
year = {2026},
author = {Cao, X and Zhou, L and Ding, Y and Ma, C and Chen, Q and Li, N and Ren, H and Yan, P and Jia, J},
title = {Study of Fecal Microbiota Transplantation Ameliorates Colon Morphology and Microbiota Function in High-Fat Diet Mice.},
journal = {Veterinary sciences},
volume = {13},
number = {2},
pages = {},
pmid = {41745910},
issn = {2306-7381},
support = {ZR2023MC164//the Natural Science Foundation of Shandong Province/ ; 2022KJ137//the Youth Innovation Team Project Program of Shandong Provincial Education Department/ ; },
abstract = {This study investigates whether fecal microbiota transplantation (FMT) can alleviate gut microbiota dysbiosis induced by a high-fat diet (HFD) through modulation of fatty acid metabolism, competition for nutrients, production of short-chain fatty acids (SCFAs), and restoration of mucus layer integrity. To elucidate the mechanisms by which FMT regulates colonic microbial function and host metabolic responses, 80 male Bal b/c mice were randomly assigned to four experimental groups (n = 20 per group): Normal Diet Group (NDG), High-Fat Diet Group (HDG), Restrictive Diet Group (RDG), and HDG recipients of NDG-derived fecal microbiota (FMT group). The intervention lasted for 12 weeks, during which body weight was monitored biweekly. At the end of the experiment, tissue and fecal samples were collected to assess digestive enzyme activities, intestinal histomorphology, gene expression related to gut barrier function, and gut microbiota composition via 16S rRNA gene sequencing. Results showed that mice in the HDG exhibited significantly higher final body weight and greater weight gain compared to those in the NDG and RDG (p < 0.05). Notably, FMT treatment markedly attenuated HFD-induced weight gain (p < 0.05), reducing it to levels comparable with the NDG (p > 0.05). While HFD significantly elevated the activities of α-amylase and trypsin (p < 0.05), FMT supplementation effectively suppressed these enzymatic activities (p < 0.05). Moreover, FMT ameliorated HFD-induced intestinal architectural damage, as evidenced by significant increases in villus height and the villus height-to-crypt depth ratio (V/C) (p < 0.05). At the molecular level, FMT significantly downregulated the expression of pro-inflammatory cytokines (IL-1β, IL-1α, TNF-α) and upregulated key tight junction proteins (Occludin, Claudin-1, ZO-1) and mucin-2 (MUC2) relative to the HDG (p < 0.05). 16S rRNA analysis demonstrated that FMT substantially increased the abundance of beneficial genera such as Lactobacillus and Bifidobacterium while reducing opportunistic pathogens including Romboutsia (p < 0.05). Furthermore, alpha diversity indices (Chao1 and ACE) were significantly higher in the FMT group than in all other groups (p < 0.05), indicating enhanced microbial richness and community stability. Functional prediction using PICRUSt2 revealed that FMT-enriched metabolic pathways (particularly those associated with SCFA production) and enhanced gut barrier-related functions. Collectively, this study deepens our understanding of host-microbe interactions under HFD-induced metabolic stress and provides mechanistic insights into how FMT restores gut homeostasis, highlighting its potential as a therapeutic strategy for diet-induced dysbiosis and associated metabolic disorders.},
}

@article {pmid41745224,
year = {2026},
author = {Spaggiari, L and Tedeschi, G and Benatti, G and De Benedittis, M and Franzè, MT and Pinetti, D and Pericolini, E and Ardizzoni, A},
title = {Untargeted Metabolomic Analysis of Cell-Free Supernatants (CFSs) from Different Clinical Isolates of Saccharomyces cerevisiae and Their Effects on Candida albicans Virulence.},
journal = {Journal of fungi (Basel, Switzerland)},
volume = {12},
number = {2},
pages = {},
pmid = {41745224},
issn = {2309-608X},
support = {not applicable//FAR Dipartimentale 2024 (Ardizzoni) and FAR Dipartimentale 2025 (Pericolini)/ ; },
abstract = {Saccharomyces cerevisiae probiotic properties are effective for the treatment of infections by the opportunistic pathogen Candida albicans. Here, we assessed the anti-Candida effect of cell-free supernatants (CFSs) from three different fecal isolates and one ATCC strain of S. cerevisiae. We evaluated C. albicans growth inhibition through CFUs, and the impairment of virulence factors (adhesion, biofilm formation, and metabolic activity) by crystal violet and XTT assays. An untargeted metabolomic analysis of the CFSs was also performed. The CFSs moderately reduced C. albicans growth, but they could impair C. albicans virulence by reducing its capacity to adhere and to form a biofilm, and by decreasing the metabolic activity of biofilm-embedded fungal cells. The untargeted metabolomic analysis indicated an overexpression of N-acetyl-DL-tryptophan and other molecules derived from its metabolism (kynurenic acid and indole-3-acrylic acid), the dipeptides glycyl-L-leucine, prolyl-leucine, and γ-L-glutamyl-L-leucine, and the unconventional nucleotide inosine in the CFSs from fecal isolates, as compared to the reference strain. Further studies are warranted to better characterize the metabolome of these CFSs. Should the effects described here also be confirmed in vivo, the possible future employment of S. cerevisiae CFSs as a postbiotic aid to the current antifungal therapy may be considered.},
}

@article {pmid41745080,
year = {2026},
author = {Kumar, S and Himanshu, and Gaur, P and Ahmad, S and Puri, P and Raj, VS and Pandey, RP},
title = {Microbiota Transplantation as a Future Novel Therapeutic Strategy Approach.},
journal = {Diseases (Basel, Switzerland)},
volume = {14},
number = {2},
pages = {},
pmid = {41745080},
issn = {2079-9721},
abstract = {Bacterial vaginosis (BV) is a leading cause of genital discomfort among women globally, and it arises from dysbiosis of the vaginal ecosystem characterized by the overgrowth of pathogenic bacteria. Current therapeutic strategies primarily rely on antibiotics and/or probiotics, which demonstrate clinical efficacy but are frequently associated with limitations such as antimicrobial resistance, high recurrence rates, and incomplete restoration of a healthy vaginal microbiota. Inspired by the success of fecal microbiota transplantation in gastrointestinal disorders, vaginal microbiome transplantation (VMT) from healthy donors has emerged as a potential alternative therapeutic approach for BV. However, experimental and early clinical studies indicate that VMT efficacy is not uniform across individuals, with considerable inter-individual variability in treatment outcomes. Host genetic factors, baseline vaginal microbial composition, immune status, and environmental influences are likely to modulate therapeutic success, underscoring the need for personalized interventions. This article critically evaluates the shortcomings of existing standardized treatments, highlights the potential advantages and challenges of VMT, and discusses emerging, precision-based therapeutic strategies for BV in light of recent research advances and ongoing clinical trials worldwide.},
}

@article {pmid41744425,
year = {2026},
author = {Sandeep, G and Pahari, S and Nayak, V and Gundamaraju, R and Mishra, P and Misra, A},
title = {The Gut-Prostate Axis: Decoding the Interplay of Environmental Factors, Microbial Metabolites, and Hormonal Regulation in Prostate Cancer Pathogenesis.},
journal = {Technology in cancer research & treatment},
volume = {25},
number = {},
pages = {15330338261424322},
pmid = {41744425},
issn = {1533-0338},
abstract = {Prostate cancer remains one of the most common malignancies in men, with its progression strongly influenced by androgen signaling. While genetic alterations are well-documented in prostate cancer, growing evidence highlights the contribution of environmental factors, particularly diet and the gut microbiome, in modulating disease risk and therapy response. The gut microbiota plays a crucial role in regulating host metabolism, immune responses, and hormone activity. Recent findings suggest that specific microbial communities influence androgen biosynthesis and metabolism through enzymes such as β-glucuronidase, altering systemic androgen availability and imp acting tumor progression. Additionally, microbial metabolites, including short-chain fatty acids, secondary bile acids, and bacterial genotoxins, can affect inflammatory pathways and cellular signaling relevant to prostate tumorigenesis. Experimental studies also indicate that modifying the gut microbiota through dietary interventions, probiotics, or fecal microbiota transplantation can influence tumor growth and improve responses to immunotherapy and hormone-based treatments. In this review we present the current knowledge on gut-prostate axis, examine the mechanistic links between microbial activity and prostate cancer biology, and discuss emerging microbiome-based strategies as potential therapies. A deeper understanding of this bidirectional crosstalk could pave the way for microbiome-informed approaches to prevention, diagnosis, and personalized treatment of prostate cancer.},
}

@article {pmid41743894,
year = {2026},
author = {Jayathilaka, NS and Wijekoon, KJ and Sachinthani, SDD and Weththasinghe, AV and Ganamurali, N and Sabarathinam, S},
title = {Enteroendocrine hormones and gut microbiota in obesity: a systematic review from mechanistic insight to precision metabolic care.},
journal = {Journal of diabetes and metabolic disorders},
volume = {25},
number = {1},
pages = {73},
pmid = {41743894},
issn = {2251-6581},
abstract = {PURPOSE: This systematic review aims to synthesize current evidence on enteroendocrine cell alterations in obesity, elucidate the mechanisms by which gut microbial taxa and metabolites regulate gut hormone release, and assess therapeutic innovations targeting the microbiota-enteroendocrine axis for precision metabolic care.

METHODS: A systematic search of PubMed, Web of Science, Scopus, and Embase was conducted from January 2015 to July 2025 following Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 guidelines. Studies examining enteroendocrine cell function, gut microbiota composition, and their metabolic interactions in human obesity, animal models, and cellular systems were included. Data were extracted on gut hormone levels, microbial community structure, short-chain fatty acid production, and therapeutic interventions. Quality assessment was performed using the Cochrane Risk of Bias tool for randomized controlled trials and Newcastle-Ottawa Scale for observational studies.

RESULTS: Microbial dysbiosis characterized by depletion of short-chain fatty acid-producing bacteria is associated with impaired gut hormone release and altered free fatty acid receptor signaling. Therapeutic strategies including glucagon-like peptide-1 receptor agonists are associated with substantial weight loss, whereas probiotics, prebiotics, and fecal microbiota transplantation show variable and generally modest metabolic effects in human studies.

CONCLUSION: The microbiota-enteroendocrine axis represents a promising therapeutic target for obesity management, supported by mechanistic and associative evidence.Multi-modal precision approaches integrating hormonal pharmacotherapy with microbiota modulation may enable more durable metabolic benefits and personalized obesity treatment.},
}

@article {pmid41743795,
year = {2026},
author = {Zhang, J and Ji, J and Dai, X and Li, B and Liu, T and Zhang, S and Yu, Y},
title = {Microplastics and Nanoplastics Cause Thyroid Dysfunction in Adolescent Mice through the Intestinal Microbiota-Mediated Hypothalamus-Pituitary-Thyroid Axis.},
journal = {Environment & health (Washington, D.C.)},
volume = {4},
number = {2},
pages = {313-323},
pmid = {41743795},
issn = {2833-8278},
abstract = {Polypropylene (PP) and poly-(ethylene terephthalate) (PET) plastic products are widely used in diet packaging and may generate microplastics (MPs) and nanoplastics (NPs) during use. However, their effects and mechanisms on causing endocrine system diseases remain unclear. Here, we established a dietary exposure mouse model using micro and nanoplastics (MNPs) and found that MNPs caused a decrease in thyroid function in adolescent mice. Fecal microbiota transplantation (FMT) was used to reconstruct the intestinal microbiota of mice to reveal the mechanisms of thyroid dysfunction. The abundance of Bacteroides in the intestinal tract significantly changed after FMT. PP-MPs and NPs affected the levels of lysophosphatidylethanolamine and fatty acid esters of hydroxy fatty acids, respectively, which competitively bound to thyrotropin receptor (TSHR) on the thyroid gland, thus affecting the thyroid function. PET-MNPs affected the level of 4-hydroxy-3-methoxyphenylglycol sulfate, which regulated the activity of sympathetic nervous system by acting on the thyrotropin-releasing hormone receptor and TSHR in mice, thereby interfering with the regulatory function of the hypothalamus-pituitary-thyroid (HPT) axis on the synthesis and secretion of thyroid hormones. This study emphasizes the key role of intestinal microbiota-mediated HPT axis in thyroid dysfunction caused by MNP exposure and provides theoretical basis for the prevention of endocrine-related diseases during adolescence caused by MNPs.},
}

@article {pmid41743374,
year = {2026},
author = {Marasco, G and Meacci, D and Sarnelli, G and Tosetti, C and Cremon, C and Savarino, EV and Barbara, G},
title = {Diarrhea management: from pathophysiology to microbiota modulation.},
journal = {Therapeutic advances in gastroenterology},
volume = {19},
number = {},
pages = {17562848261424324},
pmid = {41743374},
issn = {1756-283X},
abstract = {Diarrhea, whether acute or chronic, is a common clinical condition with numerous causes that collectively impose significant health, economic, social, and psychological burdens worldwide. Based on its duration, diarrhea is classified as acute when lasting less than 2 weeks and chronic when persisting for more than 4 weeks. From a pathophysiological standpoint, diarrhea can be categorized into four main types: osmotic, secretory, inflammatory, and motility-related. Acute diarrhea is most commonly caused by infectious gastroenteritis and tends to have a self-limited course. In contrast, chronic diarrhea presents a more complex diagnostic challenge due to its varied etiologies and clinical presentations. A shared feature among many causes of both acute and chronic diarrhea is an alteration in the gut microbiota, a condition referred to as dysbiosis. While acute infections often result in temporary microbial imbalance, chronic conditions such as irritable bowel syndrome and symptomatic uncomplicated diverticular disease are associated with persistent dysbiosis. This review aims to explore the most prevalent causes and underlying mechanisms of acute and chronic diarrhea, with a particular focus on the role of the gut microbiota. It will also examine the principal therapeutic strategies aimed at modulating intestinal microbiota, including prebiotics, probiotics, antibiotics, and fecal microbiota transplantation.},
}

@article {pmid41743065,
year = {2026},
author = {Ren, D and Chai, X and Xiang, C and Zhao, Y and Sun, P and Wang, M and Li, J and Wu, J and Yi, C and Chen, S and Li, E and Zhao, S},
title = {Acer truncatum Bunge seed oil attenuates learning and memory impairment in AD mouse model via modulating gut microbiota and metabolism.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1757330},
pmid = {41743065},
issn = {2296-861X},
abstract = {This study aimed to clarify the neuroprotective effect of Acer truncatum Bunge seed oil (ASO) and its interactions with the gut microbiota in transgenic mice with 5 × Familial Alzheimer's disease (5 × FAD). The AD-transgenic mice were fed with standard diet supplemented with 4% ASO from one to six months of age. The result show that ASO intervention can alleviate learning and memory impairment, enhance motor coordination and endurance, and reduce Aβ deposition in the brains. It also inhibit the proliferation of microglia and astrocytes, decrease the levels of IL-1β, IL-6, and TNF-α in the hippocampus and serum. Then, ASO could increase the Chao1 index and Shannon index, alter the gut microbiota composition, specifically, enhance the growth of gut bacteria correlated with the production of SCFAs, including Ruminococcaceae, Butyricicoccus, Sutterella and others, particularly those related to butyrate production. Additionally, ASO can increase the concentrations of SCFAs in fresh feces and serum, particularly butyric acid. ASO could primarily modulate the biosynthesis of unsaturated fatty acids, glycerophospholipid metabolism, and sphingolipids metabolism in serum. At the same time, Fecal microbiota transplantation (FMT) could reduce Aβ deposition, enhance learning and memory. Finally, Supplementation of sodium Buty also mitigate learning and memory impairments. This study highlights the gut microbiota might be a potential therapeutic target for AD and provides a scientific foundation for developing novel pharmaceuticals or nutraceuticals.},
}

@article {pmid41741396,
year = {2026},
author = {Garcia-Guevara, F and Resink, T and Clasen, F and Uhlén, M and Achour, A and Shoaie, S},
title = {Temporal dynamics of gut biosynthetic gene clusters link persistent colonization and engraftment in fecal microbiota transplantation.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2634469},
pmid = {41741396},
issn = {1949-0984},
abstract = {The human gut microbiome carries a large array of biosynthetic gene clusters (BGCs) that encode the production of secondary metabolites, yet their temporal dynamics and role during microbial colonization remain largely unexplored. Here, we tracked BGCs profile over time in a cohort of healthy adults, and identified two distinct groups: persistent, which are stable over time, and transient, which are more sporadic. Functional annotations indicated persistent gene clusters are enriched in antibiotic resistance mechanisms, while transient ones more frequently carry virulence-associated genes. We then examined colonization of these two groups in the context of fecal microbiome transplantation. Our results show that persistent gene clusters exhibit higher colonization rates than transient ones. These findings contribute to our understanding of how microbial metabolites influence host health, potentially guiding future therapeutic strategies targeting the microbiome.},
}

@article {pmid41738638,
year = {2026},
author = {Eriksen, LL and Støy, S and Hansen, MM and Gatten, EP and Erikstrup, C and Kelsen, J and Mullish, BH and Marchesi, JR and Thomsen, KL and Dahlerup, JF and Dahl Baumwall, SM and Hvas, CL},
title = {Dynamics in circulating immune cell subsets after faecal microbiota transplantation for recurrent Clostridioides difficile infection.},
journal = {Clinical and translational gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.14309/ctg.0000000000001008},
pmid = {41738638},
issn = {2155-384X},
abstract = {BACKGROUND: Faecal microbiota transplantation (FMT) is effective for recurrent Clostridioides difficile infection (rCDI). Adverse reactions to FMT occur early, and cellular immune responses after FMT may contribute to effects and reactions. We compared early changes in peripheral immune cell subsets and clinical outcomes in patients with rCDI who received either FMT and antibiotics or antibiotics alone in a randomized trial.

METHODS: Thirty-five patients with rCDI were randomized to vancomycin and FMT (n=20) or vancomycin alone (n=15). Blood samples were drawn before (wk0) and one week (wk1) after treatment. In three additional patients, blood samples were drawn before, and 24 hours and wk1 after FMT. Adaptive and innate immune cell subsets and gut-homing memory (CD45RO+integrinβ7+) and effector (CD45RO-integrinβ7+) T cells were analysed by flow cytometry.

RESULTS: FMT induced subtle changes in immune cell subsets with no clear pattern from wk0 to wk1. The Treg fraction tended to decrease after FMT, and a similar decrease at 24 hours indicated rapid Tregs dynamics. NKT cells increased during the first 24 hours and returned to baseline level at wk1. Regardless of FMT, patients with clinical resolution from rCDI had a decrease in non-classical monocytes and a shift in gut-homing memory to effector cells at wk1.

CONCLUSION: In rCDI, FMT induced subtle and transient dynamics in peripheral immune cell subsets. Tregs and NKT cells seemed responsive and should be further studied. Cure of CDI may be associated with an increase in circulating gut-homing T cells.},
}

@article {pmid41737395,
year = {2026},
author = {Wen, D and Liu, S and Wu, Y and Zhang, H and Zhang, K},
title = {Fecal microbiota transplantation improves functional constipation through the gut microbiome-bile acid-receptor axis.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1751593},
pmid = {41737395},
issn = {2296-858X},
abstract = {Functional Constipation (FC) is a prevalent gastrointestinal motility disorder worldwide that markedly impairs patients' quality of life, yet the currently available treatment options often show limited efficacy. In recent years, research has gradually revealed the critical role of the gut microbiota and bile acid metabolism in the pathogenesis of FC. Fecal Microbiota Transplantation (FMT), which restores the intestinal microecological balance by transferring gut microbiota from healthy donors, has demonstrated clinical efficacy in promoting bowel movements, improving stool consistency, and enhancing patients' quality of life. However, its underlying mechanisms remain incompletely understood. Current evidence indicates that FMT restores microbial diversity, increases beneficial taxa, and partially reconstructs the bile acids (BAs) profile, thereby modulating Farnesoid X Receptor (FXR) and Takeda G Protein-Coupled Receptor 5 (TGR5) mediated signaling pathways to enhance intestinal secretion and alleviate constipation-related symptoms. The resulting microbiota-bile acid-receptor pathway elucidates the mechanistic link between microbial remodeling and host gastrointestinal motility, thereby offering theoretical support for the therapeutic application of FMT in functional constipation.},
}

@article {pmid41736135,
year = {2026},
author = {Huang, H and Peng, S and Liu, Y and Chen, L and Wu, F},
title = {Fecal microbiota transplantation for advanced non-small cell lung cancer with secondary PD-1 resistance efficacy prognostic factors and microbiome diversity analysis.},
journal = {Journal of translational medicine},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12967-026-07885-w},
pmid = {41736135},
issn = {1479-5876},
support = {2025YLCE0054//Talent Program of Ganzhou Sci-Tech and Medical Joint Program/ ; 82560474//Regional Programs of the National Natural Science Foundation of China/ ; 82560461//Regional Programs of the National Natural Science Foundation of China/ ; 82360507//Regional Programs of the National Natural Science Foundation of China/ ; },
}

@article {pmid41735123,
year = {2026},
author = {D'Arcangelo, G and Paparella, R and Gravina, A and Tarani, F and Tarani, L and Aloi, M and Petrella, C},
title = {Exploring novel biomarkers in pediatric ulcerative colitis: The role of Lipocalin-2, MMP-9, and MMP-9/LCN-2 complex.},
journal = {Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.dld.2026.01.224},
pmid = {41735123},
issn = {1878-3562},
abstract = {BACKGROUND AND AIMS: Lipocalin-2 (LCN-2), Matrix Metalloproteinase-9 (MMP-9), and the MMP-9/LCN-2 complex are emerging biomarkers for ulcerative colitis (UC). While extensively studied in adults, data in children are limited. This study aimed to evaluate their serum levels in children with newly diagnosed UC, compare them with healthy controls, and assess correlations with disease severity and extent.

METHODS: In this prospective case-control study, 32 children with UC (6-18 years) and 38 healthy controls were enrolled. Baseline clinical (Pediatric Ulcerative Colitis Activity Index/ PUCAI), laboratory (albumin, hemoglobin, Erythrocyte Sedimentation Rate, C-reactive protein/CRP, fecal calprotectin), and endoscopic (extent, Ulcerative Colitis Endoscopic Index of Severity/UCEIS) data were collected. Serum LCN-2, MMP-9, and MMP-9/LCN-2 complex levels were measured by ELISA.

RESULTS: Serum LCN-2, MMP-9, and MMP-9/LCN-2 levels were significantly higher in UC patients than controls. ROC analysis indicated LCN-2 had the best diagnostic performance. Higher LCN-2 and MMP-9 levels were observed in children with more severe endoscopic disease (UCEIS > 4) or pancolitis. LCN-2 levels inversely correlated with albumin, whereas MMP-9 positively correlated with CRP and UCEIS.

CONCLUSIONS: LCN-2 and MMP-9 are promising biomarkers in pediatric UC, reflecting disease severity and extent. Their measurement may have clinical utility in monitoring disease progression and guiding management in children.},
}

@article {pmid41735080,
year = {2026},
author = {Yu, Y and Lu, L and Ji, G and Xu, H},
title = {Ecological battle of gut microbiota under drug intervention.},
journal = {Trends in microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tim.2026.01.002},
pmid = {41735080},
issn = {1878-4380},
abstract = {Ecological consequences of drug exposure in the gut microbiota remain difficult to predict. In a recent Cell study, Shi et al. have demonstrated that nutrient competition and interspecies antagonism drive drug-induced microbiome restructuring. Their predictive framework advances mechanistic understanding of drug-microbiome interactions and fecal microbiota transplantation.},
}

@article {pmid41734860,
year = {2026},
author = {Wu, QL and Zhou, YR and Chen, ZR and Liu, MX and Liu, MX and Liu, YF and Li, ZS and Zhao, QR and Zhang, YQ and Zhang, GQ and Zhang, Z and Gong, YT and Tang, C and Yang, T and Du, ZC},
title = {Roles of the gut microbiota in cancer immunotherapy: Mechanistic foundations and therapeutic opportunities.},
journal = {Critical reviews in oncology/hematology},
volume = {221},
number = {},
pages = {105230},
doi = {10.1016/j.critrevonc.2026.105230},
pmid = {41734860},
issn = {1879-0461},
abstract = {Cancer immunotherapy has revolutionized oncological treatment through diverse modalities including immune checkpoint blockade, adoptive cell therapy, therapeutic vaccines, and cytokine-based approaches. Despite these advances, clinical responses remain heterogeneous, with sustained benefit limited to a minority of patients. Emerging evidence now implicates gut microbiota as a critical systemic regulator of immunotherapy efficacy across multiple treatment platforms, mechanistically linking intestinal dysbiosis to antitumor immunity through the gut-immune-tumor axis. Specific commensal taxa and their metabolites, including short-chain fatty acids and tryptophan derivatives, regulate anti-tumor immunity through effector T cell enhancement, dendritic cell activation, and regulatory T cell suppression. This review systematically examines the microbial-metabolite-immune axis, elucidating mechanisms whereby intestinal microbes and metabolites mediate immunotherapy responses. We comprehensively evaluate microbiota-targeting strategies including dietary interventions, probiotics, prebiotics, and fecal microbiota transplantation, providing mechanistic insights and translational frameworks. We further discuss current challenges in transitioning from associative microbiome studies to mechanistic causality, standardizing intervention protocols, and integrating multi-modal microecological data, proposing future directions for engineered probiotics and precision microbial therapeutics to optimize outcomes under current immunotherapy.},
}

@article {pmid41732311,
year = {2026},
author = {Makkieh, Y and Shah, HH and Imran, SB and Pathan, SMK and Saju, AC and Majooju, M and Garg, A and Naag, T and Islam, R and Fahima, C and Ali, R},
title = {The gut-heart axis: Exploring the role of the gut microbiome in cardiovascular health - A focused systematic review.},
journal = {American heart journal plus : cardiology research and practice},
volume = {61},
number = {},
pages = {100687},
pmid = {41732311},
issn = {2666-6022},
abstract = {This focused systematic review examines the role of the gut microbiota in cardiovascular disease (CVD). The review explores mechanisms linking gut dysbiosis with CVD via microbial metabolites such as trimethylamine-N-oxide (TMAO) and short-chain fatty acids (SCFAs), which affect inflammation, endothelial function, and lipid metabolism. Interventions including dietary modifications, probiotics, prebiotics, fecal microbiota transplantation, and pharmacological agents such as statins, rifaximin, and empagliflozin are evaluated for their impact on microbial composition and cardiovascular outcomes. Probiotic strains and fiber-rich diets demonstrated modest improvements in blood pressure, lipid profiles, and inflammatory markers. Studies revealed that gut microbiome alterations influence drug metabolism and bleeding risk in patients taking oral anticoagulants. Limited evidence suggests that modulation of the microbiota may reduce chemotherapy-induced cardiotoxicity. However, only nine eligible studies met the inclusion criteria, reflecting the early and heterogeneous nature of this research area. Consequently, these findings should be interpreted as exploratory and hypothesis-generating. The focused review emphasizes the need for large-scale trials to validate microbiome-targeted strategies in CVD prevention and management. This focused systematic review is registered with PROSPERO (ID: CRD420251022190).},
}

@article {pmid41731480,
year = {2026},
author = {Liu, P and Hu, P and Jin, M and Wan, Y and Wu, J and Sun, W and Tang, Y and Huang, L and Zhang, D and Shi, D and Xie, T and Tong, Y and Zheng, H and Wang, L and He, H and Xu, X},
title = {Gut microbiota dysbiosis contributes to diabetic nephropathy via affecting renal lipid deposition and inflammatory responses.},
journal = {Journal of translational medicine},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12967-026-07832-9},
pmid = {41731480},
issn = {1479-5876},
support = {82304948//National Natural Science Foundation of China/ ; No.2022MHCX01//School-level Project Innovation Project of Minhang Hospital Affiliated to Fudan University/ ; 24ZR1461700//Shanghai Natural Science Foundation/ ; 2024MZYS07//High-Level Specialist Physician Training Program under the Collaborative Health Service System of Medical Education and Research in Minhang District/ ; 2023MHBJ04//Minhang District Central Hospital Topnotch Project/ ; 2025MHZ035//Natural Science Research Project in Minhang District/ ; },
}

@article {pmid41729099,
year = {2026},
author = {Zhang, B and Si, Y and Liu, Y and Wei, J and Li, M and Si, D and Li, H and Wang, X and Han, P and Wang, W and Bao, J and Cheng, L and Lei, Y and Ma, H and Liu, Y},
title = {Simulated microgravity induces cerebral dysfunction by disturbing protective microbiota-metabolite-microglia signaling across the gut‒brain axis.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2635820},
pmid = {41729099},
issn = {1949-0984},
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; Rats ; *Weightlessness Simulation/adverse effects ; Male ; Fecal Microbiota Transplantation ; *Microglia/metabolism ; Hippocampus/metabolism ; Rats, Sprague-Dawley ; Signal Transduction ; *Brain/metabolism ; },
abstract = {Long-duration spaceflight characterized by microgravity adversely affects operator proficiency postlanding, yet the mechanisms by which microgravity induces cerebral dysfunction refractory to short-term recovery among astronauts remain poorly defined. Here, we demonstrate that simulated microgravity (SMG) leads to chronic behavior disorders and cognitive deficits via a microbiota-metabolite-brain axis. Fecal microbiota transplantation (FMT) from long-term SMG-treated donor rats to recipients (n = 5 per group) under normal gravity (NG) induces anxiety-like behaviors and spatial working memory disturbances by impairing synaptic plasticity in the hippocampus, reproducing the phenotype of SMG-exposed rats. SMG destroys intestinal barriers and alters the gut microbiota to a proinflammatory state with an increased abundance of Proteobacteria but decreased production of linoleic acid (LA) and LA-derived metabolites, which is highly associated with neuroinflammation in the hippocampus. Mechanistically, LA can be taken up by the hippocampus under NG conditions, and then block inflammatory microglial activation by interacting with signal transducer and activator of transcription 1 (STAT1) and inhibiting its phosphorylation at Tyr 701 and Ser 727. However, the Proteobacteria, especially Pseudomonas aeruginosa, tend to be the dominant phylum in gut microbiota under SMG conditions and consume large amounts of LA, breaking LA-dependent immune homeostasis in the central nervous system (CNS). Dietary supplementation with LA significantly mitigated SMG-induced neuroinflammation and cognitive impairment. Taken together, our findings in SD rats models reveal a critical role for gut microbiota dysbiosis in simulated microgravity-associated encephalopathy, offering a novel strategy for LA replenishment to improve brain function during spaceflight.},
}

Animals
*Gastrointestinal Microbiome/physiology
Rats
*Weightlessness Simulation/adverse effects
Male
Fecal Microbiota Transplantation
*Microglia/metabolism
Hippocampus/metabolism
Rats, Sprague-Dawley
Signal Transduction
*Brain/metabolism

@article {pmid41727680,
year = {2026},
author = {Su, B and Cao, Y and Ma, L and Huang, J},
title = {BMI-stratified phenotypes of polycystic ovary syndrome: advances in gut microbiota research and personalized management strategies.},
journal = {Frontiers in endocrinology},
volume = {17},
number = {},
pages = {1734041},
pmid = {41727680},
issn = {1664-2392},
mesh = {Humans ; *Polycystic Ovary Syndrome/microbiology/therapy/pathology ; *Gastrointestinal Microbiome/physiology ; Female ; *Body Mass Index ; *Precision Medicine/methods ; *Obesity/complications/microbiology ; Phenotype ; Dysbiosis ; },
abstract = {Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine-metabolic disorder affecting 11%-13% of women of reproductive age. Based on body mass index (BMI), patients can be phenotypically classified into obese and non-obese subgroups: the obese PCOS is characterized by insulin resistance, hyperandrogenemia, and metabolic syndrome, with more pronounced metabolic risks; non-obese PCOS primarily manifests as reproductive endocrine dysfunction. In recent years, studies have shown that the Gut microbiota plays a key role in the pathogenesis of PCOS, and dysbiosis in the obese subgroup is generally more pronounced, potentially amplifying metabolic abnormalities through pathways such as short-chain fatty acids, bile acid disturbances, and endotoxin-related low-grade inflammation. This review systematically summarizes the clinically heterogeneous features of BMI-stratified PCOS and its gut microbiota characteristics, with a focus on elucidating the mechanistic differences between obese and non-obese individuals in terms of inflammation, metabolites, and endocrine regulatory pathways. Based on current evidence, individualized intervention strategies targeting different BMI subtypes are proposed, including dietary and lifestyle modifications, interventions with probiotics/prebiotics/synbiotics, and exploration of emerging precision microbiome therapies such as fecal microbiota transplantation. The interaction between BMI and gut microbiota provides new directions for stratified management and personalized treatment of PCOS; however, high-quality longitudinal and interventional studies are still needed to clarify causal relationships and optimize microbiota-targeted strategies.},
}

Humans
*Polycystic Ovary Syndrome/microbiology/therapy/pathology
*Gastrointestinal Microbiome/physiology
Female
*Body Mass Index
*Precision Medicine/methods
*Obesity/complications/microbiology
Phenotype
Dysbiosis

@article {pmid41727556,
year = {2026},
author = {Millar, BC and Cates, MJ and Torrisi, MS and Round, AJ and Warde, A and Lowery, CJ and Moore, JE},
title = {Antimicrobial Resistance: The Answers.},
journal = {British journal of biomedical science},
volume = {83},
number = {},
pages = {15559},
pmid = {41727556},
issn = {2474-0896},
mesh = {Humans ; *Anti-Bacterial Agents/therapeutic use/pharmacology ; *Drug Resistance, Bacterial ; COVID-19/epidemiology ; SARS-CoV-2 ; },
abstract = {Antimicrobial resistance (AMR) has caused a global public health crisis, contributing to approximately five million deaths in 2019 and predicted deaths of approximately ten million annually by 2050. This equates to approximately 1.4-fold more deaths annually from AMR in 2050 than the entire COVID-19 pandemic to date. To tackle this AMR pandemic, regulatory and policy frameworks have been prepared at local, national and international levels with multi-faceted proposals and advances encompassing surveillance, diagnostics, infection prevention, antibiotic prescribing and variation of existing and novel treatment approaches. This narrative review primarily focuses on research and development which have been documented over the last five years in relation to therapeutic approaches at various stages in clinical development and the potential role that vaccines can play in the fight against AMR. This review provides an overview on antibacterial drugs, including novel classes of antibiotics, which have been recently approved, as well as combination antibiotic therapy and the potential of repurposed drugs. The potential role of novel antimicrobial, antibiofilm and quorum sensing inhibitors, such as antimicrobial peptides, nanomaterials and compounds from the extreme and natural environments, as well as ethnopharmacology including the antimicrobial effects of plants, spices, honey and venoms are explored. Novel therapeutic approaches are critically discussed in terms of their realistic clinical potential, detailing recent and ongoing trials to highlight the current interest of these approaches, including immunotherapy, bacteriophage therapy, antimicrobial photodynamic therapy (aPDT), antimicrobial sonodynamic therapy (aSDT), nitric oxide therapy and microbiome manipulation including faecal microbiota transplantation (FMT). The potential of predatory bacteria as living antimicrobial agents is also discussed. Importantly, there have been many technological developments which have enhanced bioprospecting and research and development of novel antimicrobials which this review draws attention to, including artificial intelligence, machine learning and Organ-on-a-Chip devices. Finally, key messages from the recent World Health Organization report into the role of vaccines against AMR provides an interesting perspective relating to prevention which can be of significance in tackling the AMR burden.},
}

Humans
*Anti-Bacterial Agents/therapeutic use/pharmacology
*Drug Resistance, Bacterial
COVID-19/epidemiology
SARS-CoV-2

@article {pmid41727337,
year = {2026},
author = {Toumazi, D and Charalambous, C and Constantinou, C and Nicolaou, N},
title = {From the gut to the brain: The involvement of the gut microbiota in the development and progression of glioblastoma.},
journal = {Neuro-oncology advances},
volume = {8},
number = {1},
pages = {vdaf267},
pmid = {41727337},
issn = {2632-2498},
abstract = {Glioblastoma (GB) is the most malignant tumor in the adult central nervous system (CNS), presenting substantial treatment challenges due to its infiltrative nature, heterogeneity and immunosuppressive environment it creates. Current therapeutic efforts are focused on enhancing our understanding of GB and developing effective therapies. An emerging area of interest is the bidirectional gut-brain axis, which mediates communication between gut microbiota and CNS. The gut-brain axis allows the microbiota to modulate the immune system and inflammatory pathways through microbial metabolites, such as short-chain fatty acids (SCFAs) and tryptophan derivatives, promoting or suppressing GB progression. Understanding these interactions can lead to microbiota-targeted therapies for GB patients. Novel therapies, such as fecal microbiota transplantation to enhance immunotherapy response and using bacterial toxins to cross the blood-brain barrier, show promise in improving treatment-resistant GB treatment. Additionally, the role of probiotics and antibiotics on GB prognosis is being investigated. While more research is needed to understand the gut microbiota's role in GB, recent findings suggest promising directions for future therapies. This review examines the interplay between key immune system components and the microbiota in GB development and explores how this understanding could facilitate the development of novel therapeutic interventions.},
}