@article {pmid41886797,
year = {2026},
author = {Misra, J and Bhargav Shreevatsa, KS and Ravi, K and Abomughaid, MM and Lakhanpal, S and Gupta, R and Jha, NK and Kumar, N},
title = {Microbiota-driven neuroimmune mechanisms in brain disorders: Microglial activation, cytokine signaling, and translational implications.},
journal = {Journal of neuroimmunology},
volume = {416},
number = {},
pages = {578913},
doi = {10.1016/j.jneuroim.2026.578913},
pmid = {41886797},
issn = {1872-8421},
abstract = {Neuroinflammation is increasingly recognized as a central driver of diverse neurological and neuropsychiatric disorders. Within this framework, the microbiota-gut-brain axis (MGBA) has emerged as a critical modulator of neuroimmune signaling rather than a broad systemic regulator. Microbial-derived metabolites and immune mediators influence central nervous system (CNS) homeostasis by shaping microglial maturation and activation, regulating cytokine signaling networks, including IL-1β, IL-6, and TNF-α and modulating inflammasome pathways, such as NLRP3. These immune mechanisms intersect with blood-brain barrier (BBB) integrity, where dysbiosis-associated inflammation and altered short-chain fatty acid (SCFA) production may compromise tight junction stability and promote peripheral immune infiltration. Through immune-glial crosstalk, microbial signals can amplify or attenuate neuroinflammatory cascades, thereby influencing vulnerability to autoimmune, neurodegenerative, and neurodevelopmental disorders. This review synthesizes current mechanistic evidence linking gut microbial perturbations to CNS immune regulation, emphasizing microglial activation, cytokine-mediated signaling, and BBB immunomodulation as core pathways. By reframing the MGBA through a neuroimmune lens, we highlight emerging therapeutic strategies targeting microbiota-driven inflammatory circuits to advance precision interventions for inflammatory brain disorders.},
}

@article {pmid41886951,
year = {2026},
author = {Zuo, G and Shen, Y and Wang, L and Gao, Y and Luo, C and Wen, J and Li, J and Huang, JA and Liu, Z and Lin, Y},
title = {Low-dose epigallocatechin gallate combined with L-theanine effectively alleviate obesity and metabolic dysfunction-associated steatotic liver disease by remodeling gut homeostasis and avoiding its hepatotoxicity.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {155},
number = {},
pages = {158078},
doi = {10.1016/j.phymed.2026.158078},
pmid = {41886951},
issn = {1618-095X},
abstract = {BACKGROUND: High-dose epigallocatechin gallate (EGCG) treats obesity and metabolic dysfunction-associated steatotic liver disease but causes hepatotoxicity, limiting its application.

OBJECTIVE: To determine whether low-dose EGCG combined with L-theanine (LTA) can reproduce the metabolic benefits of high-dose EGCG without hepatotoxicity, and to clarify the role of the gut microbiota.

METHODS: Diet-induced obese C57BL/6J mice were treated with L-EGCG (80 mg/kg/d), H-EGCG (160 mg/kg/d), LTA (80 mg/kg/d), or L-EGCG+LTA for 12 weeks. Metabolic parameters, liver function, oxidative stress, and gut barrier integrity, were evaluated. 16S rRNA sequencing and fecal microbiota transplantation (FMT) confirmed the causal role of microbiota remodeling in the observed therapeutic effects.

RESULTS: Although H-EGCG effectively reduced body weight and adiposity, it induced liver injury and gut dysbiosis with depletion of commensal butyrate producers and enrichment of polyphenol-metabolizing taxa, collectively exacerbating hepatic oxidative stress and mitochondrial injury. In contrast, L-EGCG+LTA achieved weight- and lipid-lowering effects comparable to H-EGCG while significantly attenuating hepatic oxidative stress and conferring hepatoprotective effects. Two-way ANOVA confirmed that the combined effects were predominantly additive, with both agents contributing independently. The combination additively remodeled the gut microbiota, markedly enriching beneficial taxa such as Bacteroides uniformis and Oscillospiraceae. FMT from combination-treated donors recapitulated metabolic benefits to HFD-fed recipient mice.

CONCLUSIONS: Co-administration of low-dose EGCG and L-theanine additively improves metabolic health by remodeling the gut microbiota, offering a promising strategy to enhance the safety and translational potential of EGCG-based interventions.},
}

@article {pmid41888318,
year = {2026},
author = {Huang, W and Zhang, J and Shan, J and Shen, W and Du, P and Liu, J and Guo, X and Chen, Z and Zeng, W and Lin, Q and Fan, H},
title = {Lactobacillus paragasseri LPG-9 reduces placental inflammation in intrahepatic cholestasis of pregnancy by regulating TGR5 in mice.},
journal = {Communications biology},
volume = {},
number = {},
pages = {},
doi = {10.1038/s42003-026-09869-4},
pmid = {41888318},
issn = {2399-3642},
support = {32370139//National Natural Science Foundation of China (National Science Foundation of China)/ ; 32300085//National Natural Science Foundation of China (National Science Foundation of China)/ ; },
abstract = {Intrahepatic cholestasis of pregnancy (ICP), a liver disorder associated with adverse fetal outcomes, is characterized by elevated bile acid levels and placental inflammation by the TGR5. However, the interplay among the gut microbiome, bile acid metabolism, and ICP-associated placental inflammation remains unexplored. We aimed to investigate the role of the gut microbiota in regulating bile acid metabolism and placental inflammation, and to identify potential probiotic-based therapies for ICP in C57BL/6 mice. Immunohistochemical analysis of human placentas revealed significantly higher inflammation and decreased TGR5 expression in ICP compared with controls. In vivo and in vitro assays confirmed the anti-inflammatory effects of TGR5 activation. Using 16S rRNA sequencing and metabolomics, ICP mice exhibited a distinct gut microbiota composition and reduced abundance of bile salt hydrolase (BSH)-producing bacteria (e.g., Lactobacillus), accompanied by a significant decrease in the proportion of secondary bile acids. Transplanting fecal microbiota from ICP donors into healthy mice reproduced the disease phenotype of ICP, confirming the pathogenic role of gut microbiota dysbiosis. Supplementation with BSH-enriched Lactobacillus paragasseri LPG-9 remodeled the bile acid profile, thereby activating placental TGR5 to inhibit TLR4-NF-κB signaling and promoting hepatic bile acid excretion via BSEP.},
}

@article {pmid41889026,
year = {2026},
author = {Shi, Y and Li, H},
title = {Microecological Interventions against Antibiotic-Induced Dysbiosis and Related Resistome Expansion.},
journal = {Journal of microbiology and biotechnology},
volume = {36},
number = {},
pages = {e2601009},
doi = {10.4014/jmb.2601.01009},
pmid = {41889026},
issn = {1738-8872},
mesh = {*Dysbiosis/chemically induced/therapy/microbiology ; Humans ; *Anti-Bacterial Agents/adverse effects/pharmacology ; *Gastrointestinal Microbiome/drug effects ; Probiotics/administration & dosage ; Prebiotics/administration & dosage ; Fecal Microbiota Transplantation ; Bacteria/drug effects/genetics/metabolism ; Drug Resistance, Bacterial ; Animals ; Synbiotics/administration & dosage ; Biofilms/drug effects ; },
abstract = {Antibiotic exposure and the emergence of antimicrobial resistance are critical global health threats, with antibiotic-induced gut dysbiosis contributing to increased mortality, prolonged illness, and significant economic burden. This review introduces the complex interplay between antibiotic exposure, gut microbiota dysbiosis, and the dissemination of antimicrobial resistance genes, which collectively undermine intestinal barrier function and promote systemic inflammation. It also explores how microbial metabolites influence resistance mechanisms through metabolic regulation, alteration of bacterial communities, antibiotic biotransformation, biofilm formation, and host-microbe interactions. Microecological interventions-including probiotics, prebiotics, synbiotics, postbiotics, fecal microbiota transplantation, dietary modifications, and emerging strategies-have the potential to restore microbial homeostasis, enhance colonization resistance to invading pathogens, and mitigate the spread of resistant pathogens. By integrating ecological and therapeutic perspectives, these approaches offer a sustainable framework for combating antibiotic resistance and improving clinical outcomes.},
}

*Dysbiosis/chemically induced/therapy/microbiology
Humans
*Anti-Bacterial Agents/adverse effects/pharmacology
*Gastrointestinal Microbiome/drug effects
Probiotics/administration & dosage
Prebiotics/administration & dosage
Fecal Microbiota Transplantation
Bacteria/drug effects/genetics/metabolism
Drug Resistance, Bacterial
Animals
Synbiotics/administration & dosage
Biofilms/drug effects

@article {pmid41889649,
year = {2026},
author = {Su, R and Ma, J and Li, J and Liu, Y and Ma, T and Wang, J and Mai, Q and Ma, Q and Wang, J and Wang, H and Yang, S and Zhang, X},
title = {Fecal microbiota transplantation ameliorates alcohol-associated liver disease through coordinated restoration of short-chain fatty acid and α-linolenic acid signaling.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1744446},
pmid = {41889649},
issn = {1664-302X},
abstract = {BACKGROUND: Alcohol-associated liver disease (ALD) is closely linked to gut microbiota dysbiosis. However, the specific microbial metabolic functions that drive the transition from microbial imbalance to hepatic inflammation and metabolic injury remain unclear, limiting the development of mechanism-based therapeutic strategies.

METHODS: This study integrated human microbiome analysis with fecal microbiota transplantation (FMT) experiments in an ALD mouse model. Multi-omics approaches, including 16S rRNA gene sequencing, untargeted metabolomics, and immunological profiling, were employed to systematically characterize the interactions among gut microbiota composition, microbial-derived metabolites, and host immune responses.

RESULTS: We observed that ALD progression was characterized by an early shift in microbial composition followed by a marked decline in microbial diversity, culminating in an ecological collapse of the gut microbiota. FMT from healthy donors significantly improved liver histopathology and serum biochemical parameters, accompanied by restoration of gut microbial diversity and key metabolic functions. Metabolomic analyses revealed enhanced short-chain fatty acid (SCFA) production and activation of α-linolenic acid (ALA)-related metabolic pathways following FMT. These metabolic improvements were associated with reduced inflammatory responses and improved immune homeostasis.

CONCLUSION: Our findings demonstrate that FMT from healthy donors ameliorates ALD by restoring critical microbial metabolic functions, particularly SCFA production and ALA-related pathways. These results highlight microbial metabolic function as a promising therapeutic target for microbiome-based interventions in ALD.},
}

@article {pmid41890300,
year = {2026},
author = {Shirotani, M and Shimizu, S and Kitamura, K and Mikawa, Y and Haruna, R and Kawai, Y and Koide, S and Mohri, I and Matsuzaki, H and Tsuchiya, KJ and Tanaka, Y and Katayama, T},
title = {Safety and efficacy of a novel fecal microbiota transplantation method using hydrogen nanobubble water without antibiotics or bowel cleansing in children with autism spectrum disorder: an open-label, single-arm study demonstrating improvements in core and comorbidity symptoms.},
journal = {Frontiers in pediatrics},
volume = {14},
number = {},
pages = {1767346},
pmid = {41890300},
issn = {2296-2360},
abstract = {BACKGROUND: Autism spectrum disorder (ASD) is rising in prevalence, but effective treatments for its core symptoms remain limited. Fecal microbiota transplantation (FMT) has shown promise; however, conventional methods often require antibiotics and bowel cleansing, raising concerns regarding safety and sustainability. We developed a novel FMT method using hydrogen nanobubble water and investigated its efficacy and safety.

METHODS: This prospective, single-arm, before-and-after comparative study enrolled 30 children aged 5-12 years with ASD, selected according to inclusion and exclusion criteria. SHIN-1, a Good Manufacturing Practice (GMP)-grade prepared fecal microbial solution from a healthy screened donor, was suspended in hydrogen nanobubble water and administered via enema. Primary outcome was the Social Responsiveness Scale-2 (SRS-2), with objectivity confirmed using Gazefinder as an eye-tracking system. Secondary outcomes included sensory profile [Short Sensory Profile (SSP)], gastrointestinal symptoms [Gastrointestinal Symptom Rating Scale [GSRS], Bristol Stool Form Scale [BSFS]] and Patient Health Questionnaire-4 items (PHQ-4). Statistical analyses employed paired t-tests or Wilcoxon signed-rank tests (α = 0.05).

RESULTS: At 30 weeks, fecal microbiota reconstitution was observed, with increases in short-chain fatty acid-producing and typically taxa abundant in developing children. SRS-2 scores decreased 29% (p < 0.001), sustained at one year. The classification is as follows; 19 severe cases improved to mild and 6 to normal. Improvements were greater in children without gastrointestinal disorders (45% vs. 24%). Social Communication and Interaction (SCI), Restricted Interests and Repetitive Behavior (RRB), and subscales improved uniformly; sensory, gastrointestinal, and emotional symptoms improved by 30%-61%. No adverse events occurred.

CONCLUSION: This novel hydrogen nanobubble water-based FMT method was safe and effective, reducing both core and peripheral symptoms of ASD and suggesting broad benefits via the gut microbiota-brain axis.Clinical Trial Registration: https://jrct.mhlw.go.jp/en-latest-detail/jRCTs031230041.},
}

@article {pmid41890703,
year = {2026},
author = {Li, X and Liu, F and Zhu, Y and Shi, H},
title = {Gut Microbiota, Insulin Resistance, and Alzheimer's Disease: A Narrative Review of Mechanistic Links and Therapeutic Perspectives.},
journal = {International journal of general medicine},
volume = {19},
number = {},
pages = {593664},
pmid = {41890703},
issn = {1178-7074},
abstract = {Alzheimer's disease (AD) is increasingly regarded as a "neurometabolic syndrome" wherein systemic insulin resistance exacerbates cerebral glucose hypometabolism, tau hyperphosphorylation, and neuroinflammation. We hypothesize that gut microbiota dysbiosis produces metabolites that are associated with peripheral insulin sensitivity, potentially contributing to disruptions in cerebral insulin signaling and an increased risk of AD. We conducted integrated search of PubMed, Web of Science, and Scopus to synthesize evidence showing: (i) consistent taxonomic shifts in AD, highlighting reduced Firmicutes and increased Proteobacteria and Bacteroidetes, depletion of Ruminococcaceae and enrichment of Blautia and Bilophila; (ii) functional consequences of dysbiosis, leading to lower short-chain fatty acids, altered secondary bile‑acid signaling, elevated lipopolysaccharide and trimethylamine‑N‑oxide, and perturbed tryptophan catabolism; (iii) these microbial metabolites compromising gut and blood-brain barrier integrity, thereby triggering chronic inflammation, potentially modulating the PI3K‑Akt‑GSK‑3β pathway, and linking peripheral insulin resistance to cerebral dysfunction; and (iv) a translational discussion of therapeutic strategies that target both microbiota and insulin pathways, including dietary modulation, probiotics and prebiotics, fecal microbiota transplantation, intranasal insulin, metformin, and metabolite-based agents, show promise. This review uniquely integrates taxonomic, functional, and therapeutic literature to propose a mechanistic microbiota-insulin resistance-AD axis and highlights the need for longitudinal and interventional trials.},
}

@article {pmid41890764,
year = {2026},
author = {Lai, J and Wang, Y and Zeng, L and Deng, Q and Qiao, Y and Liao, J and Sun, C and Geng, Y and Wu, H and Huang, D and Zhao, X and Wu, D},
title = {Melatonin alleviates airway inflammation and anxiety-depression in asthma via gut microbiota-SCFA axis-mediated inhibition of microglial activation.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1763305},
pmid = {41890764},
issn = {1664-3224},
mesh = {Animals ; *Melatonin/pharmacology/therapeutic use ; *Gastrointestinal Microbiome/drug effects ; *Asthma/drug therapy/metabolism/immunology ; *Microglia/drug effects/metabolism/immunology ; Mice ; *Fatty Acids, Volatile/metabolism ; *Depression/drug therapy/metabolism/etiology ; *Anxiety/drug therapy/metabolism ; Disease Models, Animal ; Fecal Microbiota Transplantation ; Male ; Signal Transduction ; Cell Line ; Inflammation ; },
abstract = {BACKGROUND: Asthma frequently co-occurs with anxiety and depression, yet the mechanisms underlying this lung-brain comorbidity remain elusive. The gut-lung-brain axis has emerged as a potential key mediator.

METHODS: Using an ovalbumin (OVA)-induced murine asthma model, we administered melatonin or sodium butyrate via drinking water. We assessed airway inflammation, lung function, anxiety- and depression-like behaviors, gut microbiota composition, short-chain fatty acid (SCFA) levels, and the MAPK/P65/NLRP3 signaling pathway in the hippocampus and BV2 microglial cells. Fecal microbiota transplantation (FMT) and antibiotic depletion experiments were conducted to establish causality.

RESULTS: Both melatonin and sodium butyrate significantly alleviated airway inflammation, improved lung function, and ameliorated anxiety- and depression-like behaviors in asthmatic mice. Melatonin increased gut-derived butyrate levels and restored gut microbiota balance. FMT from melatonin-treated donors replicated the therapeutic benefits, whereas antibiotic-mediated microbiota depletion abrogated the effects of melatonin. Mechanistically, both treatments inhibited the activation of the MAPK/P65/NLRP3 pathway in hippocampal microglia and LPS-stimulated BV2 cells.

CONCLUSION: Our findings demonstrate that melatonin mitigates asthma-related airway inflammation and neuropsychiatric comorbidity by modulating the gut microbiota-SCFA axis and suppressing microglial activation via the MAPK/P65/NLRP3 pathway. This study highlights a novel systemic mechanism and potential therapeutic strategy for asthma and its comorbidities.},
}

Animals
*Melatonin/pharmacology/therapeutic use
*Gastrointestinal Microbiome/drug effects
*Asthma/drug therapy/metabolism/immunology
*Microglia/drug effects/metabolism/immunology
Mice
*Fatty Acids, Volatile/metabolism
*Depression/drug therapy/metabolism/etiology
*Anxiety/drug therapy/metabolism
Disease Models, Animal
Fecal Microbiota Transplantation
Male
Signal Transduction
Cell Line
Inflammation

@article {pmid41890815,
year = {2026},
author = {Xiong, Z and Dong, X and Yuan, Y and Lu, L and Deng, X},
title = {Gut Microbiota Mitigates Chronic Itch and Cutaneous Inflammation in DNFB-Induced Atopic Dermatitis Mice.},
journal = {Journal of inflammation research},
volume = {19},
number = {},
pages = {573709},
pmid = {41890815},
issn = {1178-7031},
abstract = {BACKGROUND: Chronic itch is the most prominent symptom of atopic dermatitis (AD), which severely impacts the quality of life of patients and persists even after medication. Gut microbiota dysbiosis is considered to contribute to AD, however, the roles of gut microbiota in the modulation of chronic pruriceptive processing currently remain unclear. The present study aimed to elucidate the potential regulatory role of the gut microbiota in AD-associated chronic itch.

METHODS: In this study, the 1-fluoro-2,4-dinitrobenzene (DNFB)-induced mouse model of AD-associated chronic itch was established. Differences in gut microbiota composition between model and healthy controls were analyzed using high-throughput 16S rRNA gene sequencing. In addition, we performed oral fecal microbiota transplantation (FMT) from model mice to antibiotic cocktail-treated healthy mice and observed whether they could induce itch behavior. Furthermore, feces from healthy mice were transplanted into model mice to evaluate their effects on itch symptoms and skin inflammation.

RESULTS: The DNFB induced significantly itch behaviors and an altered gut microbiota composition. The gut microbiota from chronic itch mice through oral administration could induce itch behaviors in antibiotic cocktail-treated healthy mice. While, oral FMT from healthy mice to chronic itch mice not only significantly alleviated scratching behavior but also ameliorated skin damage and inflammation. Following FMT administration from healthy donors, remarkable alterations were observed in the metabolomic profiles of mice with DNFB-induced chronic itch.

CONCLUSION: These findings highlight the potential link between gut microbiota dysbiosis and chronic itching in AD, suggesting that targeting the gut microbiota may be a therapeutic strategy for chronic itch.},
}

@article {pmid41891399,
year = {2026},
author = {Elsheikh, M and Ibrahim, MA and Fares, S and Bhongade, M and Adhem, K and Ramirez-Morales, XI and Kaseb, AO and Petrosino, J and Hassan, MM and Jalal, PK},
title = {Influence of Gut Microbiota on Response to Immune Check Point Inhibitors in MASLD Patients With HCC: Unraveling the Connection.},
journal = {Cancer medicine},
volume = {15},
number = {4},
pages = {e71738},
doi = {10.1002/cam4.71738},
pmid = {41891399},
issn = {2045-7634},
support = {R21CA293626/CA/NCI NIH HHS/United States ; },
mesh = {Humans ; *Gastrointestinal Microbiome/immunology/drug effects ; *Immune Checkpoint Inhibitors/therapeutic use/pharmacology ; *Liver Neoplasms/drug therapy/immunology/microbiology/complications ; *Carcinoma, Hepatocellular/drug therapy/immunology/microbiology/complications ; Dysbiosis/microbiology ; Drug Resistance, Neoplasm ; Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; },
abstract = {Immune checkpoint inhibitors (ICIs) have emerged as a promising treatment for various cancers, including advanced hepatocellular carcinoma (HCC). However, a significant proportion of patients with HCC, particularly those with metabolic dysfunction-associated liver disease (MASLD), exhibit resistance to ICI therapy. Studies have revealed that the presence of specific gut bacteria, such as Akkermansia, Bifidobacterium, and Lachnoclostridium, is associated with improved outcomes with ICI-treated HCC patients. Conversely, the overgrowth of bacteria like Enterobacteriaceae is linked to resistance to therapy. This review investigates the role of gut microbiota in shaping immune checkpoint inhibitor responses in MASLD-related hepatocellular carcinoma, focusing on how dysbiosis may contribute to ICI resistance and exploring microbiome modulation strategies, such as fecal microbiota transplantation and probiotics, aiming to optimize therapeutic outcomes.},
}

Humans
*Gastrointestinal Microbiome/immunology/drug effects
*Immune Checkpoint Inhibitors/therapeutic use/pharmacology
*Liver Neoplasms/drug therapy/immunology/microbiology/complications
*Carcinoma, Hepatocellular/drug therapy/immunology/microbiology/complications
Dysbiosis/microbiology
Drug Resistance, Neoplasm
Fecal Microbiota Transplantation
Probiotics/therapeutic use

@article {pmid41892839,
year = {2026},
author = {Lista, AR and Ayala Mosqueda, CV and Palacios, R and García Mansilla, MJ and Rodríguez Sojo, MJ and Ho Plágaro, A and Garcia Garcia, J and Gálvez, J and Rodríguez Nogales, A and Ruiz Malagón, AJ and Rodríguez Sánchez, MJ},
title = {Modulation of Microbiome-Mitochondria Axis as a Novel Approach for Treatment of Obesity: A Scoping Review.},
journal = {Medical sciences (Basel, Switzerland)},
volume = {14},
number = {1},
pages = {},
doi = {10.3390/medsci14010124},
pmid = {41892839},
issn = {2076-3271},
support = {PI18/00826, PY20-01157, PI20/01447, B-CTS-664-UGR20, PI19/01058, PI24/02089 and JDC2022-049478-I, CD23/00117, IFI21/00030//Instituto de Salud Carlos III/ ; },
mesh = {Humans ; *Obesity/therapy/microbiology/metabolism ; *Gastrointestinal Microbiome/physiology ; *Mitochondria/metabolism ; Animals ; Probiotics/therapeutic use ; Energy Metabolism ; Fecal Microbiota Transplantation ; Prebiotics ; },
abstract = {Background: Obesity is a multifactorial, chronic disease characterised by excessive fat accumulation, low-grade inflammation, and metabolic dysfunction. Emerging evidence suggests that the gut microbiome-mitochondria axis may play a significant role in the pathophysiology of obesity, particularly in regulating energy metabolism, inflammatory responses, and mitochondrial function. However, most mechanistic insights into this axis derive from preclinical animal studies, while human evidence remains limited and largely associative. Mitochondrial dysfunction disrupts cellular energy balance, increases reactive oxygen species production, and may exacerbate gut dysbiosis, further contributing to metabolic disturbances. In addition, factors such as micronutrient deficiencies also play a relevant role in obesity development and progression. Objectives: This review aims to examine the bidirectional interactions between the gut microbiome and mitochondrial systems in obesity, with a focus on the underlying molecular mechanisms and their potential as therapeutic targets. Methods: Evidence from experimental models and clinical studies was analysed to evaluate how modulation of the microbiome-mitochondria axis through probiotics, prebiotics, dietary strategies, and faecal microbiota transplantation influences mitochondrial function, inflammation, and metabolic regulation. Results: Preclinical studies indicate that the gut microbiome modulates mitochondrial activity through the production of bioactive metabolites, including short-chain fatty acids, secondary bile acids, and tryptophan-derived compounds, which influence mitochondrial efficiency, lipid metabolism, and glucose regulation. Dysbiosis reduces these beneficial metabolites, impairing mitochondrial signalling and promoting adiposity and insulin resistance. Interventions targeting this axis have shown potential in restoring metabolic balance, improving mitochondrial function, and mitigating obesity-related complications such as hyperlipidaemia and glucose intolerance. Conclusions: Targeting the microbiome-mitochondria axis represents a promising therapeutic strategy for obesity, with the evidence based largely on preclinical findings. However, further well-designed human studies are required to clarify causality, optimise interventions, assess long-term safety and efficacy, and establish standardised clinical protocols for implementation.},
}

Humans
*Obesity/therapy/microbiology/metabolism
*Gastrointestinal Microbiome/physiology
*Mitochondria/metabolism
Animals
Probiotics/therapeutic use
Energy Metabolism
Fecal Microbiota Transplantation
Prebiotics

@article {pmid41894083,
year = {2026},
author = {Li, Y and Jiang, M and Pang, J and Ma, C and Zhang, H and Yin, F and Jia, Y and Zou, X and Zuo, T and Zhang, H},
title = {High-altitude exposure remodels the gut microbiota: health and disease.},
journal = {MedScience},
volume = {},
number = {},
pages = {},
pmid = {41894083},
issn = {3091-4981},
abstract = {With the increasing number of individuals travelling to or residing in high-altitude regions, understanding the physiological and pathological consequences of such environments has become increasingly important. High-altitude exposure poses significant challenges to human health, primarily due to hypobaric hypoxia, which triggers a cascade of responses, including energy deficiency, oxidative stress, and inflammation. One of the critical consequences is the disruption of the gut barrier, which facilitates the translocation of the gut microbiota and further exacerbates local and systemic inflammation. Notably, the gut microbiota, a dynamic environmental sensor, undergoes significant remodelling in high-altitude environments. The modified production of microbial metabolites such as bile acids influences gut homeostasis as well as glucose and lipid metabolism, and ultimately contributes to individual variability in high-altitude acclimatization. These changes have been implicated in the pathogenesis of altitude-related illnesses such as acute and chronic mountain sickness, as well as in metabolic and gastrointestinal disorders such as diabetes, obesity, irritable bowel syndrome, colorectal cancer, cholelithiasis, and osteoporosis. Preliminary explorations have demonstrated the therapeutic potential of microbiome-based interventions such as faecal microbiota transplantation in acute and chronic mountain sickness. Further research into gut microbiota modulation may provide applicable options for promoting high-altitude acclimatization and preventing high-altitude illness.},
}

@article {pmid41880553,
year = {2026},
author = {Liao, Y and Jiang, R and Zhang, H and Zhang, W},
title = {The dual roles of microorganisms in inflammatory diseases: initiators and regulators.},
journal = {Critical reviews in clinical laboratory sciences},
volume = {},
number = {},
pages = {1-33},
doi = {10.1080/10408363.2026.2637106},
pmid = {41880553},
issn = {1549-781X},
abstract = {Research on the microbiome is reshaping the conceptual foundations of inflammatory diseases. As a dynamic component of the host ecosystem, microbial communities collectively influence inflammatory responses and homeostatic balance through their metabolites, structural signals, and interactions with immune pathways. Dysbiosis can amplify immune activation and metabolic disturbances, leading to persistent inflammation, whereas specific commensal taxa and their metabolites possess the capacity to suppress excessive immune responses and restore homeostasis. This bidirectional regulatory capacity positions the microbiome as a central node that both drives and modulates inflammatory networks. Multi-omics investigations have delineated the systemic architecture of microbe-host interactions, revealing cross-system axes such as the gut-brain, gut-liver, and skin-gut pathways that constitute a signaling framework integrating inflammation and immunity, thereby reshaping our understanding of disease pathogenesis. Within this framework, inflammation is redefined as an adaptive strategy for maintaining systemic stability rather than merely a singular pathological reaction. Therapeutic approaches including fecal microbiota transplantation (FMT), engineered microbial strains, and interventions targeting metabolic signaling are propelling microecological medicine into an era of precision modulation. As systems biology converges with spatial omics, research on the microbiome is shifting from descriptive pathology toward mechanistic control, establishing it as a critical nexus linking immunity, metabolism, and disease evolution. This transformation heralds a paradigm shift in medicine from merely "suppressing inflammation" to actively "reconstructing ecological order."},
}

@article {pmid41883804,
year = {2026},
author = {Han, Y and Wang, Z and Xie, J and Yang, G and Su, M and Wang, S and Yang, M and Yu, H and Li, M and Wang, L and Zhang, Y and Hou, B},
title = {Host-gut microbiota interactions in health and disease: mechanisms and intervention strategies.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1785607},
pmid = {41883804},
issn = {1664-302X},
abstract = {The mammalian gut microbiota is a complex and dynamic "microbial organ" that interacts with its host. The gut microbiota contains a vast gene pool and metabolic capacity, producing key metabolites such as short-chain fatty acids (SCFAs), bile acids, vitamins, and other compounds. These metabolites regulate core physiological functions like energy metabolism, immune homeostasis, and neural behavior via the gut-brain axis (GBA), immune signaling networks, and other pathways. This review explores the bidirectional regulatory role of the gut microbiota. The gut microbiota influences the host's metabolism and immune functions through its metabolites and structural components, while the host's physiological state, internal environment, and lifestyle can alter the microbiota's composition and function, creating a complex feedback network. Furthermore, the main mechanisms of dysbiosis in diseases are also explored. Dysregulation of the gut microbiota can damage the intestinal mucosal barrier, induce chronic inflammation, disrupt metabolic and immune signaling, and contribute to diseases such as type 2 diabetes, non-alcoholic fatty liver disease, inflammatory bowel disease, rheumatoid arthritis, and neurodegenerative disorders. Microbiota-based interventions, such as probiotics, prebiotics, and fecal microbiota transplantation (FMT), can be promising in disease management, but their clinical applications face challenges, including individual genetic backgrounds, lifestyles, and environmental factors, as well as difficulties in achieving long-term colonization of specific strains. Future research needs to uncover precise causal mechanisms in host-microbe interactions, as well as develop individualized microbiota intervention strategies to provide new theoretical bases and practical tools for the prevention, diagnosis, and treatment of major diseases.},
}

@article {pmid41884305,
year = {2023},
author = {Ito, K and Haraguchi, A and Sato, S and Sekiguchi, M and Sasaki, H and Ryan, C and Lyu, Y and Shibata, S},
title = {Feeding with resistant maltodextrin suppresses excessive calorie intake in a high-fat diet, mediated by changes in mouse gut microbiota composition, appetite-related gut hormone secretion, and neuropeptide transcriptional levels.},
journal = {Frontiers in microbiomes},
volume = {2},
number = {},
pages = {1149808},
pmid = {41884305},
issn = {2813-4338},
abstract = {Consuming resistant maltodextrin (RMD) decreases food intake and increase appetite-related gut hormones, but the underlying mechanisms have remained unknown. Therefore, we aimed to elucidate the mechanisms underlying the effects of RMD feeding on food intake (appetite) using Institute of Cancer Research male mice fed with a high-fat diet (HFD-cellulose group) or HFD in which cellulose was replaced with RMD (HFD-RMD group). Feeding mice with an HFD-RMD for approximately 8 weeks inhibited excessive calorie intake and altered the gut microbiota composition. Excessive calorie intake was inhibited for several days in mice fed only with an HFD-cellulose and transplanted with fecal microbiota from the HFD-RMD group (FMT-HFD-RMD group). Moreover, in the HFD-RMD and FMT-HFD-RMD groups, serum active glucagon-like peptide (GLP)-1 and peptide tyrosine tyrosine (PYY) levels were significantly higher, and appetite-related neuropeptide gene transcription in the hypothalamus were significantly altered, compared with the HFD-cellulose and FMT-HFD-cellulose groups. These results suggested that the long-term RMD intake changed the gut microbiota composition, increased the GLP-1 and PYY secretion, and altered the appetite-related neuropeptide gene transcription in the hypothalamus, leading to suppressed excessive calorie intake in an HFD.},
}

@article {pmid41876026,
year = {2026},
author = {Celis, A and Quera, R and Núñez, P and von Muhlenbrock, C and Espinoza, R and Concha, A and Mendoza, C and Marcet, F and Araya, D and Fuentes, J and Riesco, F and Correa, P},
title = {Long-term effectiveness and safety of colonoscopy-guided Fecal Microbiota Transplantation in recurrent Clostridiodes difficile infection: a prospective case series.},
journal = {Gastroenterologia y hepatologia},
volume = {},
number = {},
pages = {502719},
doi = {10.1016/j.gastrohep.2026.502719},
pmid = {41876026},
issn = {0210-5705},
}

@article {pmid41877779,
year = {2026},
author = {Sun, S and Long, F and Su, B and Chen, J and Luo, Y and Zhong, Y and Zhang, G},
title = {The gut microbiome in colorectal anastomotic leakage: from mechanisms to precision.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1781458},
pmid = {41877779},
issn = {2296-858X},
abstract = {Anastomotic leakage after curative colorectal cancer resection remains a frequent and severe complication that increases short-term mortality, worsens long-term oncologic outcomes, and places substantial burdens on individuals and health systems despite advances in surgical technique and perioperative care. Emerging evidence redefines anastomotic failure as not only a technical event but also a biologically driven process in which the gut microbiome regulates inflammation, epithelial repair, and barrier integrity at the healing interface. This review summarizes current data on the dual role of the intestinal microbiome in promoting physiological anastomotic healing and driving pathological leakage when perioperative stressors cause dysbiosis. Mechanistic sections describe how a diverse, metabolically active community supports collagen stability through short-chain fatty acid production, immune regulation, and maintenance of mucus and tight junction architecture. In contrast, the enrichment of microbial groups such as Enterococcus faecalis, Fusobacterium nucleatum, and Alistipes onderdonkii together with fungal and viral shifts, has been associated with extracellular matrix degradation and excessive inflammation. Furthermore, the review examines microbiome-related biomarkers for risk assessment, including DNA-based microbial signatures, metabolite profiles, and host immune markers. It also discusses how integrated multi-omics models combined with machine learning may outperform traditional clinical scores for preoperative and early postoperative prediction. Finally, the article critically evaluates perioperative microbiome-directed strategies ranging from dietary prehabilitation and microbial supplementation to selective decontamination and fecal microbiota transplantation, highlighting promising signals, variability of effect, safety considerations, and key methodological limitations that currently prevent routine implementation. In summary, this review addresses three interconnected domains-mechanisms of microbiome-driven anastomotic failure, microbiome-derived biomarkers for risk stratification, and perioperative intervention strategies-underscoring that AL is best understood as a host-microbiome interaction rather than a purely technical failure. This framing offers surgeons and perioperative teams a biologically rational basis for prevention, yet clinical translation will require causal validation, standardized intervention algorithms, and interpretable computational tools embedded into real-world perioperative practice.},
}

@article {pmid41878444,
year = {2026},
author = {Chen, Y and Wang, Z and Zeng, Y and Xie, X and Liu, L and Qian, Y},
title = {Research progress on the role of gut microbiota dysbiosis in the pathogenesis of immune-mediated liver diseases.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1708826},
pmid = {41878444},
issn = {1664-3224},
mesh = {Humans ; *Dysbiosis/immunology/therapy/microbiology/complications ; *Gastrointestinal Microbiome/immunology ; Animals ; *Liver Diseases/immunology/microbiology/etiology/therapy ; Hepatitis, Autoimmune/microbiology/immunology ; Fecal Microbiota Transplantation ; },
abstract = {Gut microbiota dysbiosis plays a significant role in the pathogenesis of immune-mediated liver diseases (IMLDs), including autoimmune hepatitis (AIH), primary biliary cholangitis (PBC), and primary sclerosing cholangitis (PSC), through multiple gut-liver axis mechanisms. Microbial metabolites such as short-chain fatty acids (SCFAs) and secondary bile acids regulate hepatic immune homeostasis by activating G protein-coupled receptors (GPRs) and the farnesoid X receptor (FXR). Concurrently, disruption of the intestinal barrier integrity allows endotoxins (e.g., lipopolysaccharide) to activate hepatic macrophages via the TLR4/NF-κB pathway, triggering a pro-inflammatory cytokine cascade. Studies indicate an enrichment of Veillonella in AIH patients, while PBC patients display elevated Enterobacteriaceae and reduced Oscillospira spp. PSC is characterized by Klebsiella pneumoniae translocation and Candida albicans toxin-mediated injury. Therapeutic strategies such as fecal microbiota transplantation (FMT), probiotics, prebiotics, and bacteriophages therapy have shown efficacy in clinical settings, underscoring the potential of targeting the gut microbiota for managing IMLDs. Future research should integrate immune cell regulation by gut-derived factors and develop precision therapies based on the gut-liver axis.},
}

Humans
*Dysbiosis/immunology/therapy/microbiology/complications
*Gastrointestinal Microbiome/immunology
Animals
*Liver Diseases/immunology/microbiology/etiology/therapy
Hepatitis, Autoimmune/microbiology/immunology
Fecal Microbiota Transplantation

@article {pmid41878631,
year = {2026},
author = {MacDonald, KV and Pai, N and Burow, C and deBruyn, JC and Huynh, HQ and Otley, A and Rozario, S and Marshall, DA},
title = {Balancing safety and effectiveness: parent preferences for fecal microbiota transplant and established therapies in pediatric inflammatory bowel disease-results of a multicenter Canadian study.},
journal = {Crohn's & colitis 360},
volume = {8},
number = {1},
pages = {otag016},
pmid = {41878631},
issn = {2631-827X},
abstract = {BACKGROUND AND AIMS: Treatment decision-making in pediatric inflammatory bowel disease (IBD) is complex, with many existing and emerging options. However, little is known about parent preferences for these therapies. This multi-center Canadian study provides the first quantitative data on parent preferences for pediatric IBD treatments and explores characteristics associated with differing preferences.

METHODS: We conducted a cross-sectional survey including a discrete choice experiment (DCE) with Canadian parents (n = 159) of children diagnosed with UC/IBD-U, recruited from four pediatric IBD clinics. The DCE assessed preferences across four treatment attributes: chance of clinical remission, severity and chance of known side effects, severity of rare unknown side effects, and mode of treatment delivery. Latent class modeling was used to explore preference heterogeneity.

RESULTS: Parents prioritized safety, particularly the risk of rare unknown side effects, followed by likelihood of remission. Latent class analysis identified two distinct groups: one most concerned about rare unknown side effects, and another prioritizing treatment effectiveness. Thirty-eight percent of parents were open to fecal microbiota transplant (FMT), an emerging therapy that uses donor stool to help restore gut microbiome health. Younger parents and those with children experiencing more severe disease and on multiple medications were more likely to accept FMT. Across the cohort, many parents were willing to trade off less desirable delivery modes or increased risk in exchange for better treatment outcomes.

CONCLUSIONS: Parents value both safety and effectiveness in IBD treatment decisions. Recognizing these preferences may support shared decision-making, particularly when discussing novel therapies like FMT.},
}

@article {pmid41878811,
year = {2026},
author = {Chen, Y and Li, B and Lin, Y and Sha, W and Shi, C and Wang, M and Wang, S and Wang, J and Ma, Y and Wu, M and Fan, Z and Chen, Y and Zhou, Y and Fu, D and Li, J and Zheng, Y and Hu, L},
title = {Hypertension-Associated Acetate Deficiency Enhances Platelet Activation and Thrombosis Via Olfr78.},
journal = {Circulation research},
volume = {},
number = {},
pages = {},
doi = {10.1161/CIRCRESAHA.125.327498},
pmid = {41878811},
issn = {1524-4571},
abstract = {BACKGROUND: Arterial thrombotic events constitute the leading cause of mortality in hypertension. Gut dysbiosis induces endothelial dysfunction and systemic inflammation, contributing to hypertension and its associated cardiovascular complications. Whether these dysbiotic microbiota metabolites in hypertension directly regulate platelet hyperactivation and thrombosis remains unclear.

METHODS: Fecal microbiota transplantation, 16S rRNA sequencing, and untargeted metabolomics were performed using samples from patients with hypertension. In vivo FeCl3-induced mesenteric arteriole thrombosis model, ex vivo microfluidic whole-blood perfusion assay, and in vitro platelet functional studies defined the functional effects of acetate on platelet activation. Moreover, platelet-specific Olfr78 (olfactory receptor 78)-deficient mice were employed to explore the underlying mechanisms of acetate on platelet activation.

RESULTS: Transplantation with fecal microbiota from patients with hypertension enhanced in vivo FeCl3-injured mesenteric arteriole thrombosis and ex vivo whole blood thrombus formation compared with fecal microbiota from healthy normotensive subjects. Untargeted metabolomics revealed that gut microbiota-derived acetate was decreased in patients with hypertension, and plasma acetate concentration negatively correlated with integrin αIIbβ3 activation and P-selectin exposure. Acetate demonstrated superior antiplatelet efficacy against ADP-induced aggregation, dense-granule secretion, α-granule secretion, and integrin αIIbβ3 activation than collagen or thrombin-induced platelet activation. Mechanistic studies using platelet-specific Olfr78[-/-] mice revealed that acetate bound to and activated Olfr78, a receptor not previously reported to be expressed in platelets, to elevate cAMP level and activate PKA, thereby increasing p-VASP and decreasing Ca[2+] mobilization as well as inactivating RhoA/ROCK2/MLC (myosin light chain) signaling to inhibit platelet activation. A high-fiber diet upregulated acetate/Olfr78 signaling in platelets to suppress microvascular thrombosis and protect against myocardial injury during myocardial infarction in mice.

CONCLUSIONS: Acetate is a negative regulator of platelet hyperreactivity and thrombus formation via the Olfr78 receptor, and acetate deficiency contributes to platelet hyperreactivity in hypertension. Lifestyle modifications, particularly high-fiber dietary intervention and acetate supplementation, exhibit potent antithrombotic effects in hypertension.},
}

@article {pmid41880488,
year = {2026},
author = {Kim, SG and Ott, R and Bretin, A and Abo, H and Wang, Y and Wang, Y and Winer, S and Winer, DA and Reddivari, L and Heaver, SL and Ley, RE and Pellizzon, M and Ngo, VL and Gewirtz, AT},
title = {Wheat fiber mitigates colitis via non-SCFA microbial metabolite-trained intestinal macrophages.},
journal = {Science advances},
volume = {12},
number = {13},
pages = {eaec5757},
doi = {10.1126/sciadv.aec5757},
pmid = {41880488},
issn = {2375-2548},
mesh = {Animals ; *Dietary Fiber/pharmacology/administration & dosage ; *Macrophages/metabolism/drug effects ; *Colitis/metabolism/pathology/microbiology/prevention & control/etiology ; *Triticum/chemistry ; Mice ; *Gastrointestinal Microbiome ; *Fatty Acids, Volatile/metabolism ; Mice, Inbred C57BL ; Disease Models, Animal ; Germ-Free Life ; Male ; Feces/microbiology ; },
abstract = {The advent of highly refined wheat products has reduced fiber consumption, which is associated with increased risk for inflammatory bowel disease (IBD). We found that enriching diets with wheat fiber (WF) protected mice against colitis, especially relative to a low-fiber diet, as assessed by clinical, histopathologic, morphologic, and immunologic parameters. WF's protection against colitis was independent of short-chain fatty acids (SCFAs) yet associated with preservation of microbiota diversity, including maintenance of Bacteroides thetaiotaomicron (B. theta), which was necessary and sufficient for WF's colitis protection. B. theta's presence in gnotobiotic mice resulted in WF-induced fecal metabolites that reprogrammed macrophages toward an M2-like phenotype. Metabolic and phenotypic reprogramming of macrophages ex vivo via WF-induced metabolites, followed by their transplantation into mice, recapitulated WF's protection against colitis. Thus, microbiota-mediated metabolism of WF promotes macrophages that reduce proneness to intestinal inflammation, suggesting a mechanism by which WF consumption may curb development of IBD.},
}

Animals
*Dietary Fiber/pharmacology/administration & dosage
*Macrophages/metabolism/drug effects
*Colitis/metabolism/pathology/microbiology/prevention & control/etiology
*Triticum/chemistry
Mice
*Gastrointestinal Microbiome
*Fatty Acids, Volatile/metabolism
Mice, Inbred C57BL
Disease Models, Animal
Germ-Free Life
Male
Feces/microbiology

@article {pmid41871943,
year = {2026},
author = {Awoniyi, M and El Hag, M and Hernandez, J and Yang, Q and Evans, N and Nemet, I and Ngo, B and Coskuner, D and Zhou, J and Farmer, M and Su, L and Zhou, H and Roach, J and Stappenbeck, T and Sartor, RB},
title = {Dysbiotic microbiota trigger colitis-associated colorectal cancer and imprint a distinctive bile acid profile in a PSC-IBD model.},
journal = {Gut},
volume = {},
number = {},
pages = {},
doi = {10.1136/gutjnl-2025-336675},
pmid = {41871943},
issn = {1468-3288},
abstract = {BACKGROUND: Primary sclerosing cholangitis-associated UC (PSC-UC) carries excess colorectal neoplasia despite often mild-appearing endoscopy, implicating persistent microscopic inflammation and microbiota-bile acid (BA) dysfunction.

OBJECTIVE: To test whether PSC-UC neoplasia is driven by transferable microbiota-mediated inflammation linked to secondary BA loss.

DESIGN: Surveillance colonoscopies (2012-2022) from PSC-UC (n=251) and UC-only (n=8839) were compared for segmental endoscopic/histological activity and dysplasia. We generated multidrug resistance protein 2 (MDR2)[-/-] × interleukin (IL)-10[-/-] double-knockout (DKO) mice and used germ-free (GF) derivation, faecal microbiota transplantation (FMT), antibiotic conditioning and cohousing with shotgun metagenomics and liquid chromatography-tandem mass spectrometry BA profiling.

RESULTS: PSC-UC showed greater inflammatory activity and a right-shifted dysplasia burden versus UC-only. Under specific-pathogen-free conditions, DKO mice developed early right-predominant colitis and multifocal dysplasia progressing with age. DKO communities were depleted of 7α-dehydroxylation capacity with near absence of deoxycholic and lithocholic acids and no enrichment of canonical bacterial genotoxins. GF DKO mice were protected, whereas live DKO donor FMT reinstated severe colitis and dysplasia; sterile-filtered stool supernatant was inactive. IL-10[-/-] donor FMT or cohousing attenuated colitis and increased recipient secondary BA, whereas wild-type/MDR2[-/-] donor transfers were non-colitogenic. In GF DKO mice, direct deoxycholic acid repletion caused hepatotoxicity.

CONCLUSION: PSC-UC neoplasia associates with transmissible microbiota-dependent inflammation and secondary BA deficiency. Controlled restoration of BA-transforming microbial functions, rather than indiscriminate secondary BA replacement, is a rational translational direction.},
}

@article {pmid41872963,
year = {2026},
author = {Kim, B and Kim, HN and Cheong, HS and Jeong, S and Kim, J and Park, DI and Joo, EJ},
title = {Fecal microbiota from hepatitis B-infected individuals alters triglyceride metabolism and microbial pathways in mice.},
journal = {Gut pathogens},
volume = {},
number = {},
pages = {},
doi = {10.1186/s13099-026-00825-5},
pmid = {41872963},
issn = {1757-4749},
support = {RS-2023-KH135855//Korea Health Industry Development Institute/Republic of Korea ; NRF-2021R1A2C4002454//National Research Foundation of Korea/ ; },
}

@article {pmid41873114,
year = {2026},
author = {Wang, D and Cui, R and You, C and Zheng, W and Wang, L and Yang, Y and Yu, H and Cui, B},
title = {Relationship Between Gut Microbiota and Cancer Neuro-Immunity.},
journal = {Microbial biotechnology},
volume = {19},
number = {3},
pages = {e70336},
doi = {10.1111/1751-7915.70336},
pmid = {41873114},
issn = {1751-7915},
support = {K2023011//Medical research key project of Jiangsu Commission of Health/ ; },
mesh = {*Gastrointestinal Microbiome/immunology ; Humans ; *Neoplasms/immunology/therapy/microbiology/pathology ; Animals ; Immunotherapy ; Probiotics ; Tumor Microenvironment/immunology ; *Neuroimmunomodulation ; Prebiotics/administration & dosage ; },
abstract = {The nervous system and the immune system are integral components of the tumour microenvironment, and neuroimmune mechanisms play critical roles in tumour metastasis, immune evasion and metabolic reprogramming. However, the relationship between the gut microbiota and cancer neuro-immunity remains poorly understood. This knowledge gap hampers our understanding of how these systems contribute to tumour progression and therapeutic resistance. This article systematically explores the interactions among the gut microbiota, the nervous system and the immune system in the regulation of tumour progression, with a particular focus on elucidating the pathways by which the gut microbiota and its metabolites modulate tumour phenotypes via neuroimmune mechanisms, and summarises the regulatory mechanisms through which cancer neuro-immunity shapes gut microbiota composition. Additionally, this article summarises the interplay between immunotherapy and cancer neuro-immunity, and explores the potential of microbiota-based interventions, such as faecal microbiota transplantation, probiotics, prebiotics and synbiotics, to enhance the efficacy of immunotherapy through neuroimmune mechanisms.},
}

*Gastrointestinal Microbiome/immunology
Humans
*Neoplasms/immunology/therapy/microbiology/pathology
Animals
Immunotherapy
Probiotics
Tumor Microenvironment/immunology
*Neuroimmunomodulation
Prebiotics/administration & dosage

@article {pmid41873461,
year = {2026},
author = {Mattavelli, E and Da Prat, V and Corallo, S and Tartara, A and Figini, S and De Simeis, F and Marino, S and Uggè, A and Caccialanza, R and Pedrazzoli, P and Lasagna, A},
title = {Harnessing the gut microbiota in extra-intestinal cancers: from causal evidence to immunotherapy strategies.},
journal = {Immunotherapy},
volume = {},
number = {},
pages = {1-13},
doi = {10.1080/1750743X.2026.2648431},
pmid = {41873461},
issn = {1750-7448},
abstract = {The gut microbiota (GM) has emerged as a key modulator of cancer development and therapeutic response beyond the gastrointestinal tract. In extra-intestinal cancers, GM composition influences oncogenesis, with specific microbial taxa and their metabolites linked to either increased or decreased cancer risk, as highlighted by Mendelian Randomization studies. Beyond cancer initiation, GM plays a critical role in shaping the efficacy and toxicity of anticancer therapies, particularly immunotherapy. We searched PubMed and ClinicalTrials.gov using the terms"gut microbiota," "immune checkpoint inhibitors," "faecal microbiota transplantation," "solid tumor" in oncology patients. Evidence indicates that SCFA-producing bacteria, Akkermansia muciniphila, and members of Lachnospiraceae and Ruminococcaceae families enhance responses to immune checkpoint inhibitors (ICIs), whereas dysbiosis and immunosuppressive bacteria are associated with poor outcomes and immune-related adverse events. Therapeutic modulation of the GM through probiotics, prebiotics, fecal microbiota transplantation, and dietary interventions shows promise in optimizing immunotherapy efficacy, yet standardized clinical protocols remain lacking. Integrating GM profiling with multi-omics and artificial intelligence approaches offers a path toward personalized microbiota-targeted interventions to improve patient outcomes. This review critically summarizes current evidence linking GM to cancer immunotherapy, discusses mechanistic insights, and outlines future perspectives for translating microbiota modulation into clinical practice.},
}

@article {pmid41873680,
year = {2026},
author = {Zhang, S and Li, P and Dai, M and Wu, X and Lu, C and Lu, G and Ren, Q and Wang, X and Si, Y and Chang, L and Tang, S and Wu, J and Yuan, L and Lyu, L and Wang, H and He, F and Ding, J and Huang, G and Pan, X and Mei, Y and Li, L and Hu, S and Huang, X and Cui, B and Zhang, F and Wen, Q},
title = {Washed Microbiota Transplantation as a Rescue Therapy for Refractory Unidentified Pathogen Intestinal Infections: Findings From a National Multi-Centre, Real-World Study.},
journal = {Microbial biotechnology},
volume = {19},
number = {3},
pages = {e70335},
doi = {10.1111/1751-7915.70335},
pmid = {41873680},
issn = {1751-7915},
support = {82400648//National Natural Science Foundation of China/ ; 82170563//National Natural Science Foundation of China/ ; 2021YFA0717004//National Key Research and Development Program of China/ ; },
mesh = {Humans ; Male ; Female ; Middle Aged ; Retrospective Studies ; *Fecal Microbiota Transplantation/methods/adverse effects ; Aged ; Treatment Outcome ; China ; Adult ; *Intestinal Diseases/therapy/microbiology ; Anti-Bacterial Agents/therapeutic use ; Prospective Studies ; Aged, 80 and over ; Diarrhea/therapy ; },
abstract = {Unidentified pathogen intestinal infections (UPIIs) represent a severe clinical dilemma, characterised by clear signs of intestinal infection yet no identifiable causative pathogen, often leading to prolonged, antibiotic-refractory illness. A nationwide retrospective study based on the prospective cohorts from September 2015 to February 2025 was conducted in China to evaluate washed microbiota transplantation (WMT) on this challenging condition. Patients diagnosed with UPIIs and then underwent WMT were included. The primary outcome was the clinical response rate one month post-WMT. Finally, among the 81 included patients, 71.6% were bedridden, 46.9% required ICU admission and 51.9% developed multiple organ dysfunction syndrome. Diarrhoea was the primary symptom, and over half received ≥ 3 empirical antibiotics. Despite the challenges, WMT achieved a one-month clinical response rate of 63.0% and a cure rate of 43.2%. Multivariate analysis identified several baseline risk factors affecting WMT efficacy, including adverse events (AEs) related to WMT (β = 1.545, p = 0.026, OR = 4.690, 95% CI 1.208-18.206), total abdominal symptom scores (TASS) before WMT (β = 0.292, p = 0.047, OR = 1.340, 95% CI 1.004-1.788) and WHO performance status score ≥ 4 (β = 1.583, p = 0.031, OR = 4.867, 95% CI 1.160-20.423). The overall AEs rate was only 8.3% (18/216). A nomogram based on logistic regression [akaike information criterion (AIC) = 93.75] was developed to predict the clinical non-response at one month after WMT. The favourable clinical outcomes observed in this study provide cohort-based evidence on using WMT for treating refractory UPIIs. These findings implied that if WMT is available, earlier WMT may be beneficial for UPIIs.},
}

Humans
Male
Female
Middle Aged
Retrospective Studies
*Fecal Microbiota Transplantation/methods/adverse effects
Aged
Treatment Outcome
China
Adult
*Intestinal Diseases/therapy/microbiology
Anti-Bacterial Agents/therapeutic use
Prospective Studies
Aged, 80 and over
Diarrhea/therapy

@article {pmid41874370,
year = {2026},
author = {Liu, C and Dan, L and Wang, X and Chen, L and Yuan, X},
title = {Gut microbiota impact on lung diseases: a mini review of clinical evidence.},
journal = {Infection and immunity},
volume = {},
number = {},
pages = {e0043025},
doi = {10.1128/iai.00430-25},
pmid = {41874370},
issn = {1098-5522},
abstract = {The gut-lung axis represents a bidirectional communication network through which the gut microbiota (GM) influences respiratory health. This mini-review synthesizes clinical evidence on the role of the GM in lung diseases. We focused exclusively on human clinical trials, randomized controlled trials, meta-analyses, and systematic reviews, sourced from major databases after duplicate removal. The evidence indicates that GM dysbiosis is a significant risk factor for the susceptibility and severity of various respiratory conditions, including asthma, chronic obstructive pulmonary disease (COPD), cystic fibrosis (CF), and infections, such as COVID-19 and pneumonia. Specific microbial signatures and metabolic profiles, particularly involving short-chain fatty acids (SCFAs), are associated with disease states and outcomes. Interventions like probiotics, prebiotics, synbiotics, and fecal microbiota transplantation (FMT) show promise in modulating the GM and improving clinical parameters, though their efficacy can be inconsistent and influenced by confounding factors. In conclusion, the GM is a promising therapeutic target for lung diseases. However, future research must prioritize large-scale, longitudinal clinical trials and deeper mechanistic investigations to establish causality and develop effective, personalized microbiome-based therapies.},
}

@article {pmid41874416,
year = {2026},
author = {Koseli, E and Tyc, KM and Buzzi, B and Akbarali, HI and Damaj, MI},
title = {The Role of the Gut Microbiome in Nicotine Withdrawal and Dependence.},
journal = {Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco},
volume = {},
number = {},
pages = {},
doi = {10.1093/ntr/ntag057},
pmid = {41874416},
issn = {1469-994X},
abstract = {INTRODUCTION: Smoking is considered a global pandemic with more than 1.3 billion people being active smokers. Increasing evidence suggests that nicotine exposure can lead to changes in the gut microbiome, increases in permeability, and impaired mucosal immune responses in the gastrointestinal tract. However, the literature on behavioral aspects of nicotine-microbiome interaction, such as dependence and withdrawal, is limited. In this study, we used homologous fecal material transplants (FMT) to modify the gut microbiome and its impact on the intensity of nicotine withdrawal in mice.

METHODS: We used osmotic minipumps as an application of chronic nicotine for 15 days and orally gavaged FMT 2x a day to the mice. We assessed the nicotine withdrawal by measuring the number of somatic signs and anxiety-like behaviors at 24 h and 1 week after the mini pump removal. Fecal samples were also collected points to identify the gut microbiome changes.

RESULTS: Fecal transplants reduced the number of somatic signs and anxiety-like behaviors in nicotine-treated mice up to a week after the removal of minipumps. The shotgun metagenomic results of the fecal samples from 24 h after minipumps removal time point show altered gut microbiome with a significant shift in the species composition between the nicotine treated and its homologous FMT treatment.

CONCLUSIONS: Our results indicate that under our experimental conditions fecal transplant can reduce the severity of nicotine withdrawal. This suggests that interactions along the gut-brain axis are important for the development of nicotine dependence and might help lower the risk of cancer and other serious health problems in humans.},
}

@article {pmid41875216,
year = {2026},
author = {Castillo-Moral, Á and Toda-Ferran, C and Bulló, M and Teichenné, J and Escoté, X},
title = {Nutraceuticals and the Microbiota-Gut-Brain Axis: A Pathway for Preventing Cognitive Decline.},
journal = {Nutrition reviews},
volume = {},
number = {},
pages = {},
doi = {10.1093/nutrit/nuag017},
pmid = {41875216},
issn = {1753-4887},
support = {//Vicente Lopez Program (Eurecat)/ ; //Autonomous Government of Catalonia/ ; 2021 SGR 00213//Departament de Recerca i Universitats de la Generalitat de Catalunya to the Nutrition and Metabolic Health Research Group/ ; 2021 SGR 01556//Precision Nutrition, Wellness and Prevention of Metabolic Diseases/ ; },
abstract = {With the global rise in aging populations, cognitive impairment and neurodegenerative diseases, such as Alzheimer's disease (AD), present a growing public health issue. Current pharmacological treatments primarily target symptoms rather than underlying causes, necessitating the exploration of alternative preventive strategies. Nutraceuticals have emerged as promising candidates for neuroprotection due to their ability to modulate oxidative stress, neuroinflammation, and mitochondrial function. This narrative review aimed to evaluate the neuroprotective potential of nutraceuticals and their interactions with the microbiota-gut-brain axis in preventing age-related cognitive decline. A comprehensive search of the scientific literature using the PubMed, Scopus, and Web of Science databases was undertaken, focusing on publications during the period 2010-2025. Nutraceuticals, including vitamins, omega-3 fatty acids, coenzyme Q10, polyphenols, and isothiocyanates, exhibit neuroprotective properties through antioxidant, anti-inflammatory, and mitochondrial-support mechanisms. The gut microbiota plays a crucial role in regulating the bioavailability and efficacy of these compounds. Microbiome-based interventions, such as prebiotics, probiotics, and fecal microbiota transplantation demonstrate potential in modulating neuroinflammatory responses and supporting cognitive function. Nutraceutical and microbiome-targeted interventions represent promising, low-risk strategies for preventing cognitive decline. Their ability to modulate neuroinflammation and oxidative stress underscores their potential for future clinical applications. Further large-scale studies are needed to validate their efficacy and explore personalized approaches adapted to individual microbiome profiles.},
}

@article {pmid41875611,
year = {2026},
author = {Yang, Z and Zhang, F and Yang, S and Anayyat, U and Mo, Y and Ying, Y and Wang, X},
title = {Orally deliverable Perilla frutescens-derived nanovesicles as natural bioactive nanocarriers for colon-targeted colitis therapy via microenvironment reprogramming.},
journal = {Biomaterials advances},
volume = {184},
number = {},
pages = {214832},
doi = {10.1016/j.bioadv.2026.214832},
pmid = {41875611},
issn = {2772-9508},
abstract = {Effective oral therapy for inflammatory bowel disease (IBD) requires overcoming gastrointestinal barriers to modulate the dysregulated mucosal niche. Here, we present edible nanovesicles derived from Perilla frutescens (PLENs) as an intrinsically stable, bioactive nanotherapeutic. Multi-omics profiling defined a robust lipid-bilayer architecture encapsulating a synergistic cargo of proteins, miRNAs, and antioxidant metabolites. This structural integrity enabled PLENs to survive gastrointestinal transit and exhibit preferential fluorescence localization with prolonged retention in the inflamed colonic region, as indicated by in vivo imaging. Upon localization, PLENs executed a "dual-hit" therapeutic strategy: they reprogrammed the immune microenvironment, accompanied by reduced activation of the TLR4/MyD88-NF-κB axis and a phenotypic shift from pro-inflammatory M1 to reparative M2 macrophages. Concurrently, PLENs fundamentally restructured the gut ecosystem, accompanied by enrichment of taxa linked to saccharolytic fermentation and recovery of cecal short-chain fatty acids. Notably, fecal microbiota transplantation (FMT) further supported that this microbial remodeling contributed to the protective phenotype, highlighting the microbiome as an important component of efficacy.},
}

@article {pmid41875758,
year = {2026},
author = {Cui, H and Liu, Q and Leung, PSC and Chow, MW and Liu, SJ and Liu, B},
title = {Gut microbiota in pathogenesis and therapeutic potentials in rheumatoid arthritis.},
journal = {Current opinion in immunology},
volume = {100},
number = {},
pages = {102760},
doi = {10.1016/j.coi.2026.102760},
pmid = {41875758},
issn = {1879-0372},
abstract = {This review comprehensively explores the emerging roles of gut microbiota in the pathogenesis and therapeutic implications of rheumatoid arthritis (RA). Clinically, RA is a challenging autoimmune disease due to unclear pathology and limitations of conventional therapies. Recent studies highlight that gut dysbiosis - characterized by reduced microbial diversity, enrichment of proinflammatory taxa, and depletion of anti-inflammatory species - is an important contributor to RA. Mechanistically, gut microbiota dysregulation drives RA through molecular mimicry, metabolite-mediated inflammation, and immune cell migration. Therapeutic strategies targeting the gut-joint axis, including probiotics, high-fiber diets, Mediterranean dietary patterns, and fecal microbiota transplantation (FMT), demonstrate promise in restoring microbial homeostasis, enhancing intestinal barrier integrity, and suppressing proinflammatory cytokines. While preclinical and clinical studies underscore the potential of microbiota-based interventions, challenges such as standardization of FMT protocols and long-term safety require further investigation.},
}

@article {pmid41778924,
year = {2026},
author = {Lawenius, L and Hägg, D and Horkeby, K and Nilsson, KH and Wu, J and Grahnemo, L and Ohlsson, C and Sjögren, K},
title = {Gut microbiota transplantation from young adult mice fails to restore low bone and muscle mass in old mice.},
journal = {American journal of physiology. Endocrinology and metabolism},
volume = {330},
number = {4},
pages = {E461-E470},
doi = {10.1152/ajpendo.00522.2025},
pmid = {41778924},
issn = {1522-1555},
support = {2021 - 01739//Swedish Research Council/ ; 2020 - 01392//Swedish Research Council/ ; 2024 - 02412//Swedish Research Council/ ; ALFGBG-720331//ALF-agreement/ ; LFGBG-965235//ALF-agreement/ ; LU2021-0096//IngaBritt och Arne Lundbergs Forskningsstiftelse (Ingabritt and Arne Lundberg Research Foundation)/ ; LU2024-0110//IngaBritt och Arne Lundbergs Forskningsstiftelse (Ingabritt and Arne Lundberg Research Foundation)/ ; NNF 190C0055250//Novo Nordisk Foundation Center for Basic Metabolic Research (NovoNordisk Foundation Center for Basic Metabolic Research)/ ; NNF 22OC0078421//Novo Nordisk Foundation Center for Basic Metabolic Research (NovoNordisk Foundation Center for Basic Metabolic Research)/ ; KAW 2015.0317//Knut och Alice Wallenbergs Stiftelse (kawforskning)/ ; KAW 2020.0230//Knut och Alice Wallenbergs Stiftelse (kawforskning)/ ; ERC//European Union/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; Mice ; *Aging/physiology ; *Fecal Microbiota Transplantation ; Male ; *Muscle, Skeletal ; Mice, Inbred C57BL ; *Bone Density/physiology ; Germ-Free Life ; *Bone and Bones ; Female ; Body Composition ; },
abstract = {Aging is associated with reduced lean and bone mass, as well as alterations in gut microbiota composition. We previously demonstrated that gut microbiota composition differs between young adult and old mice, and that transplanting gut microbiota from old donors into young germ-free mice reduces lean mass, but not bone mass, compared with transplantation from young adult donors. In this study, we investigated whether the reduced lean and bone mass observed in old mice could be restored through gut microbiota transplantation from young adult donors. Old mice (18-mo old) were treated with antibiotics to deplete their gut microbiota and subsequently transplanted with gut microbiota from either young adult (5-mo old) or old (21-mo old) donors. Recipient mice colonized with gut microbiota from young adult donors showed distinct beta and alpha diversity compared with those colonized with gut microbiota from old donors, demonstrating successful transplantation. However, no differences in lean or bone mass were observed between old mice transplanted with gut microbiota from young adult donors and those receiving gut microbiota from old donors. In conclusion, our findings demonstrate that gut microbiota composition differs in mice transplanted with young adult compared with old gut microbiota but neither reduced lean mass nor reduced bone mass in old mice can be restored through gut microbiota transplantation from young adult donors.NEW & NOTEWORTHY Aging is associated with reduced lean and bone mass and changes in gut microbiota (GM). We tested whether transplanting young adult GM could reverse these age-related conditions in old mice. GM transplantation resulted in distinct GM compositions between mice receiving young adult versus old donor GM, but neither lean nor bone mass was restored in old mice. These findings suggest that GM from young adult mice cannot restore musculoskeletal deficits in aging.},
}

Animals
*Gastrointestinal Microbiome/physiology
Mice
*Aging/physiology
*Fecal Microbiota Transplantation
Male
*Muscle, Skeletal
Mice, Inbred C57BL
*Bone Density/physiology
Germ-Free Life
*Bone and Bones
Female
Body Composition

@article {pmid41864269,
year = {2026},
author = {Melchiorri, S and Besutti, VM and Castagliuolo, I},
title = {Blastocystis spp. in Fecal Microbiota Transplantation: Evidence, Policy, and the Screening Paradox.},
journal = {International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases},
volume = {},
number = {},
pages = {108548},
doi = {10.1016/j.ijid.2026.108548},
pmid = {41864269},
issn = {1878-3511},
abstract = {OBJECTIVES: Fecal microbiota transplantation (FMT) is an established treatment for recurrent Clostridioides difficile infection (rCDI). However, the detection of Blastocystis spp. in potential donors remains controversial and often leads to donor exclusion, despite uncertain pathogenicity. This review aims to critically evaluate the available evidence on Blastocystis spp. transmission through FMT, its clinical impact, and the implications of current donor screening strategies.

METHODS: A narrative review of the literature was performed using PubMed, Embase, and Web of Science. Studies reporting Blastocystis spp. detection in FMT donors or recipients, transmission events, clinical outcomes, diagnostic methods, and microbiome associations were included and analyzed.

RESULTS: Across published reports, 34 FMT recipients were exposed to Blastocystis spp.-positive donor material. Transmission was limited to common subtypes (ST1-ST3), was transient, and was not associated with adverse clinical outcomes or reduced efficacy of FMT for rCDI. No cases of symptomatic infection were reported. Frozen stool preparations appeared to abolish parasite viability. Molecular screening methods markedly increased detection rates compared with microscopy, frequently identifying low-burden colonization of uncertain clinical relevance. Available data suggest that Blastocystis spp. carriage may coexist with a healthy microbiome and does not negatively impact FMT outcomes.

CONCLUSIONS: Current evidence indicates that Blastocystis spp. transmission through FMT in immunocompetent adults is clinically benign. Routine donor exclusion based solely on Blastocystis spp. detection may therefore be overly restrictive. A risk-based approach incorporating parasite burden, subtype, host factors, and processing methods may better balance patient safety with donor availability, supporting more sustainable FMT programs.},
}

@article {pmid41867794,
year = {2026},
author = {Alviter-Plata, A and Ahmari, N and Gadient, J and Brammer-Robbins, E and Martyniuk, CJ and Zubcevic, J},
title = {Loss of Bone Marrow β1/β2-Adrenergic Receptors Reprograms Host-Microbiota Interactions and Protects Against Diet-Induced Obesity.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.03.05.707516},
pmid = {41867794},
issn = {2692-8205},
abstract = {The gut ecosystem is shaped by multiple factors with the immune system being one of the major determinants in shaping its composition in health and disease. On the other hand, the immune system regulates its responses through the action of the sympathetic nervous system (SNS) in part through beta-adrenergic receptors 1/2 (ADRB1/2). In the past years, a clear link has been established between the immune system, SNS, and the modification of nutrient absorption by the gut microbiota in the development of diet-induced obesity. We have previously shown in male mice transplanted with bone marrow cells ADRB1/2 knock-out mice (KD) showed mild immunosuppression and microbiota changes. Post-recovery, mice were challenged with high-fat diet (HFD) for two weeks ad libitum . Our findings show that KD mice are protected against diet-induced adiposity and weight gain. Additionally, these mice showed an increase in residual calorific values and a decreased expression of the fatty acid transporter FAT/CD36. Suggesting a decreased absorption of lipids in the KD mice. Gut microbiota analysis showed that KD microbiota composition on a HFD remained stable with a significant enrichment in the Bacteroidetes phylum , which is depleted in obesity. This was associated with a switch from triglycerides to diglyceride fecal profile. Moreover, microbiome culture showed a decrease in triglycerides after an incubation with 0.1% of HFD lipid extract. Suggesting a potential role of the Bacteroidetes phylum in the metabolism of these lipids. Our findings demonstrate not only that the gut microbiota can modify nutrient absorption and susceptibility to diet-induced obesity but also that the immune system contributes to selective depletion of microbial members that would otherwise thrive on dietary lipids. Revealing a novel mechanism by which host immunity sculpts the gut ecosystem in ways that influence metabolic outcomes.},
}

@article {pmid41868372,
year = {2026},
author = {Wang, Y and Zhang, Y and Cui, Y and Zhu, J and Wang, C and Wang, S and Xiao, X and Yang, L},
title = {Gut microbiota-derived EPA alleviates neuroinflammation associated with white matter injury by influencing H3K9ac/BDNF/TrkB pathway.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1711114},
pmid = {41868372},
issn = {1664-302X},
abstract = {BACKGROUND: The objective of our investigation was to explore the features of gut microbiota dysbiosis and the concentrations of gut metabolites in relation to white matter injury (WMI). Furthermore, we sought to evaluate the influence of gut dysbiosis on neuroinflammation in WMI via intestinal metabolites, and its contribution to pathogenesis.

METHODS: A cerebral hypoxia-ischemia-induced WMI model was established in 3-day-old Sprague-Dawley rats. Liquid chromatography-mass spectrometry/gas chromatography-mass spectrometry analyses and 16S rRNA gene sequencing were undertaken to ascertain WMI biomarkers. Mechanistic experiments were used to analyse activation of the H3K9ac/BDNF/TrkB pathway and neuroinflammation.

RESULTS: The analysis of 16S rRNA sequencing disclosed gut microbiota dysbiosis in WMI rats, quantified using linear discriminant analysis effect size. Overall, 341 differentially expressed metabolic markers between the WMI and Sham groups were discovered. The Kyoto Encyclopedia of Genes and Genomes network enhancement evaluation revealed significant downregulation of 20 metabolic processes in the WMI group, which is strongly related to changes in fecal microbial metabolites, and the synthesis process of unsaturated fatty acids was the most significant. Gut microbiota dysbiosis may influence WMI by downregulating metabolites such as eicosapentaenoic acid (EPA). Fecal microbiota transplantation increased EPA concentration in the brain tissue of WMI rats. Gut microbiota-derived EPA promoted H3K9ac and BDNF/TrkB expression and inhibited the transcription of pro-inflammatory TNF-α and IL-1β molecules. These EPA-mediated effects were reversed by TrkB inhibition.

CONCLUSION: WMI induces gut dysbiosis involving down-regulation of unsaturated fatty acid synthesis. Fecal microbiota transplantation leads to increased levels of EPA. Gut microbiota-derived EPA increases levels of acetylated histone H3K9ac, causes activation of the BDNF/TrkB pathway, reduces neuroinflammation, and improves WMI-associated myelination disorders. It provides a basis for targeted treatment of white matter injury in the future.},
}

@article {pmid41869071,
year = {2026},
author = {Schotz, KM and Alizadeh, M and Rapoport, AP and Ravel, J and Von Rosenvinge, EC},
title = {Faecal microbiota transplant for chronic norovirus infection: a case report of donor microbiota engraftment without clinical success.},
journal = {Gastroenterology report},
volume = {14},
number = {},
pages = {goag015},
pmid = {41869071},
issn = {2052-0034},
}

@article {pmid41870087,
year = {2026},
author = {Wang, X and Wu, W and Yang, B and Liu, Y and Xu, Y and Wang, L and Lv, X and Gao, J and Lu, M and Yu, A and Li, N and Chen, Q and Lu, L and Zhao, D},
title = {Additive effects of fecal microbiota transplantation and infliximab on gut microbiome and metabolome in refractory inflammatory bowel disease patients.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0077425},
doi = {10.1128/msystems.00774-25},
pmid = {41870087},
issn = {2379-5077},
abstract = {UNLABELLED: Fecal microbiota transplantation (FMT) is an emerging therapy for inflammatory bowel disease (IBD), yet its efficacy in patients refractory to conventional treatments and its underlying mechanisms require further elucidation. We studied 37 IBD patients (15 ulcerative colitis [UC], 22 Crohn's disease [CD]) refractory to conventional therapies and 16 healthy donors. FMT monotherapy from a single donor induced week-4 clinical response in 12 UC and 9 biologic-naïve CD patients, with all responders sustaining remission and most achieving endoscopic remission by week 14. Integrated multi-omics revealed FMT restored microbial diversity and profoundly reorganized host-microbiota-metabolite networks. In nine refractory CD patients (7 infliximab [IFX] non-responders, 2 FMT non-responders), IFX-FMT combination led to week-4 response in 6 patients, all of whom attained clinical and endoscopic remission by week 14, with more complete microbial-metabolic restoration than monotherapy. Our findings establish that FMT induces remission in refractory IBD via ecosystem network rewiring, and that IFX-FMT exhibits additive effects, supporting further trials of microbiome-directed adjunctive strategies.

IMPORTANCE: This study provides mechanistic and clinical insights into the therapeutic effects of fecal microbiota transplantation (FMT) in inflammatory bowel disease (IBD), particularly when combined with the anti-tumor necrosis factor (anti-TNF) biologic infliximab (IFX). While both FMT and IFX achieve response in approximately 60% of IBD patients, their combined influence on the gut microbial and metabolic landscape in refractory disease has been poorly understood. Here, we demonstrate that FMT monotherapy restores gut microbial diversity and reconfigures host-microbiota-metabolite networks, correlating with clinical and endoscopic remission in patients refractory to conventional treatments. Furthermore, in Crohn's disease patients unresponsive to either therapy alone, combined IFX-FMT induced more complete microbial and metabolic normalization and achieved remission where monotherapy had failed. These findings reveal ecosystem-level network rewiring as a central mechanism of FMT efficacy and establish the additive potential of combining microbiome-targeted and immunomodulatory therapies. This work supports the development of microbiome-informed adjunctive strategies for severe or refractory IBD, highlighting an actionable path toward personalized, mechanism-based treatment regimens.

CLINICAL TRIALS: This study is registered with ClinicalTrials.gov as NCT07149441.},
}

@article {pmid41870947,
year = {2026},
author = {Zhang, L and Zeng, X and Ma, C and Wei, Y and Wang, W and Liu, T and Li, W},
title = {Acupoint catgut embedding ameliorates laparotomy-induced cognitive decline in aged mice by restoring gut microbiota.},
journal = {Neuroreport},
volume = {},
number = {},
pages = {},
doi = {10.1097/WNR.0000000000002255},
pmid = {41870947},
issn = {1473-558X},
support = {YQJH2023028//Program for Young Talents of Basic Research in Universities of Heilongjiang Province (YQJH2023028)/ ; },
abstract = {BACKGROUND: Postoperative cognitive dysfunction (POCD), a common neurological complication in elderly patients, significantly impairs recovery. Emerging evidence suggests the gut microbiota is involved in its pathogenesis. This study aimed to determine whether acupoint catgut embedding (ACE) could alleviate POCD by modulating the gut microbiota in aged mice after laparotomy.

METHODS: Eighteen-month-old male C57BL/6J mice underwent laparotomy on day 8 (excluding the Sham group). The ACE group received ACE treatment, while the anesthesia and surgery group served as surgical controls. The fecal microbiota transplantation (FMT)-ACE and FMT-AS groups received FMT from corresponding donors. Additional groups received oral indole-3-propionic acid (IPA) or vehicle-treated surgery. Hippocampal inflammation and blood-brain barrier proteins were assessed on day 9; cognitive function and intestinal markers on day 15.

RESULTS: Cognitive function was significantly improved in the ACE, FMT-ACE, and IPA groups. ACE and FMT-ACE treatments specifically elevated fecal g-Clostridia_UCG-014 abundance and serum IPA levels. These changes were accompanied by suppressed hippocampal toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) signaling and proinflammatory cytokines [tumor necrosis factor alpha, interleukin (IL)-1β], together with elevated tight junction proteins (occludin, claudin-5). Furthermore, colonic aryl hydrocarbon receptor (AhR) and IL-22 were upregulated, while serum lipopolysaccharide and diamine oxidase were reduced. Accordingly, IPA treatment mirrored the key anti-inflammatory and barrier-protective effects.

CONCLUSION: ACE alleviates POCD probably by modulating gut microbiota, specifically increasing g-Clostridia_UCG-014 abundance and metabolite IPA. These effects are potentially mediated by dual pathways: (a) suppression of neuroinflammation via TLR4/NF-κB signaling, and (b) enhancement of gut barrier integrity via AhR/IL-22 axis. Our findings highlight the therapeutic potential of ACE in targeting the gut-brain axis for POCD management.},
}

@article {pmid41871875,
year = {2026},
author = {Zhang, Y and Xu, X and Wang, S and Yin, X and Zhang, B and Zhu, Z and Ji, R and Zhu, J and He, H and Cheng, S and Han, Z and Xie, T and Zhang, X and Wang, Y and Shen, S and Kou, Y and Bao, S and Liu, Y and Cao, B and Bonny, C and Guo, X and Segal, E and Tan, Y and Shen, L and Peng, Z},
title = {Fecal microbiota transplantation combined with anti-PD-1 therapy in refractory microsatellite-stable gastric cancer: a phase I feasibility and safety study.},
journal = {Journal for immunotherapy of cancer},
volume = {14},
number = {3},
pages = {},
doi = {10.1136/jitc-2025-013823},
pmid = {41871875},
issn = {2051-1426},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; Male ; Female ; *Stomach Neoplasms/therapy/drug therapy ; Middle Aged ; Aged ; *Immune Checkpoint Inhibitors/therapeutic use/pharmacology ; Feasibility Studies ; *Programmed Cell Death 1 Receptor/antagonists & inhibitors ; Adult ; },
abstract = {BACKGROUND: The discovery and therapeutic application of immune checkpoint inhibitors (ICIs) have significantly improved clinical outcomes in cancer treatment. However, the response rate is still low in gastrointestinal (GI) cancers. The gut microbiome's impact on immune modulation is a promising area for overcoming resistance to immunotherapy.

METHODS: This study (NCT04130763) is an open-label, single-arm, single-center, phase I study assessing the safety and efficacy of fecal microbiota transplantation (FMT) from healthy donors in 10 patients with advanced GI cancer resistant to anti-programmed death-ligand 1 (PD-(L)1) treatment. 10 patients with histologically confirmed, unresectable, or metastatic GI cancers (8 gastric, 2 colorectal) who were refractory to anti-PD-(L)1 treatment were enrolled. Patients received initial FMT treatment via oral capsules (60 capsules), followed by a combination therapy phase, where maintenance FMT (10 capsules per treatment) was paired with nivolumab at 3 mg/kg every 2 weeks for six cycles. Serial biomarker assessments were conducted through both fecal and blood sampling.

RESULTS: The combination of FMT and anti-PD-1 treatment was well tolerated with no serious adverse events. The objective response rate was 20% and the disease control rate was 40%. Clinical benefits were associated with colonization of donor-derived immunogenic microbes, and an activated immune status reflected by peripheral immune cell populations. Moreover, microbial signatures were identified for anti-programmed cell death protein-1 (PD-1) responsiveness and validated in an independent cohort.

CONCLUSIONS: This phase I study demonstrates the feasibility and safety of combining FMT with anti-PD-1 therapy in patients with ICI-refractory gastric cancer. The observed preliminary efficacy signals and identified microbial signatures generate hypotheses for future trials to investigate microbiome-based approaches to enhance immunotherapy efficacy.

TRIAL REGISTRATION NUMBER: NCT04130763.},
}

Humans
*Fecal Microbiota Transplantation/methods
Male
Female
*Stomach Neoplasms/therapy/drug therapy
Middle Aged
Aged
*Immune Checkpoint Inhibitors/therapeutic use/pharmacology
Feasibility Studies
*Programmed Cell Death 1 Receptor/antagonists & inhibitors
Adult

@article {pmid41862794,
year = {2026},
author = {Tian, M and Zeng, X and Zhong, Y and Ma, B and Feng, Y and Wu, X and Liao, Y and Xu, Y and Chen, T and Tan, B},
title = {Combination of Tripterygium glycosides and Lactobacillus paracasei sensitises epithelial ovarian cancer to cisplatin via downregulating Keap1-Nrf2-GPX4 signalling pathway.},
journal = {Cellular & molecular biology letters},
volume = {},
number = {},
pages = {},
doi = {10.1186/s11658-025-00850-3},
pmid = {41862794},
issn = {1689-1392},
support = {82160766//National Natural Science Foundation of China/ ; 2024SSY07061//Jiangxi Province Key Laboratory of bioengineering drugs/ ; 20242BAB20417//Youth Fund Project of Jiangxi Provincial Natural Science Foundation/ ; },
abstract = {BACKGROUND: Epithelial ovarian cancer (EOC) is a highly heterogeneous malignancy with significant morbidity and mortality, and cisplatin (DDP) resistance remains a major obstacle in its treatment. Previous studies suggest that Tripterygium glycosides (TG), derived from Tripterygium wilfordii, may enhance EOC chemo-sensitivity to DDP, potentially involving gut microbiota, though the underlying mechanisms remain to be fully elucidated.

PURPOSE: This study sought to determine how TG enhanced chemotherapy sensitivity in EOC and to examine the involvement of gut microbiota in this process.

STUDY DESIGN: Experimental research in vivo models was conducted, including fecal microbiota transplantation (FMT) from healthy controls and validation assays with Lactobacillus paracasei.

METHODS: TG were administered alone or combined with FMT to evaluate their impact on DDP sensitivity in EOC. Mechanistic studies focused on the Keap1-Nrf2-GPX4 signalling pathway and ferroptosis induction. L. paracasei was co-administered with TG to assess synergistic effects, while Nrf2 pathway activation was tested to confirm its regulatory role.

RESULTS: TG significantly enhanced DDP sensitivity in EOC, either alone or synergistically with FMT. Mechanistically, TG inhibited the Keap1-Nrf2-GPX4 axis, inducing tumor ferroptosis. Gut microbiota, particularly the probiotic Lactobacillus, contributed to this effect: L. paracasei combined with TG amplified DDP cytotoxicity in EOC cells. Conversely, Nrf2 pathway activation attenuated the synergistic effect.

CONCLUSION: TG sensitises EOC to DDP by suppressing the Keap1-Nrf2-GPX4 pathway to trigger ferroptosis, with gut microbiota (e.g., L. paracasei) playing a synergistic role. Combining TG and probiotics may offer a promising and innovative method to improve chemotherapy efficacy in EOC, offering a foundation for future therapeutic development.},
}

@article {pmid41863247,
year = {2026},
author = {Feng, S and Huang, Q},
title = {Microbiota-driven Immunopathogenesis in Systemic Lupus Erythematosus: Cross-site Mechanisms and Intervention Strategies.},
journal = {Current molecular medicine},
volume = {},
number = {},
pages = {},
doi = {10.2174/0115665240433654260209063544},
pmid = {41863247},
issn = {1875-5666},
abstract = {Systemic lupus erythematosus (SLE) is a complex autoimmune disease whose pathogenesis involves intricate interactions with the human microbiota. Accumulating evidence reveals significant compositional and functional dysbiosis in the gut, oral, skin, and vaginal microbiota of SLE patients compared to healthy individuals. These dysbioses actively contribute to disease development and progression through a multitude of mechanisms. These include impaired epithelial barrier integrity, exemplified by the "leaky gut" phenomenon, which facilitates the translocation of microbial antigens. Molecular mimicry, where microbial antigens share structural similarities with host self-antigens, triggers the production of cross-reactive autoantibodies. Furthermore, dysregulated production of microbial metabolites, such as short-chain fatty acids, tryptophan derivatives like tryptamine, and histamine, directly modulates host immune cell function, promotes inflammatory responses, and influences epigenetic regulation. The causal role of specific microbiota in SLE is substantiated by experimental models, including fecal microbiota transplantation studies where transfer of SLE-associated microbiota can recapitulate autoimmune features in recipient germ-free mice, and mono-colonization with pathobionts like Ruminococcus gnavus or Staphylococcus aureus can drive specific aspects of the disease. This growing understanding has paved the way for novel microbiota-targeting interventions. Strategies such as dietary modifications, probiotic and prebiotic supplementation, and fecal microbiota transplantation show considerable promise in preclinical and early clinical studies for restoring microbial homeostasis, rebalancing dysregulated immune responses, and alleviating disease activity. However, challenges in patient-specific variability, understanding precise mechanisms, and ensuring longterm safety remain. Future research must focus on delineating detailed causal pathways, validating efficacy in large-scale trials, and ultimately developing personalized microbiota-targeting interventions to improve SLE management and patient outcomes.},
}

@article {pmid41863409,
year = {2026},
author = {Kaur, S and Bhandari, N and Mahajan, S and Mehta, D and Chauhan, S and Kumar, V and Rohilla, M and Mehta, S and Dhankhar, S},
title = {Molecular Pathways of Microbiota-derived Neuromodulation: An Integrative View.},
journal = {Current neurovascular research},
volume = {},
number = {},
pages = {},
doi = {10.2174/0115672026427392260131184931},
pmid = {41863409},
issn = {1875-5739},
abstract = {INTRODUCTION: The gut microbiota, also called "the forgotten organ", is a complex and dynamic ecosystem of microorganisms that is fundamental to human physiology, neurobiology, and disease. This review examines the intricate relationships between the gut microbiota and the nervous system via the microbiota-gut-brain (MGB) axis. It discusses their endocrine, immunological, and neural pathways.

METHODS: A thorough literature search was performed across databases including PubMed, Scopus, Web of Science, and Google Scholar, using keywords such as "gut microbiota," "microbiota- gut-brain axis," "neuromodulation," "serotonin," "dopamine," "GABA," "norepinephrine," "prebiotics," "probiotics," and "faecal microbiota transplantation"..

RESULTS: This article explains how the gut microbiota impacts significant body's chemical messengers such as serotonin, dopamine, GABA, and norepinephrine. These are essential for brain functioning. All of these diseases have evidence linking inflammation of the gut and the brain. Furthermore, gut dysbiosis has been responsible for some of the most serious disorders of mankind through pandemics and plagues.

DISCUSSION: Moreover, prebiotics, probiotics, faecal microbiota transplantation (FMT), synbiotics, diet, and bioactive substances such as curcumin and flavonoids are new treatment approaches. These strategies help bring back a normal balance of gut microbes for mental and neurological health. Even though preclinical studies have shown promise, bringing it to humans is not simple. Issues like the strain, the individual, and sustained use make it a substantial challenge.

CONCLUSION: Future directions of work should combine and focus human-based research efforts with precise and personalized microbiome modulation, allowing us to leverage the gut-brain axis therapeutically.},
}

@article {pmid41863784,
year = {2026},
author = {Giannakogeorgou, A and van den Ende, T and Verhaar, BJH and de Clercq, N and van Laarhoven, HWM and Nieuwdorp, M},
title = {Targeting the gut microbiota as treatment for obesity and cancer cachexia.},
journal = {Expert opinion on emerging drugs},
volume = {},
number = {},
pages = {},
doi = {10.1080/14728214.2026.2650180},
pmid = {41863784},
issn = {1744-7623},
abstract = {INTRODUCTION: Obesity and cancer cachexia represent two seemingly contrasting yet interrelated ends of the metabolic disorder spectrum, both characterized by disrupted energy homeostasis, inflammation and neuroendocrine dysfunction, and associated with increased morbidity and mortality. Existing treatments often fail to address the complex underlying pathophysiological mechanisms. Emerging research highlights the role of the gut microbiome in the pathophysiology of both conditions and how it can serve as a novel therapeutic target.

AREAS COVERED: This review explores shared and distinct pathways linking obesity and cancer cachexia. Key systems discussed include the gut-brain axis as well as skeletal muscle and adipose tissue metabolism. We discuss how the gut microbiota influences these processes through (diet-derived) gut microbial metabolites that affect specific signaling pathways. The review evaluates the efficacy and limitations of current anti-obesity and cachexia therapies and summarizes clinical and preclinical interventions targeting the gut microbiome, including pre-, pro-, postbiotics and fecal microbiota transplantation.

EXPERT OPINION: The gut microbiota holds potential as a therapeutic target in metabolic diseases, offering opportunities for precision medicine based on microbial and metabolic profiles. While early microbiota-based therapies show promise, further investigation into mechanistic pathways and novel engineered microbiota is essential to develop effective treatments for obesity and cachexia.},
}

@article {pmid41864031,
year = {2026},
author = {Zhai, Z and Yang, Y and Xu, Y and Fu, Q and Chen, S and Wu, Z},
title = {Polydisperse polystyrene microplastics exacerbate colitis through gut microbiota-butyrate-PPARγ axis disruption in mice.},
journal = {Journal of hazardous materials},
volume = {507},
number = {},
pages = {141722},
doi = {10.1016/j.jhazmat.2026.141722},
pmid = {41864031},
issn = {1873-3336},
abstract = {The escalating global prevalence of inflammatory bowel disease (IBD) parallels widespread dietary exposure to microplastics (MPs), yet causal mechanisms linking polydisperse MPs to colitis remain elusive. Here, we show that polydisperse polystyrene microspheres (PS-MS) exacerbate dextran sulfate sodium (DSS)-induced colitis in mice by disrupting a microbiota-butyrate-PPARγ signaling axis. Mechanistically, PS-MS treatment alone does not directly induce colon inflammation in healthy mice; however, it suppresses intestinal Muc2 protein expression and impairs the mucus barrier by reducing the abundance of Lachnospiraceae_NK4A136_group and butyrate levels, thereby inhibiting PPARγ signaling and aggravating colitis. An antibiotic cocktail (ABX)-mediated microbiota ablation abolishes PS-MS-induced colitis aggravation, whereas fecal microbiota transplantation (FMT) from PS-MS-exposed donors transmits susceptibility to antibiotic-treated mice, confirming microbiota-dependent pathogenesis. Exogenous sodium butyrate supplementation restores mucosal homeostasis via PPARγ activation, as evidenced by the abolition of protection following administration of the PPARγ antagonist GW9662, and by the comparable efficacy of the PPARγ agonist 5-ASA. Our findings establish the microbiota-butyrate-PPARγ axis as a critical target for counteracting the adverse effects of environmental MPs and propose butyrate-boosting therapies as a translatable strategy against IBD.},
}

@article {pmid41864264,
year = {2026},
author = {Merrick, B and Mullish, BH and Goldenberg, SD and Khanna, S and Ahuja, V and Hvas, CL and Makharia, GK and Williams, HRT},
title = {A global evaluation of the use of faecal microbiota transplant (FMT).},
journal = {International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases},
volume = {},
number = {},
pages = {108574},
doi = {10.1016/j.ijid.2026.108574},
pmid = {41864264},
issn = {1878-3511},
abstract = {BACKGROUND: Faecal microbiota transplant (FMT) is an effective therapy for recurrent Clostridioides difficile infection (CDI); its use is increasingly being investigated for other indications. Although regional surveys and national registries have provided insight into local practices, a comprehensive global overview of FMT access, implementation and governance is lacking.

METHODS: A survey regarding key aspects related to FMT use was disseminated electronically to members of the World Gastroenterology Organisation, European FMT Network, and International Society of Infectious Diseases. Responses were analysed both descriptively and using appropriate statistical methods.

FINDINGS: 80 responses were obtained from 55 countries. FMT was available in significantly more Tier 1/2, than Tier 3/4, nations (24/28 vs 8/27; p<0.001). In countries lacking access to FMT reasons included: lack of expertise/infrastructure; financial constraints; regulatory uncertainty; and perceived lack of clinical need. Most countries using FMT employed both upper and lower gastrointestinal administration routes; 18/32 (56%) used capsulised FMT. Almost all countries with access to FMT used it to treat CDI, albeit with different thresholds for the number of CDI episodes prior to use. There were many non-CDI indications for FMT in current use. Payment for stool donation was reported by 10 countries.

INTERPRETATION: This is the first global overview of FMT availability and governance, highlighting substantial international inequities and considerable heterogeneity in regulation, clinical use, donor screening, and cost. Standardisation of practice and targeted support for lower income countries is needed to ensure equitable access and to promote safe, high-quality delivery as FMT and microbiome-based therapeutics continue to evolve.},
}

@article {pmid41861987,
year = {2026},
author = {Ramirez-Amoros, C and Amesty, V and Martínez, L and Martínez Urrutia, MJ and Vilanova-Sánchez, A},
title = {Post-Pubertal Outcomes in Patients with Cloacal Malformations: Colorectal, Urological, and Gynaecological Function with Patient-Reported Sexual Outcomes.},
journal = {Journal of pediatric surgery},
volume = {},
number = {},
pages = {163087},
doi = {10.1016/j.jpedsurg.2026.163087},
pmid = {41861987},
issn = {1531-5037},
abstract = {INTRODUCTION: Long-term functional outcomes in patients with cloacal malformations remain poorly described. This study reports long-term outcomes from a tertiary referral center.

METHODS: Retrospective review of female patients with cloacal malformations treated between 1980 and 2010. Colorectal, urological, and gynaecological outcomes were obtained from medical records. Sexual function was assessed using a validated female sexual health questionnaire and compared with 15 healthy controls.

RESULTS: Eleven women were included, with a mean age at follow-up of 24.77 ± 7.41 years. Associated anomalies were present in 73% of patients, including spinal anomalies in 27%. All patients underwent neonatal stoma creation and closure, the latter at a median age of 2.55 (1.61-3.72) years. Faecal continence was achieved in 73% of patients at a mean age of 10.4 ± 3.1 years; one patient required laxatives and five required enemas. All patients achieved urinary dryness. A Mitrofanoff procedure was required in 36%, and one patient underwent bladder augmentation. End-stage renal disease developed in 36%, with three patients undergoing renal transplantation and one awaiting transplant. Three patients (27%) required vaginoplasty, and four (36%) later underwent external genitoplasty. Müllerian anomalies were present in 73%, and 91% menstruated. Sexual function assessment demonstrated increased fear of sexual activity, avoidance due to perineal appearance, reduced excitation, and greater difficulty with vaginal penetration compared with controls.

CONCLUSION: Most patients in our institution with cloacal malformations achieve satisfactory faecal and urinary continence following reconstruction. Renal dysfunction and impaired sexual function remain relevant long-term issues, supporting the need for lifelong multidisciplinary follow-up.},
}

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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