@article {pmid41963962,
year = {2026},
author = {Li, Y and Wu, H and Yang, J and Weedor, JG and Ding, H and Cui, W and Cui, B and He, Z and Zhang, W and Xing, Y and Zeng, F and Huang, X and Zheng, K and Shen, Y and Yu, Y and Pan, W and Yang, X},
title = {Clostridium butyricum ameliorates Toxoplasma gondii-induced neuropsychiatric disorders by attenuating glial-mediated synaptic pruning via the gut-brain axis.},
journal = {Journal of neuroinflammation},
volume = {23},
number = {1},
pages = {},
pmid = {41963962},
issn = {1742-2094},
support = {Nos. 202310313083Y//the Training Programs of innovation and Entrepreneurship for College Students in Jiangsu Province/ ; Nos. X202510313020//the Training Programs of innovation and Entrepreneurship for College Students in Jiangsu Province/ ; Nos. X202510313017//the Training Programs of innovation and Entrepreneurship for College Students in Jiangsu Province/ ; No. JC20250007//the Faculty Development Grant of Basic Medical Sciences in Xuzhou Medical University/ ; Nos. 82372283//the National Natural Science Foundation of China/ ; No. QL-YB022//the XZHMU-QL Joint Research Fund/ ; No. 2022M710120//China Postdoctoral Science Foundation/ ; },
abstract = {UNLABELLED: Gut microbiota dysbiosis contributes to Toxoplasma gondii (T. gondii)-induced neuropsychiatric disorders (TNDs); however, the underlying mechanisms remain largely elusive. Here, we identified the critical role of butyrate-producing bacteria in TNDs in mice. Decreased abundance of butyrate-producing bacteria was consistently observed in patients with Alzheimer’s disease and T. gondii-infected mice. Dietary supplementation with Clostridium butyricum (C. butyricum), a gut commensal butyrate-producing bacterium, reversed gut microbiota dysbiosis, ameliorated intestinal barrier disruption and inflammation, and reduced endotoxemia. Coincidentally, C. butyricum administration suppressed microglial and astrocytic activation, rescued synaptic ultrastructure damage and synaptic loss, thus alleviating cognitive impairment and anxiety/depression-like behaviors. Mechanistically, C. butyricum treatment mitigated the abnormal synaptic pruning mediated by glial cells and C1q to prevent the neuropathology induced by T. gondii infection. Importantly, fecal microbiota transplantation from C. butyricum-supplemented mice into antibiotic-treated recipients recapitulated the therapeutic effects on gut and brain pathology observed in infected mice. Together, our findings suggest that C. butyricum ameliorates TNDs by modulating glial cell-mediated abnormal synaptic pruning via the gut-brain axis, highlighting the therapeutic potential efficacy of butyrate-producing bacteria against TNDs.

SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12974-026-03761-y.},
}

@article {pmid42201625,
year = {2026},
author = {Akram, F and Zainab, S and Shabbir, I and Haq, IU},
title = {Gut microbiota and cancer immunotherapy: from dysbiosis to personalized immune checkpoint blockade optimization.},
journal = {Folia microbiologica},
volume = {},
number = {},
pages = {},
pmid = {42201625},
issn = {1874-9356},
abstract = {Cancer has become one of the most prominent causes of death worldwide due to its increasing mortality rate. Immune checkpoint blockade therapy is an effective regimen for tumor control. Still, it faces challenges, including primary resistance and interindividual variations, thereby directing the field towards a new era of immunotherapy adjuncts. Recent studies have shown that the microbiota of cancer patients influences the outcomes of ICB (immune checkpoint blockade) therapy through microbiome-immune system crosstalk. Homeostatic commensal microbial consortia aid in combating tumors by enhancing immunity, whereas dysbiotic microbes facilitate cancer development by mediating immunosuppression. Microbiota modulation via microbiome-targeted interventions, including fecal microbiota transplantation or washed microbiota transplantation from responders, biotic supplements, and dietary modifications, can convert primary resistance to durable responses and thus augment immunotherapy responsiveness in cancer treatment. This review discusses the dual nature of microbiota in mediating the development and treatment of cancer, its crucial role in shaping ICB therapy responsiveness, and the identification of microbial biomarkers into a refined Discovery-Validation-Clinical (DVC) pipeline linked to multi-omics profiling and personalized microbiome-modulation interventions for ICB therapy optimization. In addition, it presents the translational clinical decision framework that highlights patient stratification, intervention timing, and implementation barriers to support clinical translation. Ultimately, the gut microbiome emerges as a "force multiplier" of cancer ICB therapy, thereby enabling microbiome-guided precision oncology and strengthening a roadmap toward personalized cancer care.},
}

@article {pmid42202865,
year = {2026},
author = {Hoel, ME and Gimenez, AR and Elbe, A and Horecka, K and Alvarez, E and Lashnits, E},
title = {Oral fecal microbial transplant for parvovirus in the outpatient setting: a randomized controlled trial to evaluate a practical and low-cost intervention.},
journal = {Journal of the American Veterinary Medical Association},
volume = {},
number = {},
pages = {1-7},
doi = {10.2460/javma.26.01.0051},
pmid = {42202865},
issn = {1943-569X},
abstract = {OBJECTIVE: To evaluate commercially available oral capsules providing fecal microbial transplant (FMT) as a practical option for adjunctive treatment of canine parvovirus (CPV) in an outpatient setting. We hypothesized that treatment with FMT capsules would improve survival and hasten resolution of clinical signs compared to placebo.

METHODS: This blinded, randomized controlled trial evaluated oral FMT capsules in shelter dogs with CPV treated with an outpatient protocol (September 2022 to August 2024). Eligible dogs were randomized to receive adjunctive FMT or placebo, with 3 dosing regimens assessed. The primary outcome was time to recovery; secondary outcomes included survival, escalation to ICU, and resolution of clinical signs.

RESULTS: 101 dogs were enrolled, of which 52 were in the control group and 49 received FMT. Dogs that survived without escalation to ICU-level care in both the control (n = 42) and FMT groups (32) had a median duration to recovery of 5 days (P = .872). There was a 94% (49 of 52) survival rate in the control group compared to 82% (40 of 49) for the group receiving FMT (P = .051); there was no significant difference in survival between groups when controlling for age or weight (OR, 3.18; 95% CI, 0.74 to 17.28; P = .139).

CONCLUSIONS: There was no evidence that oral FMT capsules hastened recovery or improved short-term survival rate in an outpatient setting. Future work is needed to determine whether oral FMT has negative effects in dogs with CPV.

CLINICAL RELEVANCE: This study provides evidence that oral FMT treatment may not be helpful in the outpatient treatment of CPV.},
}

@article {pmid42203970,
year = {2026},
author = {Ning, K and Chen, Y and Yang, X and Dou, X and Liu, S and Wang, DE and Niu, Y and Xu, H},
title = {Gut microbiota alteration contributes to bone marrow mesenchymal stem cells connexin43 response to high-fat diet induced obesity in mice.},
journal = {International journal of obesity (2005)},
volume = {},
number = {},
pages = {},
pmid = {42203970},
issn = {1476-5497},
abstract = {BACKGROUND/ OBJECTIVE: Bone marrow mesenchymal stem cells (BMSCs) contribute to controlling adipose tissue homeostasis and may be a potential target for obesity therapy. Since lack of connexin43(Cx43) in mesenchymal stem cells (MSCs) is known to combat high-fat diet (HFD)-induced adiposity. Also, HFD is a well-known risk factor for gut microbiota dysbiosis. Here we attempt to address the interaction between HFD, gut microbiota, and Cx43 deficiency in BMSCs during the development of obesity.

METHODS: BMSC-specific Cx43 knockout (Prrx1-Cre;Cx43[flox/flox](cKO)) and control littermate (Cx43[flox/flox](flox))mice were fed a regular chow diet or a HFD for 8 weeks. Cecal microbiome composition was assessed by 16S ribosomal RNA (rRNA) sequencing, and further analyzing correlation between gut microbiota and obesogenic parameters. Moreover, transplantation fecal microbiota was used to probe the salutary effect of BMSC Cx43.

RESULTS: HFD fed cKO mice notably altered cecal microbiome composition as proved by a distinctively clustered separation from flox mice. Concomitantly, Allobaculum induced by HFD was strongly correlated positively with body weight, glucose intolerance, and adipose mass. The recipients with gut microbiota from cKO mice displayed anti-obesity phenotype as the donors.

CONCLUSIONS: Gut microbiota alteration may be one main reason for the salutary effect of BMSC Cx43 knockout on body adiposity.},
}

@article {pmid42204443,
year = {2026},
author = {Henriksen, IW and Hansen, CHF and Koch, J and Sørensen, DB and Nielsen, DS and Bartholdy, C and Hansen, AK},
title = {A Refined Method for Fecal Microbiota Transplantation Using Nutella.},
journal = {Clinical and translational science},
volume = {19},
number = {6},
pages = {e70576},
doi = {10.1111/cts.70576},
pmid = {42204443},
issn = {1752-8062},
mesh = {Animals ; *Fecal Microbiota Transplantation/methods/adverse effects/instrumentation ; Mice, Inbred BALB C ; Mice ; Feces/microbiology ; RNA, Ribosomal, 16S/genetics ; *Gastrointestinal Microbiome/genetics ; Administration, Oral ; Female ; },
abstract = {Fecal microbiota transplantation (FMT) in mice is an evolving research field, often employing oral gavage, which can be stressful and harmful for the animals and time-consuming for technicians. Voluntary intake methods, such as delivery in Nutella, have successfully been used for drug administration in mice and may likewise be a promising tool to refine traditional FMT techniques. Nutella-based FMT may improve animal welfare, reduce workload, and enhance animal safety without compromising microbiota engraftment rates. This study compared microbiota engraftment after mouse-to-mouse FMT in antibiotic-treated BALB/c mice using three methods: oral gavage, pipette delivery, and voluntary intake of a Nutella-inoculum mixture. Feces collected before and after FMT were analyzed using GridION Nanopore 16S rRNA gene amplicon sequencing. Nutella-based FMT showed similar engraftment rates as traditional methods i.e., oral gavage and pipette delivery. Oral gavage delivery resulted in greater variability and divergence from the donor composition compared to pipette delivery. Notably, the oral gavage group had the highest number of genera differing from the donor. Single-dose FMT restored microbial diversity in one study, while it was less effective in another, suggesting to add a second dose of FMT. Nutella-based FMT appears to be an efficient, reproducible, and less stressful alternative to forced-feeding methods, warranting further exploration.},
}

Animals
*Fecal Microbiota Transplantation/methods/adverse effects/instrumentation
Mice, Inbred BALB C
Mice
Feces/microbiology
RNA, Ribosomal, 16S/genetics
*Gastrointestinal Microbiome/genetics
Administration, Oral
Female

@article {pmid42204557,
year = {2026},
author = {Preetam, S and Bora, J and Porna Dutta, S and Talukdar, N and Rustagi, S and Thapliyal, S and Malik, S and Choudhary, N and Kumar, D and Kondaveeti, SB},
title = {Role of gut microbiota in cancer modulation: molecular mechanisms and emerging therapeutic strategies.},
journal = {Infectious agents and cancer},
volume = {},
number = {},
pages = {},
doi = {10.1186/s13027-026-00767-2},
pmid = {42204557},
issn = {1750-9378},
abstract = {The gut microbiota exerts profound effects on host physiology, immunity, and disease susceptibility, with growing evidence implicating its role in cancer initiation, progression, and therapy response. Dysbiosis and microbial-derived metabolites contribute to oncogenesis by modulating epithelial signalling, immune regulation, and systemic inflammation. This review synthesises current knowledge on the crosstalk between the gut microbiome and cancer, spanning molecular mechanisms, site-specific malignancies, and treatment outcomes. We discuss how microbial pathways, including NF-κB, STAT3, Wnt/β-catenin, and inflammasome activation, shape tumour biology, and how microbiota profiles correlate with cancer risk and progression in colorectal, gastric, liver, breast, gynaecological, and pulmonary cancers. Furthermore, we highlight the microbiome's impact on responses to chemotherapy, radiotherapy, and immunotherapy. Finally, we evaluate therapeutic strategies targeting the microbiota, from conventional dietary and probiotic interventions to cutting-edge approaches such as faecal microbiota transplantation, engineered bacterial strains, and microbiome-based biomarkers. Understanding these complex interactions offers novel opportunities to integrate microbiome science into precision oncology.},
}

@article {pmid42204645,
year = {2026},
author = {Zhao, N and Wu, L and Peng, S and Yang, H and Song, Y and Zhang, Y and Ding, L},
title = {Decoding the microbiome-immune crosstalk in cancer: from mechanisms to therapeutic translation.},
journal = {Biomarker research},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40364-026-00930-2},
pmid = {42204645},
issn = {2050-7771},
support = {82303235//National Natural Science Foundation of China/ ; 2025SF-YBXM-358//Key Research and Development Projects of Shaanxi Province/ ; 2025JC-YBQN-1236//Natural Science Basic Research Program of Shaanxi Province/ ; NUHSRO/2023/005/Startup/3//NUS STARTUP grant/ ; MOH-OFIRG24jan-0001, MOH-OFIRG23jul-0007 and MOH-OFIRG21nov-0007//NUS-NJU Research Collaboration Fund 2025, OF-IRG grant from National Medical Research Council/ ; NRF, CRP28-2022RS-0001//CRP grant from National Research Foundation/ ; },
abstract = {The gut microbiome plays a critical role in shaping host immunity and profoundly affects the efficacy of cancer immunotherapy. Accumulating evidence suggests that interventions designed to alter the microbial community, including fecal microbiota transplantation, probiotics, and engineered bacteria, can reprogram the tumor-immune microenvironment and enhance clinical efficacy. This Review provides a comprehensive overview of the molecular and cellular mechanisms through which the gut microbiota influences antitumor immunity, and it highlights recent clinical studies evaluating these interventions. We further examine inherent challenges, including inter-individual variability in microbial composition, difficulties in achieving stable and durable colonization, technical barriers in delivery, and potential safety concerns associated with immune activation or off-target effects. Finally, we discuss future directions for translating microbiome-targeted therapies into oncology, emphasizing the need for mechanistic insight, standardized protocols, rigorous evaluation, and integration with precision immunotherapy strategies to optimize therapeutic outcomes.},
}

@article {pmid42205476,
year = {2026},
author = {Pollicardo, C and Gotta, F and Bottino, P and Vay, D and Pizzo, V and Scaglione, S and Pontarollo, G and Novi, M and Boatti, L and Mignone, F and Melioli, G and Rapallo, F and Rocchetti, A},
title = {Defining reference values for the gut microbiota in a Southern European population.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1766733},
pmid = {42205476},
issn = {2235-2988},
mesh = {Humans ; Reference Values ; Feces/microbiology ; *Gastrointestinal Microbiome/genetics ; RNA, Ribosomal, 16S/genetics ; *Bacteria/classification/genetics/isolation & purification ; High-Throughput Nucleotide Sequencing ; Fecal Microbiota Transplantation ; Europe ; Sequence Analysis, DNA ; Male ; Female ; DNA, Bacterial/genetics ; European People ; Adult ; },
abstract = {INTRODUCTION: The clinical implementation of gut microbiota analysis requires the definition of reliable reference values derived from standardized and certified methodologies applied to a population representative of the intended clinical setting.

METHODS: In this study, 250 fecal samples were analyzed using a CE-certified 16S rRNA bacterial profiling assay for taxonomic characterization across multiple bacterial levels. Sequencing reads were quality-filtered and aligned against the RDP database (release 11, update 5); only sequences with ≥80% alignment coverage and ≥97% similarity were retained.

RESULTS: The resulting taxonomic distributions were first compared with data previously obtained from a similar population, revealing only minor differences. As an additional validation, comparative analyses were performed with data from a clinical study on fecal microbiota transplantation (FMT). Donor profiles were highly consistent with those obtained in the present study, whereas pre-transplant samples showed marked deviations from the reference ranges; post-transplant profiles progressively converged toward them.

DISCUSSION: Although the limited sample size precludes accurate assessment of rare taxa (<0.1% relative abundance), the use of a single Next-Generation Sequencing (NGS) platform and the focus on a Southern European population characterized by the Mediterranean diet allowed the establishment of the first set of gut microbiota reference values derived from a certified in-vitro diagnostic workflow. These data represent an essential step toward the integration of gut microbiota testing into clinical laboratory practice, enabling standardized interpretation of microbiota imbalance and supporting targeted medical interventions aimed at restoring microbial equilibrium.},
}

Humans
Reference Values
Feces/microbiology
*Gastrointestinal Microbiome/genetics
RNA, Ribosomal, 16S/genetics
*Bacteria/classification/genetics/isolation & purification
High-Throughput Nucleotide Sequencing
Fecal Microbiota Transplantation
Europe
Sequence Analysis, DNA
Male
Female
DNA, Bacterial/genetics
European People
Adult

@article {pmid42020750,
year = {2026},
author = {Grieshop, MP and Behr, AA and Bowden, S and Lin, JD and Molari, M and Reynolds, GZ and Brooks, EF and Doyle, B and Moore, AA and Rodriguez-Nava, G and Salinas, JL and Banaei, N and Bhatt, AS},
title = {Transposable elements are driving rapid adaptation of Enterococcus faecium.},
journal = {Nature},
volume = {653},
number = {8116},
pages = {1139-1147},
pmid = {42020750},
issn = {1476-4687},
mesh = {*Enterococcus faecium/genetics/pathogenicity/isolation & purification ; *DNA Transposable Elements/genetics ; Humans ; Genome, Bacterial/genetics ; *Adaptation, Physiological/genetics ; Metagenome/genetics ; Promoter Regions, Genetic/genetics ; Feces/microbiology ; },
abstract = {Bacterial pathogens adapt rapidly to clinical and within-host selective pressures[1]. Insertion sequences (IS) are transposable elements that can contribute to pathogenic adaptation[2], but their activity and consequences in contemporary clinical populations are not well characterized. Here, combining large-scale genomic surveys with long-read sequencing of clinical isolates and longitudinal gut metagenomes, we quantify pathogen IS dynamics from global patterns to within-host evolution. Across 19,485 publicly available high-contiguity ESKAPEE pathogen genomes, Enterococcus faecium genomes are the most IS dense, dominated by replicative ISL3 family elements, which have proliferated in clinical lineages over the past 30 years. We find extensive chromosomal structural variation, largely involving ISL3, within a new single-hospital collection of bloodstream isolates. Long-read metagenomic sequencing of 28 longitudinal stool samples from 12 haematopoietic cell transplantation (HCT) recipients demonstrates within-host IS dynamics and their regulatory consequences. In one patient, an ISL3 insertion upstream of a folate transporter formed a strong promoter, increasing transcription and improving relative fitness under folate limitation. Enhanced folate scavenging may enable E. faecium to thrive in the setting of microbiome collapse, which is common in HCT and other critically ill patients[3]. Together, these results show that a recent ISL3 expansion is driving rapid evolution in healthcare-associated E. faecium, with consequences for its metabolic fitness that may help explain its increasing clinical burden. Several other pathogens also show elevated IS loads in our survey, which suggests that IS expansion-mediated evolution might be more broadly relevant.},
}

*Enterococcus faecium/genetics/pathogenicity/isolation & purification
*DNA Transposable Elements/genetics
Humans
Genome, Bacterial/genetics
*Adaptation, Physiological/genetics
Metagenome/genetics
Promoter Regions, Genetic/genetics
Feces/microbiology

@article {pmid42186662,
year = {2026},
author = {Mueller, MK and Rousseau, SR and Hark, GM and Shaffer, LR and Rizvanović, BF and Nuelle, JAV},
title = {The Role of the Gut Microbiota in Functional Recovery after Peripheral Nerve Injury: A Narrative Review.},
journal = {Orthopedic reviews},
volume = {18},
number = {},
pages = {162156},
pmid = {42186662},
issn = {2035-8164},
abstract = {INTRODUCTION: While researchers have previously pointed to the peripheral nervous system as a method of transportation for the gut microbiota metabolites to distant organs, researchers have more recently studied the impact of gut microbiota on the peripheral nerves. The purpose of this review was to synthesize the literature on how modulation of the gut microbiota impacts functional recovery following peripheral nerve injury.

METHODS: Electronic searches were conducted in Ovid/Medline and PubMed to identify articles that discuss gut microbiome interventions following peripheral nerve injury in sciatic nerve chronic constriction injury or crush injury animal models and the effects on peripheral nerve regeneration and functional recovery.

RESULTS: Twelve articles met inclusion criteria; all were prospective studies in animal models. Four interventions were identified by the twelve studies, including probiotics, antibiotics, intermittent fasting, and naturopathic compounds. Probiotic treatment and dietary interventions targeted at modulating the gut microbiota improved histological, sensory, and motor outcomes following peripheral nerve injury. While antibiotic treatment negatively impacted recovery after peripheral nerve injury, co-treatment with probiotics or reconstitution of the gut microbiota through fecal microbiota transplantation was able to rescue these negative effects.

CONCLUSION: Alterations in the gut microbiota, whether induced by antibiotics, probiotics, intermittent fasting, or dietary interventions, impact functional recovery, neuropathic pain, and inflammatory processes. However, future research should focus on identifying the specific microbial taxa responsible for neuroregenerative effects and developing standardized protocols for probiotic treatment to optimize improvement in peripheral nerve recovery after injury.},
}

@article {pmid42187072,
year = {2026},
author = {John, JM and Manjarres, Z and Zulkifly, NI and Plumb, AN and Pratt, ML and Sadler, KE},
title = {Male-specific analgesic effects of minocycline in sickle cell disease are mediated by microglia and the microbiome.},
journal = {Pain},
volume = {},
number = {},
pages = {},
doi = {10.1097/j.pain.0000000000004008},
pmid = {42187072},
issn = {1872-6623},
abstract = {Over 50% of individuals with sickle cell disease (SCD) experience chronic pain that is phenotypically distinct from their acute, vaso-occlusive crisis pain. Chronic SCD pain is commonly managed with opioid-based drugs that are associated with unwanted side effects, incomplete pain relief, and-in this population-accessibility issues. Thus, new treatments for chronic SCD pain are desperately needed. Here, we examined the analgesic efficacy of acute minocycline treatment in transgenic SCD mice. Sickle cell disease mice exhibit gut dysbiosis and chronic inflammation. Therefore, we hypothesized that minocycline would provide robust analgesia in this model given the drug's antibiotic and anti-inflammatory properties, respectively. Six days of minocycline treatment reversed chronic mechanical hypersensitivity only in male SCD mice. We identified 2 potential mechanisms underlying these sex-specific effects. First, we observed increased microgliosis only in the dorsal horn of male SCD mice. Minocycline treatment had opposite effects on microglial number in male and female SCD spinal cords. Second, minocycline treatment altered the gut microbiota in a sex-specific fashion; fecal microbiota transplant (FMT) from minocycline-treated female SCD mice induced widespread pain in recipients, whereas FMT from minocycline-treated male SCD mice did not. In summary, these experiments highlight novel sex-specific mechanisms of minocycline analgesia and support future exploration of minocycline use for SCD pain management, but only in male patients.},
}

@article {pmid42188905,
year = {2026},
author = {Yao, Y and Yang, Z and Xie, T and Zhang, Y and Huang, F and Meng, C and Wu, Y},
title = {Multi-Omics Analyses of the Gut Microbiota and Metabolism in Cats with Different Body Conditions and the Effects of Fecal Microbiota Transplantation.},
journal = {Veterinary sciences},
volume = {13},
number = {5},
pages = {},
pmid = {42188905},
issn = {2306-7381},
abstract = {Obesity is increasingly recognized in domestic cats and is associated with metabolic disturbances such as insulin resistance and dyslipidemia. The gut microbiota is considered an important regulator of host metabolism, yet its role in feline obesity remains unclear. In this study, a multi-omics approach was used to investigate gut microbiota composition and metabolic profiles in cats with different body conditions and to evaluate the effects of fecal microbiota transplantation (FMT) on the feline gut microbiota and overall metabolism. In Experiment 1, twenty-four cats were classified as obese, normal, or lean, and their gut microbiota and serum metabolites were analyzed. In Experiment 2, fecal microbiota from obese or lean donors were transplanted into recipient cats. Although overall microbial diversity and community structure did not differ significantly among groups, Coriobacteriaceae and Collinsella were enriched in obese cats, whereas Enterobacteriaceae-related taxa were more abundant in normal-weight cats. Serum metabolomics revealed alterations mainly related to amino acid and antioxidant metabolism, including O-acetylcarnitine, glutathione, and tryptophan metabolism. FMT shifted the recipient gut microbial communities toward their respective donor profiles (obese or lean) but did not significantly affect body weight or routine serum biochemical parameters during the experimental period. These findings suggest that gut microbiota remodeling may influence metabolic processes prior to detectable phenotypic changes in cats.},
}

@article {pmid42192549,
year = {2026},
author = {Zhang, L and Quan, J and Nie, L and He, S and Lin, Y and Liu, X and Zhang, Y and Zhuang, L and Jia, C and Li, M and Wang, Q and Duan, L},
title = {Electroacupuncture prevents CUMS induced depressive-like behaviors by inhibiting microglia-mediated synaptic pruning induced by gut dysbiosis.},
journal = {Chinese medicine},
volume = {21},
number = {1},
pages = {},
pmid = {42192549},
issn = {1749-8546},
support = {82305383//National Natural Science Foundation of China/ ; 2023KQNCX017//Ordinary Universities Youth Innovative Talents Project of Guangdong Province Department of Education/ ; 20241088//Project of Guangdong Provincial Administration of Chinese Medicine/ ; 2024A04J4161, 2024A03J0354//Science and Technology Planning Project of Guangzhou/ ; },
abstract = {RATIONALE: Electroacupuncture (EA) has been widely used for depression treatment. Microbiota-gut-brain (MGB) axis plays a vital role in regulating emotional behaviors. However, the potential role of MGB axis in EA-mediated protective effects remains unclear.

METHODS: The protective effects of EA in chronic unpredictable mild stress (CUMS) induced mice were evaluated, and the gut microbiota and metabolic profiles were analyzed. Fecal microbiota transplantation (FMT) was utilized to explore the role of MGB axis in the protective effects of EA. Analyses related to synaptic pruning mediated by microglia were conducted to explore the molecular mechanisms.

RESULTS: In this study, EA treatment prevented depressive-like behaviors in CUMS mice. Mechanistically, EA ameliorated CUMS-induced gut microbiota dysbiosis and inflammation, and partially restored gut microbial metabolism, particularly affecting the abundance of Alistipes and taurine metabolism. Furthermore, EA significantly reduced systemic and hippocampal inflammation. It also attenuated aberrant synaptic pruning in the hippocampus. Moreover, FMT from CUMS mice induced depressive-like behaviors, gut inflammation and microglia-mediated aberrant synaptic pruning, whereas FMT from EA-treated donors exerted protective effects against these impairments.

CONCLUSION: Collectively, our findings suggest that EA prevented CUMS-induced depression-like behaviors and support the involvement of the MGB axis in its protective effects.},
}

@article {pmid42192558,
year = {2026},
author = {Aggad, WS and Ghosh, R and Almohaimeed, HM and Mohammedsaleh, ZM and Saleh, FM and Almars, AI and Jyothi, SR and Panigrahi, R and Kumer, A and Dhara, B},
title = {Exosome-mediated gut-brain axis signaling in neurodegenerative diseases: Mechanisms, experimental evidence, and therapeutic perspectives-A narrative review.},
journal = {Animal models and experimental medicine},
volume = {},
number = {},
pages = {},
doi = {10.1002/ame2.70226},
pmid = {42192558},
issn = {2576-2095},
support = {PNURSP2026R213//Princess Nourah Bint Abdulrahman University/ ; },
abstract = {The stomach and the brain are connected by a sophisticated two-way communication mechanism called the gut-brain axis. Extracellular vesicles, particularly exosomes, that move bioactive substances between the stomach and the brain, such as proteins, lipids, metabolites, and microRNAs, may improve the gut-brain axis. In the past years, the role of exosome-mediated communication has been recognized as significant in relation to the etiology, continued progression, and potential treatment of neurodegenerative disorders. The authors of this review article present a summary of the current understanding of the relationship of gut microbiome, exosome biogenesis, and the pathophysiological development of neurodegenerative diseases. Evidence from laboratory studies, animal studies, and newly emerging human studies suggests that microbiome-based metabolites and inflammatory mediators may modulate how exosomes are produced, what they carry, and how they interact with the blood-brain barrier. These exosomal signals may impact neuroinflammation, neuronal signaling, and the spread of pathological proteins of neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and Huntington's disease. In addition, they examine some possible ways to target the gut-brain axis from a therapeutic perspective, including manipulating the gut microbiome, providing probiotics and/or prebiotics, performing fecal microbiota transplantation, and/or using engineered extracellular vesicles as vehicles for drug delivery. The authors also outline some of the methodological differences that make it difficult to assess the effects of exosomes.},
}

@article {pmid42193296,
year = {2026},
author = {Pinton, P},
title = {Microbiome-Based Therapies in Ulcerative Colitis: Mechanisms, Clinical Evidence, and a Precision-Medicine Framework.},
journal = {Biomedicines},
volume = {14},
number = {5},
pages = {},
doi = {10.3390/biomedicines14050969},
pmid = {42193296},
issn = {2227-9059},
abstract = {Microbiome-based therapies are reshaping the therapeutic landscape for ulcerative colitis (UC), offering new avenues for disease management beyond conventional immunomodulatory and biologic treatments. UC remains a chronic, relapsing condition with significant unmet clinical needs, as many patients fail to achieve sustained remission or experience adverse effects with current therapies. The gut microbiome has emerged as a central contributor to UC pathogenesis, influencing epithelial barrier integrity, immune homeostasis, and metabolic signaling. Interventions such as fecal microbiota transplantation (FMT) and defined microbial consortia have demonstrated proof-of-concept efficacy in early-phase clinical trials, each leveraging distinct mechanistic strategies. FMT, as a broad ecological intervention, restores microbial diversity and functional redundancy, potentially addressing multiple pathogenic mechanisms simultaneously. In contrast, defined consortia enable precise targeting of specific metabolic and immunological pathways, including short-chain fatty acid production, bile-acid remodeling, epithelial barrier reinforcement, immune modulation, and succinate degradation. Recent clinical evidence suggests that consortia with broader mechanistic coverage may achieve more consistent biological activity than narrowly focused designs. This review synthesizes mechanistic and clinical insights across broad and defined microbial consortia, integrates evidence from randomized controlled trials and early-phase LBP studies, and outlines a precision-medicine framework to guide therapy selection. We highlight the importance of aligning therapeutic mechanisms with patient-specific microbial, metabolic, and immune profiles, and discuss future directions including biomarker-guided stratification, hybrid consortia, and adaptive trial designs. Advancing both broad and defined approaches, while incorporating ecological principles, mechanistic understanding, and patient stratification, will be essential to realizing the full therapeutic potential of microbiome-based therapies in UC.},
}

@article {pmid42193302,
year = {2026},
author = {Marchitto, SA and Abbatecola, G and Zeidan, RS and Morgan, L and Calvani, R and Picca, A and Schlögl, M and Tosato, M and Leeuwenburgh, C and Anton, SD and Landi, F and Marzetti, E and Cacciatore, S},
title = {The Gut-Muscle Axis in Sarcopenia: Mechanisms, Evidence Gaps and Translational Challenges.},
journal = {Biomedicines},
volume = {14},
number = {5},
pages = {},
doi = {10.3390/biomedicines14050976},
pmid = {42193302},
issn = {2227-9059},
support = {D1.2024//Università Cattolica del Sacro Cuore/ ; D1.2025//Università Cattolica del Sacro Cuore/ ; N/A//Centro Studi Achille e Linda Lorenzon/ ; P30 AG028740/AG/NIA NIH HHS/United States ; 2022YNENP3//Ministero dell'università e della ricerca/ ; },
abstract = {Sarcopenia is an age-related skeletal muscle disorder characterized by reduced muscle mass, strength, and physical performance, as well as increased risk of disability, hospitalization, and mortality. Emerging evidence suggests that gut microbiota alterations may contribute to muscle decline via a microbiota-gut-muscle axis, acting as a context-dependent modulator rather than a primary causal driver. This narrative review synthesizes mechanistic, clinical, and translational evidence linking gut dysbiosis to sarcopenia. Preclinical studies show that microbiota modulation (e.g., antibiotics, probiotics, prebiotics, postbiotics, fecal microbiota transplantation) affects muscle mass, strength, and metabolism through pathways including inflammation, mitochondrial dysfunction, altered short-chain fatty acid production, and impaired anabolic signaling. In humans, observational studies associate lower microbial diversity and reduced short-chain fatty acid-producing taxa with poorer muscle outcomes, but findings are heterogeneous and non-causal. Interventional trials remain limited and characterized by small sample sizes, with effects more consistent for functional outcomes than muscle mass. Overall, the gut microbiota represents a modifiable contributor within the complex biology of sarcopenia. Future studies should integrate microbiome profiling and multi-omics approaches within well-designed clinical trials to identify responder phenotypes and define the role of microbiota-targeted strategies within multimodal interventions.},
}

@article {pmid42194001,
year = {2026},
author = {Zhao, Z and Wang, J and Wu, Z and Ye, L and Wang, J and Wang, Y and Zhao, Y and Zhang, H and Luo, C and Tong, J},
title = {Integrated Multi-Omics Analysis Explores the Protective Effects and Potential Mechanisms of Pulsatilla chinensis on Canine Antibiotic-Associated Diarrhea.},
journal = {Biomolecules},
volume = {16},
number = {5},
pages = {},
doi = {10.3390/biom16050650},
pmid = {42194001},
issn = {2218-273X},
support = {32272904//National Natural Science Foundation of China/ ; 32373086//National Natural Science Foundation of China/ ; },
mesh = {Animals ; Dogs ; *Diarrhea/chemically induced/drug therapy/veterinary/prevention & control/metabolism ; Multiomics ; *Anti-Bacterial Agents/adverse effects ; *Pulsatilla/chemistry ; Metabolomics ; *Plant Extracts/pharmacology/chemistry ; Cytokines ; },
abstract = {Diarrhea is a common gastrointestinal disorder in animals, often worsened by antibiotic use. Pulsatilla chinensis (PC) is traditionally used for gastrointestinal issues, but its bioactive constituents and mechanisms remain unclear. This study investigated the preventive effects of PC in a canine model of antibiotic-associated diarrhea using an integrated multi-omics approach. LC-MS identified key constituents of PC, including anemoside B4, berberine, stigmasterol, and quercetin. In silico analyses predicted that stigmasterol and quercetin target EGFR and AKT1, modulating inflammation and epithelial repair via PI3K-Akt and IL-17 signaling pathways. In vivo, treatment with PC significantly reduced serum pro-inflammatory cytokines such as TNF-α and IL-6 and elevated immune markers including IgG and IgA compared to the control group. Furthermore, 16S rRNA analysis revealed that PC restored gut microbial diversity, reflected by increased Sobs and Chao1 indices, enriched beneficial Lactobacillus, and decreased the abundance of inflammation-associated taxa such as Proteobacteria, Desulfobacterota, and Escherichia-Shigella. These findings suggest that PC suppresses inflammation and remodels the gut microbiome, providing a mechanistic basis for its use as an herbal alternative to antibiotics. Future studies should include fecal microbiota transplantation and targeted metabolomics to establish causality and optimize therapeutic strategies.},
}

Animals
Dogs
*Diarrhea/chemically induced/drug therapy/veterinary/prevention & control/metabolism
Multiomics
*Anti-Bacterial Agents/adverse effects
*Pulsatilla/chemistry
Metabolomics
*Plant Extracts/pharmacology/chemistry
Cytokines

@article {pmid42194897,
year = {2026},
author = {Lau, WL and Li, W and Sumida, K and Kalantar-Zadeh, K},
title = {The Role of Diet and Gut Microbiome in CKD Progression and Therapy.},
journal = {Journal of clinical medicine},
volume = {15},
number = {10},
pages = {},
doi = {10.3390/jcm15103934},
pmid = {42194897},
issn = {2077-0383},
abstract = {There is a bidirectional relationship between chronic kidney disease (CKD) and an altered gut microbiome, with gut-derived uremic toxins contributing to cardiovascular-kidney-metabolic effects. In this review, we summarize the interplay between diet, the intestinal microbiota and systemic sequelae including CKD progression, cardiovascular morbidity and cognitive decline. We discuss the current state of knowledge regarding microbiota-modulating therapies that have the potential to delay CKD complications such as plant-dominant diets, oral adsorbents, prebiotics/probiotics, fecal microbiota transplantation and exercise.},
}

@article {pmid42197000,
year = {2026},
author = {Shehata, F and Dwyer, KM and McGee, SL and Rivera, LR},
title = {Gut Microbiome Dysbiosis in Metabolic Syndrome: Current Evidence and Emerging Perspectives.},
journal = {Nutrients},
volume = {18},
number = {10},
pages = {},
doi = {10.3390/nu18101540},
pmid = {42197000},
issn = {2072-6643},
mesh = {Humans ; *Metabolic Syndrome/microbiology/therapy ; *Dysbiosis/microbiology/complications ; *Gastrointestinal Microbiome/physiology ; Probiotics/administration & dosage ; Prebiotics/administration & dosage ; Fecal Microbiota Transplantation ; Synbiotics/administration & dosage ; },
abstract = {The gut microbiota plays a crucial role in human metabolism, and disruptions to its composition, particularly reductions in bacterial diversity, have been increasingly associated with the development of metabolic syndrome (MetS). MetS encompasses a constellation of interrelated metabolic risk factors, including central obesity, insulin resistance, dyslipidemia, and hypertension, which collectively elevate the risk of cardiovascular and cerebrovascular disease. A comprehensive understanding of the mechanisms underlying MetS is therefore critical for the development of effective preventive and therapeutic strategies. Complex interactions between the gut microbiota and host metabolic pathways are mediated by multiple factors, including microbial metabolites, inflammatory signaling, and host immune responses. This narrative review characterizes the clinical manifestations of MetS and alterations in gut microbiota composition, characterized by an overrepresentation of potentially pathogenic taxa and a concomitant decline in beneficial microbial species. In addition, we discuss current and emerging approaches to microbiota modulation, including prebiotics, probiotics, synbiotics, postbiotics, and fecal microbiota transplantation, and evaluate their potential roles in the prevention and management of MetS. We identify critical evidence gaps and propose research priorities for evidence-based clinical strategies for MetS management and prevention.},
}

Humans
*Metabolic Syndrome/microbiology/therapy
*Dysbiosis/microbiology/complications
*Gastrointestinal Microbiome/physiology
Probiotics/administration & dosage
Prebiotics/administration & dosage
Fecal Microbiota Transplantation
Synbiotics/administration & dosage

@article {pmid42197001,
year = {2026},
author = {Lupu, VV and Nedelcu, AH and Miron, I and Anton, SC and Sasaran, MO and Frasinariu, OE and Jechel, E and Bozomitu, LI and Chisnoiu, T and Anton, CR and Marginean, CO and Morariu, ID and Mihai, CM and Anton, E and Lupu, A},
title = {Early Gut Microbiota and Neurodevelopmental Trajectories: Implications for Pediatric Neuropsychiatric Vulnerability-A Narrative Review.},
journal = {Nutrients},
volume = {18},
number = {10},
pages = {},
doi = {10.3390/nu18101541},
pmid = {42197001},
issn = {2072-6643},
mesh = {Humans ; Neurodevelopment ; *Gastrointestinal Microbiome/physiology ; *Neurodevelopmental Disorders/microbiology ; Dysbiosis/microbiology ; Child ; Brain/growth & development ; Probiotics ; Prebiotics/administration & dosage ; Neuronal Plasticity ; },
abstract = {Neurodevelopment is a dynamic and multifactorial process, critical in the early stages of life, involving the formation of neural networks, the establishment of synapses, and the maturation of cognitive, social and emotional circuits. In this context, the gut microbiome emerges as an essential regulator of neurodevelopment, exerting influences through multiple biochemical and immunological mechanisms that define the "gut-brain axis". The microbiota modulates neurodevelopment by regulating neurotransmitters (serotonin, dopamine, GABA), the production of microbial metabolites, including short-chain fatty acids, the modulation of inflammatory cytokines, and vagal signaling to the central nervous system. Recent evidence highlights the role of microbiota in modulating microglia, synaptogenesis, dendritic maturation, and neuronal plasticity, emphasizing how these processes are influenced by microbial activity rather than providing a comprehensive treatise on plasticity itself. Gut microbiota disturbances, or dysbiosis, have been associated with various neuropsychiatric and neurodevelopmental disorders, contributing to cognitive, behavioral, and emotional dysfunctions. This article summarizes, in a narrative manner, the main dysbiosis patterns identified in these disorders and the biological mechanisms by which the microbiome influences neuronal development and function, including immune-neuronal interactions, metabolomic modulation, and neuroendocrine signaling. Finally, emerging directions of intervention aimed at adjusting the microbial profile, such as dietary adjustment, the use of probiotics, prebiotics, symbiotics, and fecal microbiota transplantation, are presented with the aim of positively influencing neurodevelopment and preventing or ameliorating associated dysfunctions. This review emphasizes the need for longitudinal, rigorous, and controlled clinical trials to validate the efficacy of microbiota modulation strategies and to substantiate their integration into individualized pediatric management protocols.},
}

Humans
Neurodevelopment
*Gastrointestinal Microbiome/physiology
*Neurodevelopmental Disorders/microbiology
Dysbiosis/microbiology
Child
Brain/growth & development
Probiotics
Prebiotics/administration & dosage
Neuronal Plasticity

@article {pmid42197004,
year = {2026},
author = {Wang, M and Lyu, Y and Zhang, J and Wang, Y and Yang, Y and Mao, YH},
title = {FMT from Exercise and Konjac Glucomannan Preconditioned Donors Rescues Antibiotic-Induced Dysbiosis with Enhanced Ecological Restoration in Mice.},
journal = {Nutrients},
volume = {18},
number = {10},
pages = {},
doi = {10.3390/nu18101544},
pmid = {42197004},
issn = {2072-6643},
support = {2023ZDZX2035; 2024ZDZX2061//Guangdong Scientific Research Platform and Projects for the Higher-educational Institution (Key Area Project)/ ; SL2024A04J01093//the Guangzhou Fundamental and Applied Research/ ; No.82030098//National Natural Science Foundation of China/ ; S202410585045 and 202410585015//the College Students Innovation and Entrepreneurship Training Program/ ; 2023A1515010004//the Guangdong Basic and Applied Basic Research Foundation/ ; },
mesh = {Animals ; *Dysbiosis/therapy/chemically induced/microbiology ; *Fecal Microbiota Transplantation/methods ; *Mannans/pharmacology ; *Anti-Bacterial Agents/adverse effects ; Mice ; *Gastrointestinal Microbiome/drug effects ; Male ; *Physical Conditioning, Animal ; Mice, Inbred C57BL ; },
abstract = {BACKGROUND: Although antibiotics have a wide range of applications in medical clinical practice and possess significant clinical value, their inevitable contribution to gut microbiome dysbiosis warrants attention. Our previous research has confirmed that the combined intervention of exercise and konjac glucomannan (KGM) has a better regulatory effect on gut dysbiosis in mice compared with individual interventions.

METHODS: This study aims to further investigate whether this effect can be transmitted through fecal microbiota transplantation (FMT), and to compare the recovery effects of autologous FMT (a-FMT), fecal microbiota transplantation after exercise combined with KGM intervention (EK-FMT), and combinative intervention with exercise and KGM (EXE-KGM) on gut microbiome dysbiosis. Sample sizes ranged from five to six animals.

RESULTS: The results showed that the a-FMT group recovered α diversity the fastest, including Chao, Shannon, and Simpson indices(p < 0.05), within 2 weeks after transplantation when compared with the CTL group. At the end of the experiment, the Bray-Curtis distance of the a-FMT group was closest to the CTL group, while the EXE-KGM group had delayed recovery, there was no significant difference between the EK-FMT group and the EXE-KGM group. Metagenomic analysis and metabolomics analysis indicated that the arginine synthesis and metabolism pathways (KEGG: map00471, map00473, arginine biosynthesis) played a core role in the restoration of the microbiota.

CONCLUSIONS: The results of this experiment indicate that EK-FMT group can partially transfer the regulatory effects of combined exercise and KGM intervention, a-FMT accelerates the recovery speed of the gut microbiome and arginine metabolism may play an important role in it. This finding provides a theoretical basis and practical direction for special populations to receive special donor fecal treatment.},
}

Animals
*Dysbiosis/therapy/chemically induced/microbiology
*Fecal Microbiota Transplantation/methods
*Mannans/pharmacology
*Anti-Bacterial Agents/adverse effects
Mice
*Gastrointestinal Microbiome/drug effects
Male
*Physical Conditioning, Animal
Mice, Inbred C57BL

@article {pmid42197026,
year = {2026},
author = {Alsinani, Y and Rostamkhani, F and Shirvani, H},
title = {Exercise and the Gut Microbiome: From Mechanisms to Clinical Applications.},
journal = {Nutrients},
volume = {18},
number = {10},
pages = {},
doi = {10.3390/nu18101565},
pmid = {42197026},
issn = {2072-6643},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; Animals ; *Exercise/physiology ; Fatty Acids, Volatile/metabolism ; },
abstract = {Background/Objectives: The gut microbiome is a critical regulator of host metabolism, immunity, and the gut-brain axis. Exercise is a promising non-pharmacological modulator of microbial ecology, yet human evidence remains heterogeneous and the translational gap persists. This narrative review synthesizes mechanisms, human and animal evidence, and future directions for the exercise-gut microbiome axis. Methods: PubMed, Scopus, Web of Science, and SID were searched for articles published between January 2000 and February 2025. Keywords included exercise, physical activity, gut microbiome, gut microbiota, short-chain fatty acids, and gut-muscle axis. From 218 initial records, 89 original studies (47 human, 42 animal) met inclusion criteria and were critically appraised. Results: Exercise modulates the gut microbiome via splanchnic hypoperfusion, hyperthermia, altered transit time, and immune-mediated barrier regulation. Moderate-intensity continuous training consistently increases alpha diversity and enriches butyrate-producing taxa (Faecalibacterium prausnitzii, Roseburia hominis) and mucin-degrading Akkermansia muciniphila. High-intensity interval training transiently increases intestinal permeability in untrained individuals but, following adaptation, stimulates butyrate production via lactate cross-feeding metabolism-a recent breakthrough. Effects are transient and reversible upon detraining. Animal models establish causality through fecal microbiota transplantation; human randomized controlled trials demonstrate modest, intensity-dependent, and highly individualistic responses. Emerging evidence supports the gut-muscle axis in sarcopenia and personalized exercise prescription guided by microbiome profiling. Conclusion: Exercise shows promise as a low-cost modulator of the gut microbiome for enriching health-associated taxa and improving metabolic outcomes. Definitive evidence linking exercise-induced microbial shifts to enhanced athletic performance in humans remains lacking. Future research requires diet-controlled randomized controlled trials with ≥12-week interventions, shotgun metagenomics, and mechanistic validation of the gut-muscle axis in humans.},
}

Humans
*Gastrointestinal Microbiome/physiology
Animals
*Exercise/physiology
Fatty Acids, Volatile/metabolism

@article {pmid42197071,
year = {2026},
author = {Jing, Y and Bai, X and Ji, Y and Zhai, Z and Zhao, Y and Hao, Y},
title = {Fecal Microbiota Transplantation from Toddler Donors Ameliorated DSS-Induced Colitis in Mice by Reshaping Gut Microbiota.},
journal = {Nutrients},
volume = {18},
number = {10},
pages = {},
doi = {10.3390/nu18101611},
pmid = {42197071},
issn = {2072-6643},
support = {No. 2022YFF1100105//the National Key R&D Program of China/ ; },
mesh = {Animals ; *Fecal Microbiota Transplantation/methods ; *Colitis/therapy/chemically induced/microbiology ; *Gastrointestinal Microbiome ; Dextran Sulfate ; Mice ; Male ; Disease Models, Animal ; Humans ; Colon/pathology/microbiology ; Mice, Inbred C57BL ; Dysbiosis/therapy ; Feces/microbiology ; Intestinal Barrier Function ; Cytokines/metabolism ; },
abstract = {Background/Objectives: Gut microbiota dysbiosis is a key driver of inflammatory bowel disease (IBD), and fecal microbiota transplantation (FMT) has emerged as a potential therapeutic strategy. In this study, we investigated the protective effects of toddler-derived FMT against colitis and elucidated the underlying mechanisms. Methods: Firstly, fecal microbiota from healthy toddlers was transplanted into antibiotic-pretreated mice, establishing stable colonization between days 14 and 21 post-transplantation. Results: In a dextran sulfate sodium-induced colitis model, FMT significantly ameliorated colitis symptoms, including reduced disease activity index and restored colon length. Toddler-derived FMT improved the intestinal barrier by preserving goblet cell density and enhancing MUC2 expression. Meanwhile, colonic inflammation was alleviated by FMT, which suppressed pro-inflammatory cytokines, reduced CD4[+] T cell counts, and associated with downregulation of JAK/STAT-related transcripts. 16S rRNA sequencing revealed that FMT remodeled the gut microbiota by enriching beneficial genera, including Bacteroides, Parabacteroides, Blautia, and Akkermansia, which correlated positively with colon length and negatively with inflammatory markers. Conclusions: These findings provided a theoretical foundation that toddler-derived microbiota represents a potential donor source for FMT in IBD.},
}

Animals
*Fecal Microbiota Transplantation/methods
*Colitis/therapy/chemically induced/microbiology
*Gastrointestinal Microbiome
Dextran Sulfate
Mice
Male
Disease Models, Animal
Humans
Colon/pathology/microbiology
Mice, Inbred C57BL
Dysbiosis/therapy
Feces/microbiology
Intestinal Barrier Function
Cytokines/metabolism

@article {pmid42197467,
year = {2026},
author = {Bartocci, B and Del Gaudio, A and Murgiano, M and Papa, A and Cammarota, G and Gasbarrini, A and Scaldaferri, F and Lopetuso, LR},
title = {Emerging Role of Gut Microbiota in Modulating Response to Therapies in IBD.},
journal = {Microorganisms},
volume = {14},
number = {5},
pages = {},
doi = {10.3390/microorganisms14051082},
pmid = {42197467},
issn = {2076-2607},
abstract = {The gut microbiota is increasingly recognized as a key contributor in the pathogenesis and progression of inflammatory bowel disease (IBD). Compared with healthy individuals, patients with IBD show marked dysbiosis, characterized by reduced microbial diversity, an expansion of facultative anaerobes such as Proteobacteria, and a depletion of obligate anaerobes within the Firmicutes phylum. These changes have been implicated in the perpetuation of intestinal inflammation, disruption of mucosal immune homeostasis, and altered metabolic functions, further underscoring the microbiota's relevance in IBD pathophysiology. However, microbiota-driven insights have not yet been consistently translated into therapeutic stratification or clinical decision-making. A major challenge lies in the complex and dynamic interplay between the gut microbiota and various treatment modalities, including conventional immunosuppressants, biologics, and small-molecule inhibitors. While accumulating evidence suggests that IBD treatments may modulate microbial composition and function, it remains unclear whether these changes represent a direct pharmacological effect or are secondary to inflammation control. Additionally, there is a lack of comparative data on microbiota profiles associated with differential responses to various therapeutic classes, limiting the implementation of microbiota-informed precision medicine. In this review, we synthesize current evidence on the association between gut microbiota composition and treatment outcomes, focusing on biologic agents and small-molecule therapies. Furthermore, we discuss the potential of microbiota-targeted strategies, such as fecal microbiota transplantation (FMT) and precision probiotics, in enhancing therapeutic response. A deeper understanding of host-microbe interactions could enable a more personalized and effective approach to IBD management.},
}

@article {pmid42198436,
year = {2026},
author = {Zou, Y and Hu, RT and Yu, Q and Rao, PL and Cui, HY and Wei, WJ and Cai, X and Li, HK and Shen, YH},
title = {Liuweidihuang Pill Attenuates Early Bleomycin-Induced Pulmonary Fibrosis in Mice and Is Associated with Gut Microbiome.},
journal = {Pharmaceuticals (Basel, Switzerland)},
volume = {19},
number = {5},
pages = {},
doi = {10.3390/ph19050762},
pmid = {42198436},
issn = {1424-8247},
support = {ZD2021CY001//Shanghai Municipal Science and Technology Major Project/ ; },
abstract = {Background: Pulmonary fibrosis (PF) is a chronic, progressive lung disease with limited treatment options. Liuweidihuang pill (LDP), a classical formula for kidney-yin deficiency, has been reported to have anti-inflammatory and anti-oxidative activities, suggesting potential relevance to PF. Purpose: This study evaluated whether LDP attenuates bleomycin-induced PF in mice and whether gut microbiota remodeling may contribute to its protective effects. Methods: Mice received intratracheal bleomycin followed by LDP gavage. Lung pathology was assessed by hematoxylin-eosin (HE) and Masson staining. Inflammatory cytokines, hydroxyproline (HYP), and α-SMA were measured. LDP and LDP-containing serum were profiled by UPLC-MS. The gut microbiota was analyzed using 16S rDNA sequencing. To further explore whether microbiota-related changes were associated with the protective phenotype, fecal microbiota transplantation (FMT) and probiotic VSL#3 intervention were performed. In addition, LDP-containing serum was tested in a TGF-β1-induced EMT model in A549 cells. Results: LDP reduced lung index, inflammatory infiltration, interstitial fibrosis, α-SMA expression, HYP content, and pro-inflammatory cytokine levels in bleomycin-treated mice. These effects were accompanied by gut microbiota remodeling and transcriptomic changes related to inflammation, metabolism, and fibrosis. VSL#3 partially reproduced the protective phenotype, whereas FMT showed limited efficacy. LDP-containing serum had a limited inhibitory effect on EMT inhibited EMT in vitro, suggesting that systemic host responses may contribute to the in vivo effect. Conclusions: LDP attenuated early bleomycin-induced PF and was associated with reduced inflammation and gut microbiota remodeling. These findings suggest a possible role for microbiota-host interactions in LDP-associated protection; however, causal directionality, key active effectors, and protein-level pathway validation remain unresolved.},
}

@article {pmid42198457,
year = {2026},
author = {Pastras, P and Aggeletopoulou, I and Psalti, V and Triantos, C},
title = {Gut Microbiota in Irritable Bowel Syndrome and Inflammatory Bowel Disease: Differences in Pathophysiology, Biomarkers, and Treatment Implications.},
journal = {Pharmaceuticals (Basel, Switzerland)},
volume = {19},
number = {5},
pages = {},
doi = {10.3390/ph19050783},
pmid = {42198457},
issn = {1424-8247},
abstract = {Alterations in the intestinal microbiota have been implicated in both irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD). However, their biological significance and therapeutic implications differ substantially between the two conditions. Although dysbiosis is a common feature, the mechanisms by which alterations in the microbiota contribute to disease pathophysiology and clinical expression are distinct. Some pathways are more prominent in IBS (e.g., the gut-brain axis), whereas others are more prominent in IBD (e.g., reduced microbial diversity). Equally important are pathways that appear to play a role exclusively in IBD [e.g., Adherent-invasive Escherichia coli (AIEC) and Paneth cells], as well as others that seem to be specific to IBS (e.g., mast cell activation). In IBD, microbiota changes are primarily linked to immune dysregulation, mucosal barrier impairment, and inflammation-driven pathways, whereas in IBS, they are mainly associated with functional disturbances mediated by neuroimmune signaling and microbial metabolites. Furthermore, several microbiome-associated biomarkers differ between these two diseases, and some are already assessed by international guidelines. Although the microbiota plays a key role in IBS and IBD pathophysiology, microbiome-based treatments remain limited, especially in IBD. There are clinically available treatments in IBS (e.g., rifaximin, low-FODMAP diet), but in IBD, only the probiotic VSL#3 is guideline-approved in ulcerative colitis pouchitis prophylaxis. Nevertheless, the dynamic nature of the microbiota continues to support the investigation of already studied (e.g., probiotics, fecal microbiota transplantation) and potential novel therapeutic approaches at the research level. The aim of this review is to compare the gut-microbiota-related pathophysiological pathways and biomarkers between IBS and IBD, to summarize the microbiome-related medications that have already been studied in both diseases, and to suggest new potential therapeutic options based on the gut microbiota.},
}

@article {pmid42198975,
year = {2026},
author = {Zhang, J and Bai, J and Ren, X and Ye, X and Tan, M and Yang, Y and Li, L and Fu, Z},
title = {[Fecal microbiota transplantation inhibits colonic tumor growth in mice by suppressing the TLR4/MyD88/NF-κB signaling pathway].},
journal = {Nan fang yi ke da xue xue bao = Journal of Southern Medical University},
volume = {46},
number = {5},
pages = {1139-1148},
doi = {10.12122/j.issn.1673-4254.2026.05.18},
pmid = {42198975},
issn = {1673-4254},
mesh = {Animals ; Myeloid Differentiation Factor 88/metabolism ; *Toll-Like Receptor 4/metabolism ; NF-kappa B/metabolism ; Mice ; Signal Transduction ; *Colonic Neoplasms/therapy ; *Fecal Microbiota Transplantation ; Mice, Inbred C57BL ; Transforming Growth Factor beta1/metabolism ; Cell Line, Tumor ; Killer Cells, Natural ; Male ; },
abstract = {OBJECTIVES: To explore the effects of fecal microbiota transplantation (FMT) on immune function and tumor inhibition in mice.

METHODS: C57BL/6N mice were divided into blank control group, tumor bearing model group, and FMT intervention group (n=6). In the latter two groups, the mice bearing subcutaneous MC38 colon cancer cell xenografts were treated with daily gavage of normal saline or 0.1 mL of bacterial suspension. The changes in tumor mass and volume were recorded, and peripheral blood natural killer (NK) cell counts and NKG2A and NKG2D receptor expressions were analyzed using flow cytometry; serum lipopolysaccharide (LPS) levels were measured with ELISA. The binding ability of NF‑κB to the TGF‑β1 gene promoter was analyzed with JASPAR. The mRNA and protein expressions of TLR4, MyD88, NF‑κB, TGF‑β1, perforin and granzyme in the tumor tissues were detected using RT qPCR and Western blotting, and the changes in gut microbiota were analyzed using 16S high throughput sequencing.

RESULTS: FMT significantly reduced tumor mass and volume in the tumor-bearing mice. Peripheral CD3⁻NK1.1⁺ cell counts were significantly decreased in the tumor-bearing mice regardless of FMT treatment, which, however, reversed the increase of CD3[-]NKG2A[+] cells and reduction of CD3[-]NKG2D[+] cells and reduced serum LPS levels in the mouse models. Molecular docking and JASPAR analysis confirmed LPS-TLR4 binding (binding energy: -13.1 kcal/mol) and identified NF-κB binding sites on TGF‑β1 promoter. FMT downregulated mRNA and protein expressions of TLR4, MyD88, NF‑κB and TGF‑β1 and upregulated perforin and granzyme mRNA expressions in the xenografts. FMT also restored gut microbiota diversity and composition, and reversed the increase of Proteobacteria and decrease of Lactobacillus murinus in the tumor-bearing mice.

CONCLUSIONS: FMT modulates the relative abundances of intestinal Proteobacteria and Lactobacillus murinus in tumor-bearing mice, and inhibits tumor growth by suppressing the TLR4/MyD88/NF‑κB signaling axis, down-regulating TGF-β1 expression, and promoting NK cell activation.},
}

Animals
Myeloid Differentiation Factor 88/metabolism
*Toll-Like Receptor 4/metabolism
NF-kappa B/metabolism
Mice
Signal Transduction
*Colonic Neoplasms/therapy
*Fecal Microbiota Transplantation
Mice, Inbred C57BL
Transforming Growth Factor beta1/metabolism
Cell Line, Tumor
Killer Cells, Natural
Male

@article {pmid42199152,
year = {2026},
author = {Zhang, W and Song, Y and Li, C and Luo, Y and Shao, M and Guo, F and Wei, F and Fan, X and Guo, W and Xu, F and Sang, Y and Zhang, D and Zhou, Y and Wang, L and Kang, Z and Yang, Y and Song, C and Liu, Y and Ma, X and Wang, J and Li, C and Ma, S and Zhao, L and Qin, Z and Xing, G and Zhao, Q and Li, J and Song, S and Zhao, D and Huang, T and Wang, Q and Zhao, Y and Qin, G},
title = {Canagliflozin Alleviates Diabetic Glomerular Endothelial Injury via Melibiose in a Microbiota-Dependent Manner.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e17222},
doi = {10.1002/advs.202517222},
pmid = {42199152},
issn = {2198-3844},
support = {82170839//National Natural Science Foundation of China/ ; U23A20414//National Natural Science Foundation of China/ ; 82470876//National Natural Science Foundation of China/ ; 82300930//National Natural Science Foundation of China/ ; 251111311500//Key Research and Development Program of Henan Province/ ; 242300421272//Natural Science Foundation of Henan Province/ ; LHGJ20230200//Henan Joint Construction Program/ ; SBGJ202301006//Science and Technology Research Project of Henan Province/ ; },
abstract = {Canagliflozin reduces albuminuria in patients with diabetic kidney disease (DKD) beyond its glucose-lowering effect, but the mechanisms remain unclear. We analyzed 85 patients treated with canagliflozin and 85 controls over 26 weeks to explore whether the gut microbiome and its metabolites contribute to renoprotection. Canagliflozin remodeled the gut microbiota, notably enriching Roseburia intestinalis and increasing plasma melibiose levels. In mice, canagliflozin alleviated glomerular endothelial injury and albuminuria. Similar effects were replicated by fecal microbiota transplantation, Roseburia intestinalis, or melibiose administration. Mechanistically, melibiose bound to and activated glyoxalase 1, reduced methylglyoxal, and suppressed the AGE-RAGE pathway, preserving glomerular endothelial integrity. Furthermore, oral melibiose precursor supplementation reduced albuminuria in patients with early-stage DKD. These findings suggest the involvement of a gut-kidney axis in the renoprotective effects of canagliflozin and indicate that melibiose may serve as a potential therapeutic strategy for DKD.},
}

@article {pmid41981603,
year = {2026},
author = {Liu, Y and Chen, C and Liu, H and Wang, W and Zhou, X and Guo, M and Zhao, J and Zeng, Z and Xu, L},
title = {Decoding the gut microbiota-immune dialogue: from bidirectional axis to therapeutic applications.},
journal = {Journal of nanobiotechnology},
volume = {24},
number = {1},
pages = {},
pmid = {41981603},
issn = {1477-3155},
support = {82160503, 82272812//National Natural Science Foundation of China/ ; QKHZC-2020-4Y156, QKH-JC-2018-1428, QKHJC-ZK-2022-624//Project of the Guizhou Provincial Department of Science and Technology/ ; },
abstract = {UNLABELLED: The gut microbiota (GM), a highly complex micro-ecosystem residing within the host’s gastrointestinal tract, works in conjunction with the gut immune system to form a precise bidirectional regulatory network, that maintains symbiotic homeostasis and overall host health. Cumulative evidence has demonstrated that the critical impact of the bidirectional causal relationship between the GM and the gut immune system on host development and the dynamic progression of disease. However, many challenges remain in this research field, including the mechanism complexity, therapeutic effect differences due to individual heterogeneity, long-term safety, and clinical transformation bottlenecks) that need to be urgently broken through. Therefore, the in-depth analysis of these issues is of great theoretical and practical significance for clarifying the intrinsic connection between the GM and gut immunity, particularly in elucidating the pathogenesis of related clinical diseases such as inflammatory bowel disease (IBD), tumors, and autoimmune diseases (AD). We systematically outline the interaction mechanisms between the microbiota and the immune system, including compositional structure (microbiota diversity and immune system composition), development and maturation processes (early microbiota colonization and immune system establishment), and functional regulation (immune cell differentiation and maintenance of mucosal barrier integrity), as well as their associations with clinical diseases. Finally, we discuss some key considerations for the developing of innovative treatment strategies, such as microbial-targeted interventions, fecal microbiota transplantation (FMT), and synergistic use of immunomodulatory drugs, with the aim of providing a new paradigm for the precise intervention of related diseases.

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

@article {pmid42183271,
year = {2026},
author = {Zhang, H and Zhang, K and Liu, J and Luo, H},
title = {Multidimensional exploration of the relationship between gut microbiota and colorectal cancer: focus on clinical tumorigenesis and treatment.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1807247},
pmid = {42183271},
issn = {1664-3224},
mesh = {Humans ; *Colorectal Neoplasms/therapy/microbiology/etiology/immunology/metabolism/pathology ; *Gastrointestinal Microbiome/immunology ; Animals ; Dysbiosis ; *Carcinogenesis ; Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; Prebiotics ; },
abstract = {The gut microbiota has received considerable attention in the field of colorectal cancer (CRC) research in recent years. In this review, we have explored the multifaceted relationship between the gut microbiota and CRC progression and treatment. The composition, distribution, and normal physiological functions of the gut microbiota have been summarized, along with the association between gut dysbiosis and CRC based on the body of evidence from animal experiments and clinical studies. In addition, we have discussed the mechanisms through which specific microbial configurations or microbiota-derived metabolites may contribute to colorectal carcinogenesis, including genotoxic effects, inflammation, and immune dysregulation. The impact of the gut microbiota on the efficacy of chemotherapy, radiotherapy, and immunotherapy, and new treatment strategies based on the gut microbiota, such as probiotic intervention, prebiotic application, and fecal microbiota transplantation have also been explored. Despite some promising outcomes, the specific carcinogenic microorganisms have not been identified, and it is challenging to distinguish association from causation, determine the influence of individual differences, and translate the research to clinical applications. In the future, more rigorous longitudinal studies, gnotobiotic models with defined microbial communities, and mechanistic interventional studies are needed to strengthen causal inference, and provide practical guidance for CRC prevention and treatment. Beyond summarizing reported associations, this review proposes a microbiota-immune-metabolism-therapy axis by integrating tumorigenic mechanisms, immune contexture, and treatment responsiveness into a single translational framework.},
}

Humans
*Colorectal Neoplasms/therapy/microbiology/etiology/immunology/metabolism/pathology
*Gastrointestinal Microbiome/immunology
Animals
Dysbiosis
*Carcinogenesis
Fecal Microbiota Transplantation
Probiotics/therapeutic use
Prebiotics

@article {pmid42184295,
year = {2026},
author = {Wong, SH},
title = {The human microbiome at translational crossroads: an ecological and causal perspective.},
journal = {Singapore medical journal},
volume = {67},
number = {5},
pages = {279-287},
pmid = {42184295},
issn = {2737-5935},
mesh = {Humans ; *Translational Research, Biomedical ; Probiotics/therapeutic use ; *Microbiota ; Fecal Microbiota Transplantation ; *Gastrointestinal Microbiome ; Ecology ; },
abstract = {The human microbiome has emerged as a central focus of biomedical research, driven by interest in its translational potential for chronic diseases. Although compelling associations link microbial alterations to gastrointestinal, metabolic, neuropsychiatric and systemic conditions, successful clinical translation remains limited. This perspective contends that the principal barrier is not biological relevance but the application of reductionist thinking to an inherently complex ecological system, compounded by an incomplete understanding of causality. This review examines the gradient of causal confidence across gut-organ axes, from established roles in digestive disorders to less established distal associations, as well as highlights the epistemological challenges underlying microbiome research. A critical appraisal of current strategies, including probiotics, live biotherapeutics and faecal microbiota transplantation, suggests that progress requires ecological reasoning, causal rigour and systems-level integration. Moving from association to intervention demands approaches that account for host-microbiome complexity rather than oversimplified microbial targeting.},
}

Humans
*Translational Research, Biomedical
Probiotics/therapeutic use
*Microbiota
Fecal Microbiota Transplantation
*Gastrointestinal Microbiome
Ecology

@article {pmid42184718,
year = {2026},
author = {El-Sehrawy, AAMA and Soleimani Samarkhazan, H},
title = {The silent pharmacist: Harnessing the gut microbiome to improve therapy in hematologic malignancies.},
journal = {Translational oncology},
volume = {70},
number = {},
pages = {102833},
doi = {10.1016/j.tranon.2026.102833},
pmid = {42184718},
issn = {1936-5233},
abstract = {The gut microbiome, a complex ecosystem of microorganisms, is now recognized as a key determinant of drug efficacy and toxicity, giving rise to the field of pharmacomicrobiomics. This review decodes the profound influence of the gut microbiome on treatment outcomes for hematologic malignancies. We explore the tripartite mechanistic pathways through which gut microbes act: the direct enzymatic biotransformation of chemotherapeutic agents, the indirect immunomodulation of systemic and anti-tumor responses, and the preservation of mucosal barrier integrity to prevent devastating complications like graft-versus-host disease (GVHD). The manuscript details how the microbiome interacts with specific drug classes, from conventional chemotherapies like cyclophosphamide to cutting-edge immunotherapies like immune checkpoint inhibitors and CAR-T cells, shaping their clinical success. Furthermore, we discuss the translational potential of targeting this "silent pharmacist" through fecal microbiota transplantation, next-generation probiotics, and dietary interventions. Finally, we highlight the main translational opportunities, current limitations, and future clinical priorities for integrating microbiome science into hematology, paving the way for more personalized and improved cancer care.},
}

@article {pmid41850660,
year = {2026},
author = {Baca, A and Félix, J and Díaz-Del Cerro, E and Yépez-Notario, C and Requena, T and Martínez de Toda, I and De la Fuente, M},
title = {Gut microbiota transfer from old mice accelerates aging in adults.},
journal = {Mechanisms of ageing and development},
volume = {231},
number = {},
pages = {112177},
doi = {10.1016/j.mad.2026.112177},
pmid = {41850660},
issn = {1872-6216},
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; Mice ; *Aging/physiology ; Female ; *Longevity ; Oxidative Stress ; Feces/microbiology ; *Fecal Microbiota Transplantation ; Behavior, Animal ; },
abstract = {The gut microbiota communicates with the homeostatic systems (nervous, immune, and endocrine). As we age, there is an increase in oxidative stress, which can deteriorate these systems, the microbiota, and the communication between them. It has been suggested that the microbiota influence the aging process, though its specific effects remain unclear. This study aimed to assess the impact of transferring microbiota from old to adult mice on behavioral, immune, and redox parameters, as well as their rate of aging and longevity. Adult female mice were divided into three groups (N = 10/group): old microbiota (received 200 μL of old mice feces resuspended in PBS/3 days week/2 weeks, after a previous intestinal lavage with polyethylene glycol), adult microbiota (received adult mouse feces following the same procedure), and control (no manipulation). Feces were collected after treatment for microbiota and short-chain fatty acid analyses. After microbiota transfer, behavioral tests were performed, and peritoneal leukocytes were extracted to analyze immune and redox parameters, and to quantify biological age. These parameters were re-evaluated in old age, and the animals' longevity was recorded. The results showed that old microbiota group was characterized by the increase of Akkermansia, Anaerostipes, Dubosiella, and Ruminococcus, among others. In addition, the group displayed elevated levels of anxiety, impaired immune function, and increased oxidative-inflammatory stress, effects that continued into old age. These changes translated into higher biological age and lower longevity. In conclusion, microbiota transfer from old to adult mice disrupts neuroimmune homeostasis, increases oxidative-inflammatory stress and accelerates aging process, reducing longevity.},
}

Animals
*Gastrointestinal Microbiome/physiology
Mice
*Aging/physiology
Female
*Longevity
Oxidative Stress
Feces/microbiology
*Fecal Microbiota Transplantation
Behavior, Animal

@article {pmid42174754,
year = {2026},
author = {Chen, Y and Zhao, J and Zhao, J and Chen, Q and Dong, S and Jia, S and Zhao, Y and Hao, D and Yin, Y and Lin, S and Chen, Y and Zhuang, Y and Peng, H},
title = {Effects of fecal microbiota transplantation and probiotics on the gut microbiome in antibiotic-treated septic patients: A pilot randomized controlled trial.},
journal = {Virulence},
volume = {17},
number = {1},
pages = {2668764},
doi = {10.1080/21505594.2026.2668764},
pmid = {42174754},
issn = {2150-5608},
mesh = {Humans ; *Gastrointestinal Microbiome/drug effects ; *Probiotics/administration & dosage/therapeutic use ; *Fecal Microbiota Transplantation ; Pilot Projects ; Male ; Middle Aged ; Female ; *Sepsis/therapy/microbiology/drug therapy ; *Anti-Bacterial Agents/therapeutic use/adverse effects ; Aged ; Prospective Studies ; Critical Illness ; Dysbiosis/therapy ; Treatment Outcome ; Feces/microbiology ; Adult ; RNA, Ribosomal, 16S/genetics ; },
abstract = {Broad-spectrum antibiotics, essential for sepsis management in critically ill patients, cause significant gut dysbiosis. Restoring gut microbiota may improve outcomes, but the efficacy of interventions like fecal microbiota transplantation (FMT) and probiotics in this setting remains underexplored. This study aims to evaluate the feasibility and potential efficacy of FMT versus probiotics on gut microbiome restoration and inflammatory markers in critically ill, antibiotic-treated sepsis patients. In this single-center, prospective, exploratory pilot RCT, 40 sepsis patients were were randomized 2:1:1 to: Control (n = 20, antibiotics treatment), Probiotics (n = 10, antibiotics treatment combined one week of probiotics), and FMT (n = 10, antibiotics treatment combined one week of FMT) groups. Gut microbiota composition was analyzed using 16S rDNA sequencing, and clinical inflammatory markers were assessed at baseline, one week, and two weeks post-treatment. FMT significantly mitigated antibiotic-induced reductions in microbial diversity. At 2 weeks, the FMT group exhibited higher alpha-diversity (Chao1 index, p = 0.0125; Shannon/Simpson trends p = 0.06) compared to Control and Probiotics groups. FMT increased beneficial Bacteroides abundance and reduced Enterobacteriaceae. BugBase analysis revealed FMT significantly lowered pathogenic potential of gut microbiota (p = 0.021). Donor-recipient analysis showed FMT shifted recipient microbiomes toward donor enterotype. This study provides preliminary evidence that FMT, but not the probiotic regimen, effectively restores gut microbiome diversity and composition, reduces pathogenic potential, and may improve clinical outcomes in critically ill sepsis patients after broad-spectrum antibiotics. This study was registered on ClinicalTrials.gov (NCT05578196).},
}

Humans
*Gastrointestinal Microbiome/drug effects
*Probiotics/administration & dosage/therapeutic use
*Fecal Microbiota Transplantation
Pilot Projects
Male
Middle Aged
Female
*Sepsis/therapy/microbiology/drug therapy
*Anti-Bacterial Agents/therapeutic use/adverse effects
Aged
Prospective Studies
Critical Illness
Dysbiosis/therapy
Treatment Outcome
Feces/microbiology
Adult
RNA, Ribosomal, 16S/genetics

@article {pmid42177552,
year = {2026},
author = {Zou, F and Wu, Z and Wang, S and Xu, M and Xia, P and Hu, Y and Fang, T and Hu, P and Huang, C and Deng, F},
title = {Microbiota-derived butyrate inhibits colonic epithelial pyroptosis and mitigates DSS-induced colitis via interacting with aryl hydrocarbon receptor.},
journal = {Journal of translational medicine},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12967-026-08264-1},
pmid = {42177552},
issn = {1479-5876},
support = {82470586//National Natural Science Foundation of China/ ; },
abstract = {BACKGROUND: Intestinal barrier defects cause antigen translocation and immune dysregulation. The pyroptosis of colonic epithelial cells (CECs) disrupts the colonic barrier, and its inhibition might be a therapeutic approach for ulcerative colitis (UC), but the mechanisms are not fully understood.

METHODS: A DSS-induced UC model was established to assess the level of colonic epithelial cell pyroptosis. 16S rDNA sequencing and LC‒MS/MS were applied to screen potential candidate bacterial species and metabolites. The roles of target metabolites were evaluated in vivo using GSDMD-knockout mice. FHC cells treated with LPS + ATP were used as a cellular model of pyroptosis, and the underlying molecular mechanism was explored mainly by siRNA transfection and lentivirus infection.

RESULTS: We found that DSS-treated mice exhibited increased levels of pyroptosis in the colon. Fecal microbiota transplantation (FMT) significantly suppressed mucosal inflammation and CEC pyroptosis, accompanied by increased levels of butyrate-producing bacteria and butyrate in feces. Butyrate treatment alleviated DSS-induced colitis in mice. Moreover, GSDMD knockout mitigated DSS-induced colitis in mice, whereas a butyrate intervention failed to further ameliorate colitis in GSDMD-knockout mice. Mechanistically, we found that butyrate significantly inhibited LPS + ATP-induced pyroptosis by activating its receptor, aryl hydrocarbon receptor (AhR), in FHC cells, while silencing AhR suppressed this effect. The overexpression of cGAS in FHC increased the level of pyroptosis, whereas the administration of butyrate inhibited the activation of the cGAS-STING pathway. Treatment with a cGAS inhibitor significantly reversed the increase in pyroptosis caused by AhR knockdown in pyroptotic FHC cells.

CONCLUSIONS: Gut microbiota-derived butyrate levels were increased after FMT. Butyrate suppressed the proinflammatory cGAS-STING-NF-κB signaling axis via AhR to inhibit CEC pyroptosis and thereby alleviate UC.},
}

@article {pmid42177905,
year = {2026},
author = {Liu, T and Wang, H and Lu, D and Yan, C and Hang, F and Ma, B and Meng, X},
title = {Emodin inhibits the formation of gallstones by affecting the intestinal flora and expression of hepatic HIF1α.},
journal = {International immunopharmacology},
volume = {183},
number = {},
pages = {116878},
doi = {10.1016/j.intimp.2026.116878},
pmid = {42177905},
issn = {1878-1705},
abstract = {BACKGROUND: Gallstone disease is a prevalent digestive disorder worldwide; however, current therapeutic approaches remain limited. Emodin, a natural anthraquinone compound, exerts diverse biological effects including anti-inflammatory activity and metabolic regulation. To elucidate the mechanism by which emodin inhibits gallstone formation, we conducted in vivo experiments, multi-omics analysis, and network pharmacology.

METHODS: Six-week-old C57BL/6 mice were used to establish an in vivo model with emodin intervention. Fecal microbiota transplantation (FMT), 16S rRNA gene sequencing, and serum metabolomics sequencing were employed to investigate the effects of emodin on gut microbiota and serum metabolites. Network pharmacology was applied to predict the regulatory effects of emodin on liver-related genes, which were further verified by fundamental experiments. The correlations between gut microbiota, serum metabolites, and liver genes were explored. Statistical analysis was performed using GraphPad Prism 9.0.

RESULTS: The medium dose of emodin (30 mg/kg) showed the optimal inhibitory effect on gallstones formation. Emodin reshaped the intestinal flora structure in mice with gallstones and increased the abundance of Limosilactobacillus reuteri (L. reuteri) in vivo. By elevating serum tauroursodeoxycholic acid (TUDCA) levels in mice, emodin downregulated the expression of hepatic HIF1α and upregulated the expression of AQP8.

CONCLUSIONS: Emodin inhibited gallstone formation in mice through two complementary mechanisms. First, emodin modulated the gut microbiota to promote the proliferation of L. reuteri; second, it increased serum TUDCA levels, thereby regulating the HIF1α-AQP8 pathway to alleviate cholestasis. In addition, we speculate that L. reuteri may elevate serum TUDCA content via several indirect pathways.},
}

@article {pmid42178721,
year = {2026},
author = {Schulze, K and Goldschmidt, I and Melk, A and Boehne, M and Woltemate, S and Ballmaier, M and Kleiner, S and Lehmann, E and Kramer, M and Vital, M},
title = {Altered SIgA-targeting of gut microbiota is associated with long-term dysbiosis in pediatric solid organ transplant recipients.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2675078},
doi = {10.1080/19490976.2026.2675078},
pmid = {42178721},
issn = {1949-0984},
mesh = {Humans ; *Dysbiosis/microbiology/immunology/etiology ; *Gastrointestinal Microbiome ; Child ; Male ; Female ; *Immunoglobulin A, Secretory/immunology/genetics ; *Transplant Recipients ; Tacrolimus/adverse effects ; Bacteria/classification/genetics/isolation & purification ; Adolescent ; Immunosuppressive Agents/adverse effects/therapeutic use ; *Organ Transplantation/adverse effects ; Feces/microbiology ; Child, Preschool ; Liver Transplantation/adverse effects ; },
abstract = {The composition of the gut microbiota (GM) is altered in solid organ transplantation (SOT) recipients, where the degree of dysbiosis is associated with long-term survival and is believed to be influenced by immunosuppression therapy. At the interface stands secretory (S)IgA, however, little is known about its role in governing dysbiosis in the context of SOT. We performed quantitative metagenomic analyses of the GM accompanied by SIgA sequencing in 48 pediatric SOT recipients (age = 10.6 ± 4.7 y) receiving either heart (n = 11), kidney (n = 10) or liver transplantation (n = 27), and compared the results to age-matched healthy controls (HC, n = 16). We confirmed compositional and functional dysbiosis in SOT recipients, with the degree of dysbiosis being associated with tacrolimus (TAC) levels. Overall, SOT recipients exhibited higher SIgA levels than HC, along with an increased percentage of bacteria targeted and altered target spectra. Furthermore, altered SIgA responses were associated with the degree of dysbiosis. A mechanistic model connecting immunosuppression, GM composition and SIgA-targeting is proposed, suggesting that GM dysbiosis in SOT recipients is mediated by the immune system through the SIgA response; direct drug-mediated effects on fecal communities were not observed in in vitro experiments. Our study provides new insights into factors that contribute to persisting dysbiosis in SOT recipients.},
}

Humans
*Dysbiosis/microbiology/immunology/etiology
*Gastrointestinal Microbiome
Child
Male
Female
*Immunoglobulin A, Secretory/immunology/genetics
*Transplant Recipients
Tacrolimus/adverse effects
Bacteria/classification/genetics/isolation & purification
Adolescent
Immunosuppressive Agents/adverse effects/therapeutic use
*Organ Transplantation/adverse effects
Feces/microbiology
Child, Preschool
Liver Transplantation/adverse effects

@article {pmid42178957,
year = {2026},
author = {Ciesielski, P and Zaniewska, M and Waliszewski, M and Dziewa, N and Kołodziejczak, M},
title = {Treatment for full-thickness rectal prolapse using the abdominal access: An evaluation of 94 cases.},
journal = {Polski przeglad chirurgiczny},
volume = {98},
number = {2},
pages = {8-12},
doi = {10.5604/01.3001.0055.5841},
pmid = {42178957},
issn = {2299-2847},
mesh = {Humans ; *Rectal Prolapse/surgery ; Female ; Middle Aged ; Male ; Treatment Outcome ; Prospective Studies ; Adult ; Aged ; *Digestive System Surgical Procedures/methods ; Surgical Mesh ; },
abstract = {Introduction: Full-thickness rectal prolapse (FTRP) is a multifactorial disease that can be treated with different surgicaltechniques. There is still no standard surgical procedure, and the selection of the surgical technique is based on the individualassessment and the experience of the surgeon. The benefits to patients should focus on repair of bowel prolapse, reduction ofconstipation, and an improvement in pelvic floor muscle insufficiency.Aim: Aim of this study was to evaluate clinical and functional outcomes after abdominal surgery for FTRP in a prospective single- -center observational study.Materials and methods: Between 2016 and 2022, a total of 94 consecutive patients (46.2 18.2 years) underwent abdominal surgery due to FTRP using an abdominal approach. They were operated on with ventral mesh rectopexy (VMR) (55 pts.) or resection and suture rectopexy - Frykman-Goldberg procedure (FG) (39 pts.). Before and after the surgery, clinical and functional outcomes were measured. The follow-up period ranged from 1 to 6 years (mean: 26 months).Results: At last follow-up, constipation occurred in 27.6% of VMR and 31.3% of FG patients (p = 0.754; calculated among patients with available postoperative constipation status). The Wexner incontinence score was significantly better in the VMR group (1.0 2.1 vs. 3.6 5.0, p = 0.009). There were no differences in the EQ5D indices between the groups (1.7 2.0 vs. 2.4 2.8, p = 0.257).Conclusions: Both surgical procedures revealed comparable rates of recurrence and complications. While QoL was similarbetween groups, VMR yielded a significantly greater improvement in the Wexner incontinence score.},
}

Humans
*Rectal Prolapse/surgery
Female
Middle Aged
Male
Treatment Outcome
Prospective Studies
Adult
Aged
*Digestive System Surgical Procedures/methods
Surgical Mesh

@article {pmid42180552,
year = {2026},
author = {Chen, Y and Wei, X and Yi, X and Jiang, DS},
title = {Interactions between the gut microbiome and ferroptosis in degenerative diseases: Novel mechanisms and potential therapeutic strategies.},
journal = {Acta pharmaceutica Sinica. B},
volume = {16},
number = {5},
pages = {2711-2729},
pmid = {42180552},
issn = {2211-3835},
abstract = {Degenerative diseases are a group of medical conditions characterized by the progressive and irreversible deterioration of cells, tissues, and organs over time. Emerging evidence highlights the alteration and functions of the gut microbiome in the development of degenerative diseases. Ferroptosis, a regulated form of cell death characterized by iron-dependent lipid peroxidation, has been implicated as a pivotal factor in the regulatory effect of the gut microbiome on degenerative diseases. Moreover, gut metabolites, particularly short-chain fatty acids and trimethylamine N-oxide, are closely related to iron overload, redox imbalance, and lipid peroxidation. Recently, microbiome-based therapies, such as fecal microbiota transplantation, have been considered novel therapeutic strategies. In this review, we focus on degenerative diseases and explore the interactions between the gut microbiome and ferroptosis, aiming to provide new insights into the underlying mechanisms and clinical implications.},
}

@article {pmid42181429,
year = {2026},
author = {Lopez Garri, S and Lingier, P and Dassonville, M and Tulelli, B},
title = {Long-Term Quality of Life and Functional Outcomes in Patients With Anorectal Malformations: A Retrospective Multicenter Study in Brussels, Belgium.},
journal = {Cureus},
volume = {18},
number = {4},
pages = {e107561},
pmid = {42181429},
issn = {2168-8184},
abstract = {Introduction Anorectal malformations (ARMs) are congenital conditions requiring surgical correction. Despite surgical intervention, patients often experience persistent fecal and urinary dysfunction, significantly impacting their quality of life (QoL). This multicenter retrospective study aimed to assess QoL in ARM patients, identify factors influencing QoL deterioration, and propose improved management strategies. Methods We retrospectively analyzed data from 39 ARM patients who underwent surgery between 1999 and 2019 at two Belgian hospitals. Patients completed the Hirschsprung's Disease Anorectal Malformation Quality of Life Questionnaire (HAQL). We also reviewed their medical records. Descriptive statistical analysis was performed. Results At a median follow-up of 106 months, functional outcomes showed high rates of constipation (87%), fecal incontinence (54%), and fecal soiling (87%). Fecal incontinence was more prevalent in patients with bulbar rectourethral and recto-vesical fistulas. Postoperative complications occurred in 72% of patients, primarily in those with high ARMs, and correlated with increased constipation and abdominal pain. Management gaps were observed: only 47% of constipated patients and 56% of incontinent patients underwent anorectal manometry, and only 50% of constipated patients utilized physiotherapy. QoL assessment revealed persistent digestive functional disorders and physical symptoms across age groups, which improved with age. However, emotional and body image issues persisted into adulthood. Conclusion Patients with ARMs frequently experience significant functional digestive disorders and impaired QoL. Suboptimal management, particularly regarding the use of anorectal manometry and physiotherapy, contributes to these challenges. A long-term, multidisciplinary follow-up is crucial. This follow-up should include systematic dietary support, perineal rehabilitation, and targeted interventions guided by anorectal manometry to improve QoL in this population.},
}

@article {pmid42181890,
year = {2026},
author = {Gamal, NK and Fakhry, R and Hatem, Y and Rashed, E and Marzouk, R and Bukr, AKM and Akawi, N and George, MY},
title = {Neurodegeneration at the crossroads: the gut-brain axis and blood-brain barrier in Parkinson's disease - a review.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1813134},
pmid = {42181890},
issn = {1663-9812},
abstract = {Parkinson's disease (PD), which is one of the most common neurodegenerative illnesses, involves abnormal deposition of α-Synuclein and loss of dopaminergic neurons in the substantia nigra. Beyond this, there is increasing evidence that the gut-brain axis (GBA) and blood-brain barrier (BBB) interfere in disease initiation and progression. Dysbiosis of the gut microbiota affects the intestine and the BBB, allowing microbial metabolites and proinflammatory mediators to enter the CNS, causing neuroinflammation and neurodegeneration. Studies show that α-Synuclein pathology can originate in the gut and reach the brain via the vagus nerve. This review summarizes the connections among GBA, BBB, and PD, focusing on oxidative damage, inflammatory cascades, decreased expression of tight junction proteins, and signaling pathways such as TLR4/MyD88/NF-κB. In addition, we discuss therapeutic strategies that target the microbiota-BBB axis, such as probiotics, fecal microbiota transplantation, natural compounds (e.g., piperine, anethole, polymannuronic acid, Paeonia lactiflora), and stem cell therapy, which have demonstrated neuroprotective potential in animal models. Overall, the literature emphasizes the importance of restoring gut homeostasis and BBB integrity, and suggests that getting this axis right may offer novel opportunities for PD treatment. Future research is crucial to validate the efficacy of this approach clinically and to develop tailored therapies to prevent or delay PD progression.},
}

@article {pmid42182017,
year = {2026},
author = {Li, J and Qiu, X},
title = {Neurodevelopmental disorders and the gut microbiome: insights into ADHD and tic disorders.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1779746},
pmid = {42182017},
issn = {1664-302X},
abstract = {This review examines the relationship between tic disorders (TD), attention deficit hyperactivity disorder (ADHD), and the gut microbiota within the framework of the gut-brain axis. We summarize current evidence on the clinical characteristics and neurobiological features of TD and ADHD, and discuss how genetic susceptibility, environmental exposures, and dietary factors may interact with gut microbial composition. We further review studies comparing the gut microbiota of affected individuals and healthy controls, with attention to recurrent taxa-level findings, functional hypotheses, and emerging microbiome-targeted interventions such as probiotics and fecal microbiota transplantation. Importantly, most available human studies remain associative rather than mechanistic, and cross-study comparability is limited by heterogeneity in sequencing approaches, cohort characteristics, medication exposure, and dietary control. Overall, current findings support the gut microbiota as a relevant component of neurodevelopmental disorders such as ADHD and TD, while highlighting the need for larger longitudinal and mechanistic studies to clarify causality and therapeutic potential.},
}

@article {pmid42182071,
year = {2026},
author = {Qin, R and Yu, P and Wang, H and Zhou, J and Gong, R and Duan, Y and Jia, H and Xie, M and Zhou, Y and Hu, J},
title = {Gut-bone axis crosstalk: Microbiota-driven immune-metabolic-neural networks in bone disorders and precision interventions.},
journal = {Journal of orthopaedic translation},
volume = {58},
number = {},
pages = {101126},
pmid = {42182071},
issn = {2214-031X},
abstract = {UNLABELLED: The gut microbiota regulates bone metabolism via a complex gut-bone axis involving short-chain fatty acids (SCFAs), immune modulation, and neuroendocrine signals. However, the precise mechanisms remain unclear, and microbiota-targeted interventions (probiotics, prebiotics, fecal microbiota transplantation) are not yet optimized for clinical use. This review systematically synthesizes the immune-metabolic-neural interaction network within the gut-bone axis, highlighting non-linear crosstalk among SCFAs, bile acids, tryptophan derivatives, immune cells (macrophages, Treg/Th17), and vagus nerve signaling. We critically assess translational hurdles, including heterogeneous study designs, confounding factors, and lack of causal evidence. Based on this network perspective, we propose a framework for future research that prioritizes multi-omics approaches, stratified interventions, and rigorous trials. This synthesis advances understanding of how gut dysbiosis drives bone disorders and paves the way for precision skeletal medicine.

This review identifies microbial markers for risk stratification of bone metabolic disorders and discusses SCFA-based strategies and fecal microbiota transplantation (FMT) in conditions including osteoporosis, impaired fracture healing, rheumatoid arthritis, and glucocorticoid-associated osteonecrosis. It provides testable hypotheses for large-scale randomized controlled trials (RCTs), directly supporting translation of microbiome research into clinical practice for bone disorders.},
}

@article {pmid42182110,
year = {2026},
author = {Zhang, Z and Holton, M and Ferrer, DM and Tripp, AD and Richter, A and Dixit, PD and Urtecho, G},
title = {Metagenome-scale Modeling to Assess Microbiome Metabolic Complementarity for Precision Microbiota Transplantation Therapies.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.05.15.725570},
pmid = {42182110},
issn = {2692-8205},
abstract = {Fecal microbiota transplantation (FMT) holds therapeutic promise beyond recurrent Clostridioides difficile infection, but clinical outcomes remain unpredictable, in part because existing computational models do not fully capture the metabolic compatibility between donor and recipient communities. Here, we present a metagenome-scale metabolic modeling framework that quantifies metabolic niche complementarity between donor and recipient microbiomes to predict transplantation outcomes. Using MICOM-derived community metabolic models, we show that donor taxa whose metabolic flux profiles are more dissimilar from the recipient community engraft at significantly higher rates in both murine and human FMT cohorts. In a human IBS trial, metabolic models accurately predicted post-FMT community composition via leave-one-out cross-validation and recapitulated disease-associated alterations in short-chain fatty acid, sulfur, and gas metabolism. We then performed 2,548 in silico FMT simulations between IBS-D/M patients and donors from the OpenBiome biobank to demonstrate a platform for personalized donor screening. This screen identified super-donors characterized by high taxonomic diversity, broad metabolic niche coverage, and community interaction networks dominated by cross-feeding rather than competition, as quantified by a flux-derived ecological network balance index that strongly predicted engraftment potential. This framework provides a mechanistic, scalable tool for rational donor-recipient matching that could guide personalized microbiome-based therapies.},
}

@article {pmid42183070,
year = {2026},
author = {Dou, M and Xu, J and Ye, X and Liu, J and Shi, L},
title = {Fecal Microbiota Transplantation From Healthy Donors Reduces Glycemic Variability in Streptozotocin-Induced Diabetic Rats via Enhanced Hepatic Glycogen Synthesis.},
journal = {International journal of endocrinology},
volume = {2026},
number = {},
pages = {8852077},
pmid = {42183070},
issn = {1687-8337},
abstract = {BACKGROUND: Blood glucose fluctuations in patients with brittle diabetes have been a problem for clinicians. A recent study found that transplanting the intestinal flora of healthy people to patients with brittle diabetes can improve their blood glucose fluctuations. However, the underlying mechanism remains unclear.

METHODS: Streptozotocin-induced diabetic rats were assigned to receive fecal microbiota transplantation (FMT) from healthy donors or to remain untreated, while normal rats received FMT from brittle diabetes donors or remained untreated. Groups included the normal control group (NC group), the diabetic group (DM group), normal rats with FMT from brittle diabetic patients (NC-DMFMT group), and diabetic rats with FMT from normal individuals (DM-NCFMT group). Blood glucose variability, rat liver glucokinase, and glycogen levels, as well as intestinal short-chain fatty acid content, were detected in each group of rats. Gut microbiota composition was analyzed using 16S rDNA sequencing.

RESULTS: Compared with the standard deviation of blood glucose (SDBG) (1.664 ± 0.427 mmol/L) in the NC group, that of the DM group (6.879 ± 1.475 mmol/L) was higher. However, the DM-NCFMT group reduced SDBG (4.387 ± 0.619 mmol/L) vs. the DM group (p < 0.05). Hepatic glycogen (27.57 ± 5.254 mg/L) was lower in the DM group than in the NC group (55.48 ± 9.467 mg/L) but increased in the DM-NCFMT group (37.59 ± 1.283 mg/L) vs. the DM group. The abundance of Bifidobacteria in the DM group was decreased compared to that in the NC group. In contrast, Bifidobacterium abundance in the DM-NCFMT group increased after standard human flora transplants (p < 0.05). Correlation and stepwise regression analysis indicated that Bifidobacteria reduced SDBG partly by promoting hepatic glycogen synthesis, with an effect share of 23.01%.

CONCLUSION: Normal individual fecal microbiota transplantation improves glucose variability in DM rats, potentially mediated by enhanced hepatic glycogen synthesis.},
}

@article {pmid42173875,
year = {2026},
author = {Nie, X and Li, Q and Tao, Z and Xu, Y and Li, B and Xie, J and Nie, S},
title = {Faecalibacterium prausnitzii-derived extracellular vesicles ameliorate experimental colitis through regulating barrier immunity and gut microbiota.},
journal = {NPJ science of food},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41538-026-00897-2},
pmid = {42173875},
issn = {2396-8370},
support = {SKLF-ZZB-202543//State Key Laboratory of Food Science and Resources, Nanchang University/ ; 20242BAB21031//Natural Science Foundation of Jiangxi/ ; 20232BCD44003//Technological Project of Jiangxi Province/ ; },
abstract = {Ulcerative colitis (UC) is closely linked to intestinal barrier dysfunction and gut dysbiosis. Bacterial extracellular vesicles (bEVs) act as key mediators of bacteria-host crosstalk, with great potential in regulating host health. Recent studies have shown that EVs derived from gut commensal bacteria offer therapeutic advantages in treating UC. Herein, we explored the therapeutic effect of Faecalibacterium prausnitzii-derived EVs (PEVs) in DSS-induced colitis mice. Results showed PEVs significantly improved intestinal barrier damage, restored Th17/Treg balance and alleviated gut dysbiosis. Further fecal microbiota transplantation (FMT) confirmed that feces from PEVs-treated mice transferred beneficial effects to recipient colitis mice. Collectively, our findings indicate that commensal gut microbiota-derived nanovesicles have the potential to serve as candidates for UC treatment.},
}

@article {pmid42173912,
year = {2026},
author = {Huang, Y and Hu, Y and Zhao, Y and Li, Y and Liu, Y and Wang, M and Wang, Q and Hu, H},
title = {Ulcerative colitis-driven gut dysbiosis exacerbates periodontal bone loss through the gut-oral axis /Th17/Treg imbalance.},
journal = {NPJ biofilms and microbiomes},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41522-026-01015-6},
pmid = {42173912},
issn = {2055-5008},
support = {gzwkj2025-445//the Science and Technology Fund of Guizhou Provincial Health Commission(gzwkj2025-445)/ ; QKHJC-MS[2026]895//Guizhou Provincial Science and Technology Programme/ ; 17zy-002//Outstanding Young Talent Project of Zunyi Medical University/ ; HZ[2024]340//the Zunyi Science and Technology Program/ ; },
abstract = {Ulcerative colitis (UC) and periodontitis, both microbial dysbiosis-driven chronic inflammatory disorders, coexist and mutually exacerbate, but the causal mechanisms remain unclear. Using ligature-induced periodontitis plus DSS-colitis mice, we found UC doubles alveolar bone loss, heightens systemic inflammation, oxidative stress, and osteoclastogenesis. 16S rRNA and LC-MS metabolomics showed UC enriches oral pathogens, depletes gut Firmicutes, expands Bacteroides, and correlates with suppressed amino-acid/bile-acid biosynthesis. Fecal microbiota transplantation (FMT) from DSS donors into antibiotic-pretreated periodontitis-prone mice replicated aggravated bone loss, systemic inflammation, gut-barrier leakage, and Th17/Treg imbalance, while healthy-donor FMT protected. GC-MS revealed 35-60% reductions in acetate, propionate, and butyrate; keystone taxa Parabacteroides and Muribaculum inversely correlated with SCFAs and host inflammatory genes. Collectively, UC-driven gut dysbiosis is a transmissible causal factor that simultaneously remodels oral and intestinal biofilms, erodes epithelial barriers, and amplifies osteoclastic bone resorption. SCFAs-producing microbes or supplementation may be potential therapeutics for UC-associated periodontitis patients.},
}

@article {pmid42172084,
year = {2026},
author = {Oliveira, JM and Luxo, C and Matos, AM},
title = {Human Polyomaviruses of Clinical Relevance: Modes of Transmission and Associated Pathologies.},
journal = {Reviews in medical virology},
volume = {36},
number = {3},
pages = {e70166},
doi = {10.1002/rmv.70166},
pmid = {42172084},
issn = {1099-1654},
support = {//Fundação para a Ciência e a Tecnologia/ ; },
mesh = {Humans ; *Polyomavirus Infections/transmission/virology/pathology/diagnosis ; *Polyomavirus/pathogenicity/classification/genetics/physiology/isolation & purification ; Seroepidemiologic Studies ; Clinical Relevance ; },
abstract = {Polyomaviruses are non-enveloped viruses with double-stranded circular DNA genome. Currently, 13 members of the Polyomaviridae family have been classified as human polyomavirus (HPyVs). Despite high seroprevalence values have been reported for the majority of the HPyVs worldwide, the main mode of transmission remains to be elucidated, and simple and common routes, such as faecal-oral and respiratory have been suggested. In general, HPyVs are responsible for asymptomatic primary infection, followed by asymptomatic lifelong persistent infection. In situations of severe immunosuppression, viral reactivation of some HPyVs may occur and result in the development of associated clinical manifestations. JCPyV is the causative agent of Progressive Multifocal Leukoencephalopathy, BKPyV is associated with nephropathy among kidney transplant recipients, MCPyV with Merkel Cell Carcinoma and TSPyV with Trichodysplasia spinulosa. The association of certain HPyVs with severe diseases, in addition to the high seroprevalence of the majority of HPyVs, emphasises the need to address various knowledge gaps that still exists in the natural history of these viruses, including the transmission routes and the pathogenic mechanisms. The present review summarises current information on HPyV transmission routes and associated diseases, including diagnosis and available treatment options, highlighting the need for further studies.},
}

Humans
*Polyomavirus Infections/transmission/virology/pathology/diagnosis
*Polyomavirus/pathogenicity/classification/genetics/physiology/isolation & purification
Seroepidemiologic Studies
Clinical Relevance

@article {pmid42172181,
year = {2026},
author = {Gomes, JV and Ribeiro, SPO and Nascimento, GMCD and Santos, DOD and Paula, DJG and Lima, SCS and Simão, TA},
title = {The human microbiome in cancer: Not just a sidekick anymore.},
journal = {Genetics and molecular biology},
volume = {49Suppl 1},
number = {Suppl 1},
pages = {e20250236},
pmid = {42172181},
issn = {1415-4757},
abstract = {The human microbiome is increasingly recognized as a dynamic element in cancer biology. Studies across breast, prostate, lung, colorectal, and cervical tumors reveal that microbial communities influence carcinogenesis, immune regulation, and treatment outcomes. When the balance of these microorganisms is altered, inflammation becomes chronic, metabolism is disrupted, and signaling pathways such as NF-κB, IL6-STAT3, and β-catenin are activated. Bacterial metabolites and genotoxins, including colibactin and bile acids, may damage DNA and reshape the epigenetic landscape. Distinct microbial profiles have been linked to prognosis and to patient responses to chemotherapy and immunotherapy. The presence of beneficial taxa, such as Akkermansia muciniphila and Ruminococcus, has been associated with improved response to immune checkpoint inhibitors. At the same time, antibiotic-induced depletion of gut microbiome can reduce therapeutic efficacy. Strategies that help restore microbial balance, including probiotics, dietary interventions, and fecal microbiota transplantation, are being explored as complementary therapies. Although methodological differences and contamination remain challenges, the growing body of evidence indicates that the microbiome is a measurable and modifiable component of tumor ecosystems with strong potential for diagnostic, prognostic, and therapeutic applications in precision oncology.},
}

@article {pmid42172659,
year = {2026},
author = {Liu, C and Yin, X and Yuan, X},
title = {Gut microbiota dysbiosis and osteoporosis: pathogenesis and novel intervention strategies.},
journal = {Future microbiology},
volume = {},
number = {},
pages = {1-12},
doi = {10.1080/17460913.2026.2678122},
pmid = {42172659},
issn = {1746-0921},
abstract = {Osteoporosis represents a major global public health challenge, with current pharmacological treatment often limited by substantial side effects. Recent research identifies the gut-bone axis as a key regulatory pathway linking gut microbiota to bone metabolic homeostasis. This review synthesizes findings from PubMed, Web of Science, and Scopus (up to March 2026) to elucidate how gut microbiota dysbiosis drives osteoporosis pathogenesis through interconnected mechanisms: aberrant immune modulation, altered microbial metabolites, impaired nutrient absorption, endocrine disruption, and systemic inflammation stemming from intestinal barrier failure. Consequently, these pathways disrupt the delicate balance of bone remodeling. Based on these insights, we outline novel microbiota-targeted therapeutic strategies, including probiotics, prebiotics, fecal microbiota transplantation, natural bioactive compounds, traditional Chinese medicine, and nanomaterials. These interventions aim to prevent and manage osteoporosis by reshaping the intestinal microecology via multi-target modulation. Future endeavors should prioritize in-depth mechanistic exploration, personalized precision interventions, and enhanced clinical translation to integrate these strategies into comprehensive osteoporosis care frameworks.},
}

@article {pmid42172982,
year = {2026},
author = {Yan, S and Zhang, Y and Fan, Q and Jia, W and Dai, Y and Li, X and Lu, S and Sheng, Y and Sun, S and Lin, R and Tang, Y and Zhao, C},
title = {Evodiamine targets ZO-1 to ameliorate cholestatic liver disease: Intestinal homeostasis as the core mediator of gut-liver axis repair and bile acid metabolism remodeling.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {157},
number = {},
pages = {158288},
doi = {10.1016/j.phymed.2026.158288},
pmid = {42172982},
issn = {1618-095X},
abstract = {BACKGROUND: Cholestatic liver disease (CLD) is a complex and multifactorial chronic disorder that requires a systematic and integrative management. Evodiamine (EVO), a natural alkaloid derived from Evodiae Fructus, has demonstrated significant therapeutic potential in ameliorating digestive diseases. However, the beneficial effects of EVO on CLD and the underlying mechanisms remain poorly understood.

OBJECTIVE: This study aims to elucidate the mechanisms through which EVO modulates the progression of CLD, with a particular focus on the regulation of gut-liver axis homeostasis.

METHODS: The therapeutic efficacy of EVO in bile duct ligation (BDL)- and α-naphthyl isothiocyanate (ANIT)-induced CLD rat models was systematically evaluated. An integrative approach combining network pharmacology with multi-omics analyses (transcriptomic, metagenomic sequencing, targeted bile acid metabolomics) was employed to identify significantly altered molecular networks. Fecal microbiota transplantation (FMT) was conducted to validate the functional role of gut microbiota in the hepato-intestinal protective effects. Direct molecular targets as well as the functional validation were confirmed through molecular docking, pull-down assays, surface plasmon resonance and cellular thermal shift assay.

RESULTS: EVO achieved significant synchronous hepato-intestine protection in both CLD rats: it markedly ameliorated hepatic injury and hepatic fibrosis, downregulated pro-inflammatory cytokine levels, while preserving intestinal barrier integrity and alleviating intestinal inflammation. Mechanistically, EVO exerted these protective effects by directly targeting the tight junction protein ZO-1 and enhancing its expression and stability. Furthermore, EVO restored intestinal microbial homeostasis, corrected dysregulated BA metabolism-specifically normalizing deoxycholic acid (DCA) levels. FMT experiments demonstrated that the synchronous hepato-intestinal beneficial effects of EVO were partially mediated by gut microbiota.

CONCLUSION: EVO exerts a protective effect against CLD by directly targeting ZO-1 to strengthen intestinal barrier function, thereby restoring gut microbial balance and rebalancing BAs metabolism (especially DCA levels) in the gut-liver axis. This study uncovers a novel ZO-1-dependent mechanism of EVO in CLD, highlighting EVO as a promising candidate for the treatment of CLD and providing new insights into gut-liver axis-targeted therapies.},
}

@article {pmid42168337,
year = {2026},
author = {Tao, M and Liu, Y and Guo, H and Gao, S and Wang, Y and Yan, X and Zhu, Y},
title = {The role of the gut microbiota in radiation enteritis: from mechanistic insights to therapeutic applications.},
journal = {Communications biology},
volume = {9},
number = {1},
pages = {},
pmid = {42168337},
issn = {2399-3642},
support = {BK20250559//Natural Science Foundation of Jiangsu Province (Jiangsu Provincial Natural Science Foundation)/ ; 82403008//National Natural Science Foundation of China (National Science Foundation of China)/ ; 2024M762749//China Postdoctoral Science Foundation/ ; },
mesh = {*Gastrointestinal Microbiome/radiation effects ; Humans ; *Enteritis/microbiology/therapy/etiology ; *Radiation Injuries/microbiology/therapy ; Dysbiosis/microbiology ; Animals ; Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; Radiotherapy/adverse effects ; },
abstract = {Radiation enteritis (RE) is a severe adverse reaction after abdominal and pelvic radiotherapy, with a complicated pathogenesis and no effective treatment. Although gut microbiota dysbiosis was reported to play a critical role in RE, related molecular characteristics and intervention strategies have not been extensively summarized. In this review, the mechanisms of RE, including injury to intestinal stem cells, damage to the vascular endothelium, reshaped immune microenvironment, and mucosal barrier dysfunction, are discussed. In addition, radiation-induced gut microbiota dysbiosis is characterized by decreased abundance of beneficial bacteria such as Faecalibacterium prausnitzii and Bifidobacterium bifidum, and increased abundance of detrimental bacteria such as Escherichia-Shigella and Enterococcus. Beneficial and detrimental bacteria affect the development of RE by regulating inflammatory signaling pathways such as NF-κB and JAK/STAT3, and through their metabolites such as bile acids and short-chain fatty acids. Accordingly, several microbiome-targeted therapeutic strategies, including antibiotic administration, dietary interventions, fecal microbiota transplantation, probiotic administration and engineered bacteria, have been developed to mitigate RE. However, some challenges still remain for these therapeutic strategies. The goal of this review is to highlight the crucial role of gut microbiota dysbiosis in the pathogenesis of RE, thereby accelerating the development of individualized microbial therapies against this disease.},
}

*Gastrointestinal Microbiome/radiation effects
Humans
*Enteritis/microbiology/therapy/etiology
*Radiation Injuries/microbiology/therapy
Dysbiosis/microbiology
Animals
Fecal Microbiota Transplantation
Probiotics/therapeutic use
Radiotherapy/adverse effects

@article {pmid42168694,
year = {2026},
author = {Sahu, P and Satapathy, T},
title = {The Gut-Liver Axis in Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD): Mechanisms, Microbiome Interactions and Therapeutic Targets.},
journal = {Probiotics and antimicrobial proteins},
volume = {},
number = {},
pages = {},
pmid = {42168694},
issn = {1867-1314},
abstract = {Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized as a multifactorial condition in which the gut-liver axis plays a central pathogenic role. While a large body of literature has described associations between gut microbiota alterations and MASLD, a critical synthesis of the mechanistic pathways linking microbial activity to liver injury remains lacking. This review specifically focuses on gut-derived microbial metabolites as key mediators of disease progression. We examine how short-chain fatty acids, bile acids, lipopolysaccharide (LPS), trimethylamine-N-oxide (TMAO) and microbially derived ethanol influence hepatic lipid metabolism, inflammation and fibrogenesis through defined molecular pathways, including FXR signaling, TLR4 activation and immune-metabolic crosstalk. Importantly, we highlight inconsistencies in human microbiome studies, limitations in establishing causality and the challenges in translating preclinical findings into effective therapies. Although microbiome-targeted interventions such as probiotics, bile acid modulators and fecal microbiota transplantation show promise, their clinical efficacy remains variable due to interindividual heterogeneity and lack of mechanistic precision.By integrating current mechanistic evidence with translational insights, this review identifies critical knowledge gaps and proposes future directions for metabolite-focused therapeutic strategies. A more precise understanding of gut-derived signaling pathways will be essential to move from associative microbiome research toward targeted and personalized interventions in MASLD.},
}

@article {pmid42168704,
year = {2026},
author = {Zhang, X and Mallick, H and Rahnavard, A},
title = {Meta-analytic microbiome target discovery for immune checkpoint inhibitor response in advanced melanoma.},
journal = {Communications medicine},
volume = {6},
number = {1},
pages = {},
pmid = {42168704},
issn = {2730-664X},
support = {2109688//National Science Foundation (NSF)/ ; 2109688//National Science Foundation (NSF)/ ; },
abstract = {BACKGROUND: Immune checkpoint inhibitors have transformed melanoma therapy, yet only a subset of patients achieve durable responses. Gut microbes have been linked to response, but reported biomarkers vary across studies. We aim to identify reproducible microbial features and test their generalizability across cohorts and treatment settings.

METHODS: We reprocessed stool metagenomic sequencing data from 15 melanoma cohorts (763 samples from 484 individuals), including 12 cohorts treated with immune checkpoint inhibitors alone and 3 trials combining immune checkpoint inhibitors with fecal microbiota transplantation. Using a unified analysis pipeline, we profiled microbial species, metabolic pathways, and biosynthetic gene clusters, and analyzed their associations with treatment response using Tweedie regression, random-effects meta-analysis, and multimodal integration with leave-one-dataset-out validation.

RESULTS: Here, we show that responders in immune checkpoint inhibitor-only cohorts are enriched for several short-chain fatty acid-producing commensals, whereas non-responders show higher abundance of taxa associated with disrupted gut communities. In fecal microbiota transplantation plus immune checkpoint inhibitor trials, response associates with distinct communities and shifts in amino-acid, nucleotide and cofactor metabolism. Across cohorts, multiview prediction models repeatedly select gene clusters linked to antimicrobial peptides and surface polysaccharides, but cross-study discrimination remains modest.

CONCLUSIONS: Microbiome signatures of response are treatment-context dependent and are not captured by a single universal species. These harmonized findings prioritize microbial taxa and functions for mechanistic studies and future microbiome-informed interventions.},
}

@article {pmid42169007,
year = {2026},
author = {Lu, Y and Rong, X and Wei, L and Yang, J and Zhang, K and Tan, Y and Zhao, N and He, X and Lu, C and Li, L},
title = {Baicalein mitigates epithelial barrier impairment and microbiota dysbiosis in allergic asthmatic mice via the gut‑lung axis.},
journal = {Chinese medicine},
volume = {21},
number = {1},
pages = {},
pmid = {42169007},
issn = {1749-8546},
support = {ZB2025013//The Fundamental Research Funds for the Central public welfare research institutes/ ; CI2023C065YLL//Scientific and technological innovation project of China Academy of Chinese Medical Sciences/ ; 102160222020040009016, 160202001000210007//Scientific Research Facility Special Foundation for Operation and Maintenance/ ; },
abstract = {BACKGROUND: Allergic asthma (AA) may result in repeated episodes of chest constriction and coughing. In its most serious manifestations, it can cause death by asphyxiation. Currently, no efficacious therapeutic interventions exist to avert or counteract these serious outcomes. Baicalein (BAI) is a core quality marker of the traditional Chinese medicine Scutellaria baicalensis, but the mechanism of its oral action remains unclear.

OBJECTIVE: Assess the therapeutic efficacy of BAI in AA mice models and investigate its mechanism of action.

STUDY DESIGN AND METHODS: Evaluate the efficacy of BAI on ovalbumin-induced AA mice. To assess alterations in the pulmonary and gut microbial communities, 16S rRNA sequencing was employed. The integrity and restoration of the lung and intestinal epithelial lining were evaluated via immunohistochemistry. Furthermore, gas chromatography-mass spectrometry quantified fecal levels of short-chain fatty acids (SCFAs) in AA mice, and flow cytometry was used to analyze the content of ILC2 cells in colon tissue. Finally, the role of beneficial bacteria and their metabolites in inhibiting AA was further confirmed through fecal microbiota transplantation (FMT).

RESULTS: Oral BAI effectively alleviated AA-related lung epithelial damage and microbiota dysbiosis, while elevating the production of the tight junction proteins. Moreover, BAI mitigated colonic epithelial damage, inhibited ILC2s activation in the colon, enriched the abundance of gut probiotics capable of producing SCFAs, especially Akkermansia muciniphila (A. muciniphila), and increased the content of SCFAs such as propionic acid in feces. The FMT experiment conducted after gavage with broad-spectrum antibiotics confirmed that BAI mediated reversal of microbial dysbiosis plays a key role in the treatment of AA, significantly increasing the expression of GPR41 mRNA in colon tissue and inhibiting the activation of ILC2s.

CONCLUSION: The potential prebiotic BAI mitigates AA via targeting A. muciniphila and its metabolites, which consequently inhibits epithelial damage and type 2 immune activation.},
}

@article {pmid42171840,
year = {2026},
author = {Yu, Y and Tian, M and Sun, S and Wang, H and Qin, M and Gao, Y and Jia, X and Gao, Q and Jiang, F},
title = {Fecal Microbiota Transplantation from Exercise-Preconditioned Mice Attenuates Post-stroke Cognitive Impairment by Preserving Gut and Blood-Brain Barrier Integrity.},
journal = {Neurochemical research},
volume = {51},
number = {3},
pages = {},
pmid = {42171840},
issn = {1573-6903},
support = {2108085MH252//Natural Science Foundation of Anhui Province/ ; 2023AH040288//Natural Science Research Program for Universities in Anhui Province/ ; 2024byfy004//the Science and Technology Programme of Bengbu Medical University/ ; No. 82070265//National Natural Science Foundation of China/ ; },
mesh = {Animals ; *Blood-Brain Barrier/metabolism ; *Fecal Microbiota Transplantation/methods ; *Physical Conditioning, Animal/physiology ; *Cognitive Dysfunction/therapy/etiology ; *Gastrointestinal Microbiome/physiology ; Male ; Mice ; Mice, Inbred C57BL ; *Stroke/complications ; },
abstract = {Exercise preconditioning reduces post-stroke cognitive impairment (PSCI), but the contribution of the gut microbiota (GM) to barrier protection remains unclear. We examined whether exercise-preconditioned GM contributes to PSCI improvement and preservation of gut and blood-brain barrier (BBB) integrity. Mice were preconditioned with 4 weeks of voluntary wheel running prior to stroke induction. We assessed cognitive function, GM composition, fecal short-chain fatty acid (SCFA) levels, inflammation, and gut-blood-brain barrier (BBB) integrity. Then, we used fecal microbiota transplantation (FMT) to evaluate how GM contributes to the benefits of voluntary exercise. Our results showed that exercise remodeled the GM composition and elevated SCFAs levels. Also, exercise suppressed systemic, colonic, and neuroinflammation, enhanced the barrier-related protein (Occludin, Claudin-5, and ZO-1) levels, maintained barrier integrity, and alleviated cognitive dysfunction after ischemic stroke. FMT from exercised mice partially reproduced the cognitive and anti-inflammatory benefits. SCFA levels were associated with reduced inflammatory markers and increased expression of barrier-related proteins. The findings suggest that exercise preconditioning is associated with coordinated preservation of gut and BBB integrity and improved cognition after stroke. Moreover, FMT from exercised mice conferred partial protection against PSCI.},
}

Animals
*Blood-Brain Barrier/metabolism
*Fecal Microbiota Transplantation/methods
*Physical Conditioning, Animal/physiology
*Cognitive Dysfunction/therapy/etiology
*Gastrointestinal Microbiome/physiology
Male
Mice
Mice, Inbred C57BL
*Stroke/complications

@article {pmid42171841,
year = {2026},
author = {Gómez-Montañez, E and Rojas-Salazar, YL and Rojas-Salazar, JG},
title = {Microbiome in Gastrointestinal Tumors: Implications in Oncogenesis and Therapeutic Response : Microbiome in Gastrointestinal Tumors.},
journal = {Current oncology reports},
volume = {28},
number = {1},
pages = {},
pmid = {42171841},
issn = {1534-6269},
mesh = {Humans ; *Gastrointestinal Neoplasms/microbiology/therapy/pathology ; *Gastrointestinal Microbiome ; *Carcinogenesis ; *Dysbiosis/microbiology ; Tumor Microenvironment ; *Microbiota ; },
abstract = {PURPOSE OF REVIEW: To provide an updated overview of the role of the human microbiome in the initiation, progression, and therapeutic response of gastrointestinal tumors, emphasizing molecular, immunological, and metabolic mechanisms, as well as its potential as a target for novel therapeutic strategies.

RECENT FINDINGS: Emerging evidence demonstrates that microbiome dysbiosis contributes to carcinogenesis across gastrointestinal malignancies, including colorectal, gastric, hepatic, and pancreatic cancers. Microbial-derived metabolites, such as short-chain fatty acids and secondary bile acids, modulate key signaling pathways involved in cell proliferation, apoptosis, and genomic stability. In addition, the microbiome influences the tumor microenvironment and immune responses, shaping variability in treatment outcomes. Both preclinical and clinical studies have shown that microbiome composition affects the efficacy and toxicity of chemotherapy and immunotherapy. Notably, specific microbial signatures are being explored as non-invasive biomarkers for early detection and prognostic stratification, while microbiome modulation strategies, such as diet, probiotics, antibiotics, and fecal microbiota transplantation, have demonstrated potential to enhance therapeutic response. The bidirectional interaction between the microbiome and the host plays a central role in gastrointestinal tumorigenesis and treatment response. Although this field holds significant promise for precision oncology, its clinical translation remains limited by interindividual variability, methodological heterogeneity, and insufficient longitudinal evidence. Future efforts should focus on standardization, validation of microbiome-based biomarkers, and integration of multi-omics and artificial intelligence approaches to enable clinically actionable applications.},
}

Humans
*Gastrointestinal Neoplasms/microbiology/therapy/pathology
*Gastrointestinal Microbiome
*Carcinogenesis
*Dysbiosis/microbiology
Tumor Microenvironment
*Microbiota

@article {pmid42171928,
year = {2026},
author = {Bi, Q and Zhang, L and Wan, H and Zhang, J},
title = {Harnessing the gut microbiota to enhance immune checkpoint inhibitor efficacy: from mechanistic insights to clinical translation.},
journal = {Molecular biology reports},
volume = {53},
number = {1},
pages = {},
pmid = {42171928},
issn = {1573-4978},
support = {HUST: 32500006//Fundamental Research Funds for the Central Universities/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/immunology/drug effects ; *Immune Checkpoint Inhibitors/therapeutic use/pharmacology ; Animals ; *Neoplasms/immunology/therapy/microbiology/drug therapy ; Tumor Microenvironment/immunology/drug effects ; Fecal Microbiota Transplantation/methods ; Immunotherapy/methods ; Translational Research, Biomedical ; },
abstract = {Immune checkpoint inhibitors (ICIs) targeting PD-1/PD-L1 and CTLA-4 pathways have revolutionized cancer therapy, yet their efficacy is frequently limited by primary or secondary resistance. Emerging evidence underscores the gut microbiota as a decisive regulator of ICI therapeutic outcomes. This review systematically delineates the multi-dimensional mechanisms through which the microbiota modulates anti-tumor immunity, specifically focusing on the molecular remodeling of immune signaling by microbial metabolites such as short-chain fatty acids (SCFAs) and bile acids, cross-reactive immunity driven by antigenic molecular mimicry, and the spatial restructuring of the tumor microenvironment mediated by the gut-tumor axis. Clinically, fecal microbiota transplantation (FMT) has demonstrated the potential to reverse ICI resistance, while the development of live biotherapeutic products (LBPs) and precise prebiotic combinations offers a standardized path for niche-specific intervention. Despite these advances, critical challenges persist, including the biological mismatch in cross-species animal models, the context-dependency arising from individualized microbial signatures, and the cognitive gap in the temporal dynamics of microbe-drug interactions. Deciphering the non-linear correlation between microbial succession and host immune response will be essential for integrating microbiota-driven strategies into personalized oncology frameworks.},
}

Humans
*Gastrointestinal Microbiome/immunology/drug effects
*Immune Checkpoint Inhibitors/therapeutic use/pharmacology
Animals
*Neoplasms/immunology/therapy/microbiology/drug therapy
Tumor Microenvironment/immunology/drug effects
Fecal Microbiota Transplantation/methods
Immunotherapy/methods
Translational Research, Biomedical

@article {pmid42159494,
year = {2026},
author = {García-Vidal, C and Gallardo-Pizarro, A and Aiello, TF and Kwon, M and Salavert, M and Pitart, C and Suarez-Lledó, M and Soriano, A and Mensa, J},
title = {Antibiotic therapy in febrile neutropenia in haematological patients: current considerations and future challenges.},
journal = {Revista espanola de quimioterapia : publicacion oficial de la Sociedad Espanola de Quimioterapia},
volume = {},
number = {},
pages = {},
doi = {10.37201/req/165.2026},
pmid = {42159494},
issn = {1988-9518},
abstract = {The management of febrile neutropenia (FN) in oncohematological patients is undergoing a paradigm shift driven by a deeper understanding of patients' pathophysiological heterogeneity, the increasing speed and accuracy of microbiological diagnostics, the emergence of new antibiotics, and the incorporation of predictive artificial intelligence (AI) as a tool to support clinical decision-making. Our objective is to provide an updated and comprehensive overview of the factors influencing antibiotic treatment in FN. We propose that its management should be based on three essential pillars. First, accurate risk stratification for bacterial infection. Second, ensuring that patients receive appropriate empirical antibiotic therapy, tailoring the initial choice according to the results of surveillance cultures from oropharyngeal and/or fecal microbiota. Finally, prioritizing antibiotic choices that preserve intestinal microbiota eubiosis as much as possible. Reducing colonization and overgrowth of facultative aerobic/anaerobic flora (Enterobacteriaceae, non-fermenting Gram-negative bacilli, and Enterococcus spp.) while preserving strict anaerobic flora decreases the risk of bacterial translocation and complications such as graft-versus-host disease (GVHD) after allogeneic hematopoietic stem cell transplantation (allo-HSCT) or loss of CAR-T functionality. This decision model, grounded in objective criteria, aims to balance the need for effective empirical coverage with responsible antibiotic use.},
}

@article {pmid42159959,
year = {2026},
author = {Zhang, Z and Jiang, F and Li, Z and Lin, L and Qi, B and Han, D and Ran, C and Mao, S and Wang, J and Zhou, Z and Wang, M and Li, J and Wang, G and Kang, S and Zhang, T},
title = {Animal gut microbes and microbiomes in the 21st century and beyond.},
journal = {Science China. Life sciences},
volume = {},
number = {},
pages = {},
pmid = {42159959},
issn = {1869-1889},
abstract = {Animal gut microbiomes-comprising bacteria, archaea, fungi, viruses, and protozoa-are fundamental to host evolution, physiology, and ecosystem resilience. This review synthesizes 21st-century advances in their diversity, spatiotemporal dynamics, and functional roles across the animal kingdom. Although high-throughput metagenomics has transformed the field, major biases remain: most studies still focus on domesticated vertebrates and fecal samples, leaving substantial "microbial dark matter" in wild hosts, invertebrates, and non-bacterial domains unexplored. We highlight how gut microbiomes mediate adaptation to environmental extremes, including hypoxia, temperature stress, and toxins, and how industrialization disrupts these communities, contributing to biodiversity loss and disease risk. We further integrate eco-evolutionary theory, multi-omics, and spatial modeling to clarify cross-kingdom interactions and functional networks. Finally, we discuss translational applications-including probiotics, fecal microbiota transplantation (FMT), phage therapy, and synthetic consortia-and emphasize the need for global collaborative initiatives, artificial intelligence (AI)-driven discovery, and standardized databases to unlock the full potential of animal gut microbiomes for biodiversity conservation, climate resilience, and planetary health in the coming decades.},
}

@article {pmid42160026,
year = {2026},
author = {Zhao, M and Hou, J and Wang, J and Zhu, X and Zou, A and Wang, Y and Liu, Z and Xianyu, Y},
title = {Food-Derived Biohybrid Probiotic Extracellular Vesicles for Synergistic Therapy of Inflammatory Bowel Disease.},
journal = {Small (Weinheim an der Bergstrasse, Germany)},
volume = {},
number = {},
pages = {e73858},
doi = {10.1002/smll.73858},
pmid = {42160026},
issn = {1613-6829},
support = {LZ26B050002//Natural Science Foundation of Zhejiang Province/ ; 2025C02124//"Pioneer" and "Leading Goose" R&D Program of Zhejiang/ ; 82470544//National Natural Science Foundation of China/ ; 2026YFE0214400//National Key Research and Development Program of China/ ; },
abstract = {Inflammatory bowel disease is a chronic gastrointestinal disorder characterized by persistent intestinal inflammation, microbiota dysbiosis, and impaired mucosal barrier function. Conventional treatments, including pharmacological agents, biologics, and fecal microbiota transplantation, are limited by adverse effects, immune suppression, recurrence, and low patient acceptance. In this study, food-derived probiotic extracellular vesicles (EVs) from Lactiplantibacillus plantarum with dietary polysaccharide (chitosan) and polyphenol (tannic acid) are developed as a synergistic therapeutic strategy for inflammatory bowel disease. The engineered biohybrid with dual-functional coating confers gastrointestinal stability and colon-targeted delivery, while scavenging reactive oxygen species and preserving the intrinsic microbiota-regulating properties of probiotic EVs. Multi-omics approach reveals correlations among microbial community shifts, short-chain fatty acids, oxidative stress modulation, inflammatory cytokine profiles, and disease severity indices. This work provides a promising approach and reveals the synergistic mechanisms of engineered probiotic EVs in reshaping gut microbiota, modulating metabolic networks, and improving the inflammatory microenvironment for the treatment of inflammatory bowel disease.},
}

@article {pmid42161263,
year = {2026},
author = {Ni, M and Junker, K and Liu, Y and Fan, Y and Li, Y and Qiao, W and Zhang, XS and Ksiezarek, M and Mead, EA and Tourancheau, A and Jiang, W and Blaser, MJ and Valdivia, RH and Davey, LE and Fang, G},
title = {Epigenetic phase variation in the gut microbiome enhances bacterial adaptation.},
journal = {Cell host & microbe},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.chom.2026.04.019},
pmid = {42161263},
issn = {1934-6069},
abstract = {The human microbiome continuously adapts to variations in diet and host physiology. Epigenetic phase variation (ePV) mediated by bacterial DNA methylation can generate phenotypic heterogeneity within clonal populations. ePVs have been characterized in human pathogens, but their roles in commensals remain unclear. Here, we cataloged ePVs in infant and adult gut microbiomes, revealing genome-wide and site-specific ePV in response to antibiotics and fecal microbiota transplantation. Long-read metagenomics revealed genome-wide ePV mediated by structural variations of DNA methyltransferases. Analysis of public short-read metagenomic datasets further revealed a high prevalence of genome-wide ePVs in the human microbiome. Site-specific ePVs were identified and associated with antibiotics or probiotic engraftment. Focusing on an Akkermansia muciniphila isolate, we find a specific ePV regulating mucC, a gene of unknown function but whose heterologous expression enhances bacterial tolerance to antibiotics via a bet-hedging strategy. Thus, epigenetic modifications are used by gut bacteria to adapt to fluctuating environments.},
}

@article {pmid42162499,
year = {2026},
author = {Gu, R and Li, J and Qi, J and Sun, R and Wu, H and Jin, B},
title = {Odoribacter laneus protects intestinal barrier by bile acid-FXR axis in acute pancreatitis.},
journal = {AMB Express},
volume = {},
number = {},
pages = {},
doi = {10.1186/s13568-026-02071-z},
pmid = {42162499},
issn = {2191-0855},
support = {2023YP44//the Cultivation Foundation of The Second Hospital of Shandong University/ ; },
abstract = {Odoribacter laneus (O. laneus) is a promising probiotic. Acute pancreatitis (AP) is an acute abodominal disease accompanied by intestinal barrier dysfunction and gut dysbiosis. However, the effects of O. laneus in AP remain unexplored. We established AP model of C57BL/6 mice. Western blotting and immunohistofluorescence were used to detect the expression of intestinal tight junction proteins and FXR/NLRP3 pathway. The changes of gut microbiota and bile acids (BAs) were analyzed by 16 S rRNA gene and targeted metabolomics sequencing. The fecal microbiota transplantation (FMT) was used to investigate the role of gut microbiota in O. laneus treatment. O. laneus effectively reduced systemic inflammation, pancreatic damage, and intestinal barrier dysfunction in AP mice. We observed significant enrichment of pathogens along with depletion of second BAs (7-KDA) in AP mice, and these alterations were reversed by O. laneus. FMT experiment showed that the protective roles of O. laneus depended on gut microbiota. O. laneus ameliorated AP via activating intestinal FXR and inhibiting NLRP3 inflammasome in vivo. In vitro and vivo studies showed that 7-KDA protected AP. Taken together, O. laneus could mitigate AP-induced intestinal barrier dysfunction by reversing the disorderd gut microbiota, BAs metabolism, and modulating FXR/NLRP3 pathway.},
}

@article {pmid42162728,
year = {2026},
author = {Suresh, G and Nath, M and Tiwari, A and Halder, N and Chawla, R and Velpandian, T},
title = {Gut Microbiome Dysbiosis in Uveitis - Mechanistic Insights and Emerging Therapeutic Strategies.},
journal = {Experimental eye research},
volume = {},
number = {},
pages = {111073},
doi = {10.1016/j.exer.2026.111073},
pmid = {42162728},
issn = {1096-0007},
abstract = {Recent studies have suggested the existence of a gut-eye axis, thus bringing the role of gut microbiota (GM) in the development of ocular inflammation in uveitis into focus. The proposed mechanisms for GM dysbiosis-induced uveitis include molecular mimicry, increased intestinal permeability by disruption of barrier integrity, immunomodulation, and alterations. Data from observational clinical studies indicate distinctive microbial signatures associated with uveal inflammation. Based on these findings, novel therapeutic modalities targeting the GM, such as antibiotics, probiotics, prebiotics, fecal microbiota transplantation, biologics, and dietary interventions have been proposed. While initial studies have shown promising results, there is limited clinical evidence supporting their therapeutic efficiency in the management of uveitis. The complexity and diversity of the GM, along with the lack of controlled clinical trials pose a significant challenge to the development of targeted therapeutics. Additionally, further studies are needed to elucidate the molecular mechanisms linking GM dysbiosis and ocular inflammation for developing specific biomarkers for diagnosis, as well as personalized GM-targeted patient interventions.},
}

@article {pmid42162772,
year = {2026},
author = {Aumpan, N and Watanabe, J and Yuan, Y and Kanno, T and Leontiadis, GI and Chan, FKL and Moayyedi, P},
title = {Fecal microbiota transplantation for symptom improvement in patients with irritable bowel syndrome: systematic review and meta-analysis of randomized controlled trials.},
journal = {Gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.1053/j.gastro.2026.04.039},
pmid = {42162772},
issn = {1528-0012},
abstract = {BACKGROUND: Fecal microbiota transplantation (FMT) could improve symptoms of irritable bowel syndrome (IBS) in some previous trials. We updated a prior meta-analysis of randomized controlled trials (RCTs) determining this issue.

METHODS: We searched CENTRAL, MEDLINE, and Embase (via Ovid) from inception to February 20[th], 2026 to identify potential studies. We included RCTs that reported the proportion of patients with IBS symptom improvement assessed between 4 and 24 weeks after FMT. For primary outcome, we estimated risk ratios (RR) of proportion of patients with IBS symptoms not improved. Data were pooled using a random effects model. The certainty of evidence was assessed using GRADE.

RESULTS: Thirteen RCTs involving 693 patients were eligible for this review. For the intention-to-treat analysis, FMT may reduce IBS symptoms at 12 weeks compared with placebo, but the evidence is very uncertain (RR of symptom not improved with FMT compared to placebo = 0.72; 95% CI 0.50-1.03). However, in the per-protocol analysis, FMT was statistically significant at improving symptoms (RR 0.67; 95% CI 0.46-0.97). Overall adverse events were not different in both groups (RR 0.98; 95% CI 0.75-1.29). The subgroup analysis reported IBS symptom improvement using single dose of FMT (RR 0.62; 95% CI 0.41-0.93), and when IBS was diagnosed by Rome IV criteria (RR 0.38; 95% CI 0.17-0.86).

CONCLUSIONS: This systematic review suggested there was very low certainty of evidence that FMT improved IBS symptoms. FMT was effective in some subgroup analyses and in the overall per protocol analysis but this needs to be interpreted with caution.},
}

@article {pmid42164024,
year = {2026},
author = {Hariyanto, TI},
title = {From dysbiosis to decolonization: The emerging role of fecal microbiota transplantation in antimicrobial resistance.},
journal = {Infectious medicine},
volume = {5},
number = {2},
pages = {100253},
pmid = {42164024},
issn = {2772-431X},
}

@article {pmid42164832,
year = {2026},
author = {Kumar, A and Krishan, B and Dhiman, S and Sharma, A and Thadiyan, V and Azmi, W},
title = {Beyond antibiotics: innovative and translational strategies to overcome antimicrobial resistance.},
journal = {3 Biotech},
volume = {16},
number = {6},
pages = {201},
pmid = {42164832},
issn = {2190-572X},
abstract = {The rapid rise of antimicrobial resistance demands therapeutic strategies that extend beyond conventional antibiotics. However, most existing reviews describe emerging alternatives without systematically linking their mechanistic advances to translational readiness and clinical implementation barriers. This review addresses this gap by integrating evidence across multiple beyond-antibiotic approaches, including antimicrobial peptides, bacteriophage therapy, CRISPR-based antimicrobials, nanotechnology-enabled delivery systems, anti-virulence agents, host-directed immunotherapies, microbiome modulation (engineered probiotics and fecal microbiota transplantation), and drug-repurposing or combination therapies. The principal contribution of this synthesis is a comparative framework that maps mechanisms of action, engineering innovations, and translational evidence across these diverse strategies. Advances such as peptidomimetics, engineered phages, and nanoparticle carriers that enhance stability, targeting, and therapeutic efficacy are highlighted, along with synergistic strategies including phage-antibiotic and CRISPR-nanocarrier combinations. The review further identifies major barriers limiting clinical translation, including delivery efficiency, toxicity and ecological concerns, large-scale production challenges, cost, inconsistent clinical outcomes, and regulatory fragmentation for biologics and live therapeutics. To facilitate clinical implementation, the study proposes a translational roadmap emphasizing standardized evaluation assays, physiologically relevant infection models, integrated rapid diagnostics, and regulatory frameworks tailored for emerging antimicrobial platforms, thereby supporting the development of sustainable therapies for the post-antibiotic era.},
}

@article {pmid42166227,
year = {2026},
author = {Kaushik, K and Sharma, M and Sharma, R and Reza, A and Sharma, G and Panwar, S and Nagraik, R and Negi, P and Sharma, A},
title = {Gut microbiota: The hidden hallmark of aging.},
journal = {Acta microbiologica et immunologica Hungarica},
volume = {},
number = {},
pages = {},
doi = {10.1556/030.2026.02808},
pmid = {42166227},
issn = {1588-2640},
abstract = {Aging is the natural process of changes that are accumulated over time and are responsible for the ever-increasing susceptibility to diseases and death. Extensive research has been done to understand the role of gut microbiota in aging, however, limited progress has been made. Thus, considering the need of the hour we have tried to give a new perspective to this body of research by delving deep into all major factors that are associated with gut microbiome and aging. This review presents a holistic view of the relation between gut microbiome and aging starting from hallmarks of aging and evolution of gut microbiome over lifespan to intricate mechanisms like inflammaging, immunosenescence, gut-brain axis, mitochondrial dysfunction, nutrient imbalance and cardiac implications. In addition, it highlights different therapies like fecal microbiota transplantation, omics and metabolomics studies, and gut modulation therapies that show a promising future towards regulation of gut microbiota for aging interventions. More importantly, this review is an addition to the existing literature which advocates gut microbiome as an additional hallmark of aging, summarising the known status of the research in this field, contributing to developing gut microbiota targeted healthy aging.},
}

@article {pmid42166402,
year = {2026},
author = {Peta Martinez, NA and Reinoso Arnaldi, M and Santiago-Rodriguez, TM and Rodriguez-Fernandez, IA},
title = {Microbiota-Based Interventions Differentially Rescue Gut and Social Behavior Phenotypes in Drosophila with Kdm5 Deficiency.},
journal = {Developmental neuroscience},
volume = {},
number = {},
pages = {1-32},
doi = {10.1159/000552681},
pmid = {42166402},
issn = {1421-9859},
abstract = {INTRODUCTION: Autism spectrum disorder (ASD) is a lifelong neurological and developmental disorder that is often accompanied by gastrointestinal (GI) issues. The bidirectional communication system known as the gut microbiota-brain axis may help explain how GI dysfunction contributes to neurological symptoms. Loss-of-function mutations in the histone demethylases KDM5A, KDM5B or KDM5C are found in patients with intellectual disability and ASD. Here, we use a genetically tractable Drosophila model of loss-of-function of the ASD-associated chromatin regulator Kdm5 to investigate how host genetic disruption influences gut microbial composition and social behavior. Previous studies using a Drosophila Kdm5 loss-of-function (Kdm5LOF) revealed gut microbial dysbiosis, reduced abundance of Lactiplantibacillus plantarum, and impaired social behavior. While L. plantarum supplementation rescued intestinal abnormalities, it did not restore social behavior.

METHODS: We evaluated multiple microbiota-based interventions, including probiotic supplementation with Lactiplantibacillus plantarum, Lactobacillus helveticus, their combination, and fecal microbiota transplantation (FMT), to determine their capacity to modulate gut microbial composition and behavior in adult Kdm5LOF flies. Gut bacterial abundance was quantified using colony-forming unit (CFU) assays and full-length 16S rRNA gene sequencing. Social behavior was assessed using the social distance assay, while anxiety-like behavior and locomotion were evaluated using the open field test. Gut-specific Kdm5 knockdown was used to assess tissue-specific contributions to microbiota and behavioral phenotypes.

RESULTS: Kdm5 deficiency resulted in reduced abundance of culturable Lactobacillus, Acetobacter, and Enterobacter species, accompanied by impaired social behavior. L. plantarum supplementation restored gut microbial abundance in both whole-body Kdm5LOF and gut-specific Kdm5 knockdown models but did not significantly rescue social behavior. In contrast, L. helveticus significantly improved social interaction in Kdm5LOF flies despite minimal effects on gut bacterial abundance, revealing a dissociation between microbial restoration and behavioral outcomes. Gut-specific Kdm5 knockdown phenocopied both microbial and social defects observed in Kdm5LOF mutants. Notably, FMT from healthy donors partially restored Lactobacillus abundance, reshaped gut microbial community structure, and partially improved social behavior in Kdm5LOF recipient flies.

CONCLUSIONS: Together, these findings identify Kdm5 as a key regulator of gut microbial viability and social behavior and demonstrate that microbiota-based interventions exert strain- and phenotype-specific effects. Our results reveal that restoration of microbial abundance alone is insufficient to rescue social behavior and highlight the importance of functional host-microbe interactions in gut-brain communication. This work establishes Drosophila as a tractable platform for dissecting epigenetic regulation of microbiota-behavior relationships in the context of disruption of an ASD-associated gene and for studying microbiota-based modulation of host physiology and behavior. All experiments were conducted in adult flies, and thus these findings reflect post-developmental effects of Kdm5 disruption.},
}

@article {pmid42167887,
year = {2026},
author = {Cui, D and Zhou, Y and Zhou, Y and Ge, R and Mao, H and Mathesh, M and Han, L and Yang, W and Yan, F},
title = {Gut microbiota dysbiosis and metabolic alterations in rheumatoid arthritis: a barrier to periodontal repair.},
journal = {RMD open},
volume = {12},
number = {2},
pages = {},
doi = {10.1136/rmdopen-2026-006931},
pmid = {42167887},
issn = {2056-5933},
mesh = {Animals ; *Dysbiosis/metabolism/etiology ; *Arthritis, Rheumatoid/metabolism/etiology/microbiology/pathology ; *Gastrointestinal Microbiome ; Rats ; Male ; Disease Models, Animal ; Fecal Microbiota Transplantation ; Arthritis, Experimental/metabolism ; Rats, Sprague-Dawley ; Metabolomics/methods ; X-Ray Microtomography ; RNA, Ribosomal, 16S/genetics ; Bone Regeneration ; Biomarkers ; },
abstract = {OBJECTIVE: To investigate the impact of rheumatoid arthritis (RA) on periodontal healing and the underlying mechanisms.

METHODS: Mandibular periodontal bone defect (PBD) and collagen-induced arthritis (CIA) models were established in male Sprague-Dawley rats aged 6 weeks, assigned to four groups: control (CON), CIA, PBD and CIA+PBD. Periodontal repair was evaluated at 1, 3 and 6 weeks. To examine the contribution of gut microbiota, pseudo-germ-free rats with PBD received 3-week faecal microbiota transplantation (FMT) from either healthy or CIA donors. Arthritis severity was assessed by paw thickness and arthritis index, while bone microarchitecture was examined by micro-CT and histology. Gut microbiota and metabolites were analysed using 16S ribosomal RNA high-throughput sequencing and untargeted metabolomics.

RESULTS: CIA was found to significantly impair periodontal bone healing and suppress osteogenesis-related markers, including runt-related transcription factor 2 and alkaline phosphatase. Compared with CON rats, CIA and PBD, CIA+PBD groups exhibited gut microbial dysbiosis and metabolic alterations, particularly in arachidonic acid and tryptophan pathways. FMT from CIA donors further increased osteoclast numbers and delayed bone regeneration. Furthermore, gut-derived factors from CIA animals were associated with increased macrophage expression of pro-inflammatory cytokines, including tumour necrosis factor-alpha and interleukin-1 beta.

CONCLUSION: Overall, RA-related gut microbiota dysbiosis and metabolic disturbances are linked to impaired periodontal healing, potentially through enhanced inflammatory responses. This study highlights a microbiome-immune-metabolic axis that may influence periodontal regeneration in RA.},
}

Animals
*Dysbiosis/metabolism/etiology
*Arthritis, Rheumatoid/metabolism/etiology/microbiology/pathology
*Gastrointestinal Microbiome
Rats
Male
Disease Models, Animal
Fecal Microbiota Transplantation
Arthritis, Experimental/metabolism
Rats, Sprague-Dawley
Metabolomics/methods
X-Ray Microtomography
RNA, Ribosomal, 16S/genetics
Bone Regeneration
Biomarkers

@article {pmid42154370,
year = {2026},
author = {Benekos, K and Katsanos, A and Laspas, P and Panos, GD and Vagiakis, I and Fousekis, FS and Luca, R and Zhou, B and Kostoulas, C and Georgiou, I and Katsanos, KH and Skondra, D and Konstas, AG},
title = {An Update and Overview of the Ocular and Extraocular Microbiome and Its Impact on Ophthalmic Care.},
journal = {Advances in therapy},
volume = {},
number = {},
pages = {},
pmid = {42154370},
issn = {1865-8652},
abstract = {The microbiome has been described as the last human "organ" and is currently the topic of great research interest worldwide. The application of culture-independent methods, like 16S ribosomal next-generation sequencing, has offered researchers the opportunity to identify bacterial populations that were impossible to detect previously using conventional culture methods. Further standardization of these new approaches to characterizing the microbiome is desirable. The present review discusses the mounting evidence suggesting that alterations in the microbiome and microbial metabolites, such as short-chain fatty acids in the gut, mouth, and ocular surface, may play a key role in the pathogenesis of ocular pathologies such as ocular surface disease, glaucoma, uveitis, age-related macular degeneration, and diabetic retinopathy. Clarifying the probable role of the microbiome in ocular diseases would not only offer valuable insights into pathogenesis but could also enable the development of novel therapeutic approaches. As yet, microbial-based therapeutic applications in ophthalmology are limited. Nevertheless, recently emerging strategies utilizing probiotics and prebiotics, or even fecal transplantation to regulate microbiome composition, offer promising research avenues for developing future innovative therapies for ocular diseases. Further studies employing standardized methodological protocols are needed to ensure the reproducibility of results and to eventually unlock the precise links between the microbiome and the eye.},
}

@article {pmid42155010,
year = {2026},
author = {Kim, JS and Loe, A and Ma, SF and Ranjan, P and Lipinski, JH and Mikhail, SG and Gurczynski, SJ and Zhou, X and Huffnagle, GB and Downward, JE and Metcalf, JD and Falkowski, N and Stringer, KA and Dickson, RP and Huang, Y and Moore, BB and Martinez, FJ and Murray, S and Noth, I and O'Dwyer, DN},
title = {Gut microbiota associate with disease severity and survival in idiopathic pulmonary fibrosis.},
journal = {American journal of respiratory and critical care medicine},
volume = {},
number = {},
pages = {},
doi = {10.1093/ajrccm/aamag249},
pmid = {42155010},
issn = {1535-4970},
abstract = {RATIONALE: Gut microbiota modify immunity. Dysregulated immunity plays a key role in the pathogenesis of IPF. However, the role of gut microbiota in IPF pathogenesis is unknown.

OBJECTIVES: Determine associations between gut microbiota, disease severity and lung transplant-free survival in IPF.

METHODS: Gut microbiota from patients enrolled in the CleanUP-IPF trial were characterized using fecal swab samples (n = 411). CleanUP-IPF investigated the clinical efficacy of long-term anti-microbials in IPF. 16S rRNA gene amplicon sequencing and shotgun metagenomic sequencing were performed to comprehensively profile gut microbial communities. Associations between baseline microbiota with disease severity, transplant-free survival, and treatment heterogeneity were analyzed using principal component analysis, multivariate generalized linear models, additive models and Cox regression models.

MEASUREMENTS AND MAIN RESULTS: Gut microbiota composition varied significantly with sex, age, and proton pump inhibitor use. Gut microbial diversity and community composition were significantly associated with impaired gas exchange (percent predicted (pp) DLCO). Several genera including the Lachnospiraceae unclassified genus were associated with improved transplant-free survival (HR 0.34 95% CI 0.14-0.87, P = .02) in patients not assigned to anti-microbial treatment. Patients with a higher abundance of the Lachnospiraceae unclassified genus exposed to long term co-trimoxazole had worse survival (HR 6.09 95% CI 1.36-27.27, P = .02). Survival in pirfenidone treated patients was significantly associated with a higher abundance of the gut Lachnospiraceae unclassified genus.

CONCLUSIONS: In exploratory post-hoc analysis, gut microbiota correlated with disease severity, associated with treatment heterogeneity and transplant-free survival in patients with IPF.},
}

@article {pmid42156770,
year = {2026},
author = {Chernova, VO and Ng, RW and Yang, L and Ip, M and Corcione, S and Benech, N and van Prehn, J and Kuijper, EJ and Contarino, MF},
title = {Safety and efficacy of faecal microbiota transplantation in Parkinson's disease.},
journal = {NPJ Parkinson's disease},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41531-026-01376-x},
pmid = {42156770},
issn = {2373-8057},
support = {NL1903//Stichting ParkinsonFonds/ ; },
abstract = {The gut microbiota may influence Parkinson's disease's (PD) pathophysiology. Faecal Microbiota Transplantation (FMT) may therefore improve symptoms. We reviewed five randomized controlled trials (RCT), three cohort studies, one case series, and two single case reports (total of 236 subjects). FMT methods varied (donor selection, FMT preparation method, pre-treatment, administration). Mild, self-limiting gastrointestinal symptoms were the most common adverse events (AEs). Constipation improved consistently after FMT. Motor and non-motor outcomes were heterogeneous, with improvements mainly reported in uncontrolled studies. One RCT demonstrated motor improvement at 8-12 weeks, another only after one year, while others showed no significant changes. In most RCTs, changes fell within or just beyond the minimal clinically important differences (MCID). Five studies reported taxonomic shifts, most consistently increased within the phylum Firmicutes. Large, well-designed RCTs with optimized FMT protocol for patient selection, FMT preparation and delivery, and donor selection are needed to determine whether FMT can affect PD symptoms or disease progression.},
}

@article {pmid42157185,
year = {2026},
author = {Wu, R and Teng, X and Cai, Y and Liu, Y and Zhang, W and Li, Z and Fan, J},
title = {Integrated multi-matrix metabolomics reveals gut microbiota-driven systemic metabolic alterations and therapeutic remodeling by fecal microbiota transplantation in autism spectrum disorder.},
journal = {Journal of translational medicine},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12967-026-08217-8},
pmid = {42157185},
issn = {1479-5876},
support = {ZX-KYXM2025001//Autism Research Special Fund of Zhejiang Foundation for Disabled Persons/ ; },
abstract = {BACKGROUND: Gut dysbiosis is deeply implicated in the pathophysiology of autism spectrum disorder (ASD); however, the mechanisms by which fecal microbiota transplantation (FMT) regulates host systemic metabolic homeostasis remain incompletely understood. Specifically, this study aims to address three core objectives: (1) to characterize the paired fecal and urinary metabolic signatures of ASD; (2) to map the microbiota-metabolite interaction networks; and (3) to evaluate the longitudinal metabolic remodeling effects of FMT. Through these objectives, we seek to elucidate the pathological mechanisms from a systems biology perspective.

METHODS: We employed a multi-omics strategy, integrating 16 S rRNA sequencing with untargeted metabolomics on paired fecal and urinary samples from children with ASD (n = 33) and healthy controls (HCs) (n = 27). Furthermore, we conducted an exploratory longitudinal evaluation of the metabolic remodeling effects of FMT in a subset of patients (n = 7) using paired samples collected at baseline and 3 months post-treatment.

RESULTS: We observed consistent metabolic dysregulation across both gut and peripheral matrices in children with ASD. These alterations were characterized by specific molecular signatures: impaired lipid metabolism (depletion of lysophosphatidylcholine [LPC] 18:2), downregulated cholinergic signaling (reduced methacholine), and the accumulation of neuroactive toxins (elevated tetraethylammonium [TEA]). Integrated multi-omics analysis correlated these metabolic deviations with a reduced abundance of beneficial commensals, such as Faecalibacterium. Preliminary data from the FMT intervention demonstrated a potential reversal of these metabolic phenotypes toward a healthy baseline, with trends indicating targeted restoration of core metabolic markers including LPC 18:2 and methacholine.

CONCLUSIONS: This study reveals that FMT may exert neuroprotective effects by ameliorating lipid metabolic defects and replenishing precursors of the cholinergic anti-inflammatory pathway (CAP). These findings delineate an ASD-specific gut-kidney metabolic axis, providing a preliminary theoretical basis for precision ASD treatment strategies targeting the microbiota-metabolism axis.},
}

@article {pmid42157525,
year = {2026},
author = {Aware, C and Woods, C and Khodakivskyi, P and Dwivedi, AK and Zuckerman, A and Govindarajan, M and Ivanich, K and Yu, W and Cui, J and Gu, Z and Goun, E and Ericsson, AC and Zafonte, R and Balchandani, P and Lin, AL},
title = {Stroke-induced gut microbiome dysbiosis accelerates Alzheimer's disease progression.},
journal = {Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism},
volume = {},
number = {},
pages = {271678X261449017},
doi = {10.1177/0271678X261449017},
pmid = {42157525},
issn = {1559-7016},
abstract = {Stroke survivors face an elevated risk of developing Alzheimer's disease (AD), yet the biological mechanisms linking these conditions remain poorly defined. Here, we show that a stroke-induced gut microbiome is a key driver of AD-related pathology. Fecal microbiota transplantation (FMT) from stroke patients into young triple-transgenic Alzheimer's disease (3xTg-AD) mice accelerated tau phosphorylation, increased neuroinflammation, and disrupted metabolic homeostasis in both the brain and gut, compared with FMT from healthy donors. Mice receiving stroke-derived microbiota exhibited persistent, donor-specific dysbiosis and broad metabolic reprogramming involving redox balance, nucleotide metabolism, and energy pathways in cecal contents and brain tissue. These metabolic disturbances were accompanied by widespread and region-specific transcriptional changes revealed by single-cell spatial transcriptomics, including glial activation, impaired neuron-glia communication, and dysregulation of mitochondrial, amyloid-processing and inflammatory pathways across cortical and hippocampal regions. Collectively, these findings identify post-stroke gut dysbiosis as a mechanistic contributor to heightened neurodegenerative vulnerability and AD risk, highlighting the gut-brain axis as a potentially modifiable target for preventing post-stroke dementia.},
}

@article {pmid42158036,
year = {2026},
author = {Maung Myint, T and Hand, J and Lowe, A and Kotton, CN and Chen, SC and Beardsley, J and Teixeira-Pinto, A and Wong, G and Chan, S},
title = {Management of Norovirus Infection in Solid Organ Transplant Recipients: A Scoping Review.},
journal = {Transplantation direct},
volume = {12},
number = {6},
pages = {e1944},
pmid = {42158036},
issn = {2373-8731},
abstract = {BACKGROUND: Norovirus infection causes significant morbidity in solid organ transplant (SOT) recipients, yet few treatments are available, and evidence for efficacy is sparse. In this scoping review, we identify and evaluate potential interventions for managing norovirus infections in SOT recipients.

METHODS: We searched electronic databases from inception to July 6, 2025. Eligible studies were analyzed for participants' characteristics, intervention types, and reported outcomes.

RESULTS: After screening 245 abstracts, 58 studies were included (1 randomized controlled trial, 27 cohort studies, 5 case series and 25 case reports), mainly from the United States. Transplant types included kidney (n = 36), liver (n = 12), cardiac (n = 12), pulmonary (n = 7), pancreas (n = 6), small bowel (n = 7), and multiorgan (n = 13) transplants. The most frequently reported primary outcome was resolution of gastrointestinal (GI) symptoms. Interventions were diverse: immunosuppression modification (n = 14), nitazoxanide (n = 6), IVIG (n = 3), oral immunoglobulin (n = 10), combination of these (n = 19), fecal transplant (n = 2), supportive management (n = 4), and others not classified (n = 5). Limited quality evidence for the resolution of gastrointestinal symptoms was reported for immunosuppression modification (n = 7/14), nitazoxanide (n = 4/6), IVIG (n = 2/3), oral immunoglobulin alone (n = 10/10), fecal transplant (n = 2/2), supportive treatment (n = 4/4), and a combination of treatments (n = 10/19). A lack of clinical improvement was described in 13 of 58 studies.

CONCLUSIONS: A wide range of interventions has been used to manage norovirus infections in SOT recipients; however, the evidence is limited to observational studies, and the findings are uncertain. High-quality randomized controlled trials are needed to establish treatment efficacy and safety.},
}

@article {pmid42158204,
year = {2026},
author = {Chen, C and Zhu, L and Huang, Y and Wang, YY and Kong, L and Lu, S and Shang, X},
title = {Gut microbiota-intestinal barrier crosstalk: mechanistic advances, disease relevance, and public health implications.},
journal = {Frontiers in public health},
volume = {14},
number = {},
pages = {1777910},
pmid = {42158204},
issn = {2296-2565},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Public Health ; *Intestinal Mucosa/microbiology ; },
abstract = {BACKGROUND: The intestinal barrier is a critical interface between the host and the external environment, and growing evidence indicates that bidirectional crosstalk between the gut microbiota and the intestinal barrier is a key determinant of intestinal and systemic health. Disruption of this interaction has been implicated in the development of multiple chronic non-communicable diseases, including inflammatory, metabolic, neurodegenerative, and immune-mediated conditions. However, previous reviews have often examined gut microbiota or intestinal barrier dysfunction separately, with less emphasis on their bidirectional interaction as an integrated mechanistic and public health framework.

OBJECTIVE: This review aims to synthesize current mechanistic advances in gut microbiota-intestinal barrier crosstalk, evaluate its relevance across major disease domains, and examine its potential implications for chronic disease prevention and public health practice. In particular, this review highlights the gut microbiota-intestinal barrier axis as a unifying framework linking microbial metabolism, mucosal homeostasis, systemic inflammation, and prevention-oriented health strategies.

METHODS: We conducted a structured review of recent studies published between 2019 and 2025 in PubMed, Scopus, and Web of Science, with emphasis on both foundational and emerging evidence. The review focused on microbiota-derived metabolites, epithelial junction integrity, mucosal immune regulation, disease-associated barrier dysfunction, and microbiota-targeted interventions. Evidence from mechanistic, preclinical, and clinical studies was integrated to identify major advances, translational opportunities, and current limitations in the field.

RESULTS: Current evidence indicates that gut microbiota regulate intestinal barrier integrity through metabolites such as short-chain fatty acids (SCFAs), indole derivatives, and bile acids, which influence tight junction expression, mucin production, epithelial repair, and mucosal immune balance. Conversely, barrier dysfunction may promote microbial translocation, endotoxemia, and chronic low-grade inflammation, thereby contributing to diseases such as inflammatory bowel disease, type 2 diabetes, metabolic-associated fatty liver disease, and neurodegenerative or neuropsychiatric disorders. Microbiota-targeted interventions, including prebiotics, probiotics, dietary approaches, and fecal microbiota transplantation, have shown potential to restore barrier-related homeostasis. However, the current evidence remains constrained by heterogeneity in study design, incomplete causal validation, inconsistent clinical outcomes, and limited standardization of intervention strategies, all of which restrict clinical translation and large-scale public health implementation.

CONCLUSION: The gut microbiota-intestinal barrier axis is an important determinant of health and disease and may represent a promising target for future prevention-oriented strategies. By integrating mechanistic evidence with disease relevance, translational limitations, and public health perspectives, this review provides a more coherent framework for understanding microbiota-barrier crosstalk. Future research should prioritize causal validation, standardized methodologies, and equitable implementation pathways to support the development of scalable preventive and therapeutic strategies.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Public Health
*Intestinal Mucosa/microbiology

@article {pmid41922969,
year = {2026},
author = {Wei, C and Zhou, X and Xia, X and Feng, W and Wang, L and Li, X},
title = {Cold environment is associated with worse outcomes in ischemic stroke patients and the underlying gut microbial mechanism.},
journal = {BMC microbiology},
volume = {26},
number = {1},
pages = {},
pmid = {41922969},
issn = {1471-2180},
support = {42275197//National Natural Science Foundation of China/ ; TJWJ2023XK007//Key Projects of Tianjin Municipal Health Commission/ ; TA-10207 PRC//Asian Development Bank Technical Assistance Project/ ; TJYXZDXK-3-017C//Tianjin Key Medical Discipline (Specialty) Construction Project/ ; },
abstract = {BACKGROUND: Increasing evidence suggests that cold environment is a potential risk factor for acute ischemic stroke (AIS) and is associated with poor prognosis, however, its underlying mechanisms remain unclear. Since gut dysbiosis and AIS are causally related and cold environment can induce changes in the gut microbiota, we wondered whether cold-season-related gut dysbiosis aggravates stroke progression.

METHODS: In total, 101 patients with AIS were enrolled and divided into two groups: cold-season onset ischemic stroke (CIS) and non-cold-season onset ischemic stroke (NCIS). Gut microbiota composition was analyzed using 16 S rRNA gene sequencing, and signature taxa were identified via linear discriminant analysis effect size (LEfSe). Correlations between key microbial taxa and clinical parameters were assessed using Spearman rank analysis. To evaluate the potential causal role of gut microbiota in cold season stroke, fecal microbiota transplantation (FMT) was performed in mice, followed by middle cerebral artery occlusion (MCAO).

RESULTS: The composition of gut microbiota in the CIS group significantly differed from the NCIS group. The characteristic microbiota of the CIS group was distinguished by an elevated relative abundance of Escherichia-Shigella and Enterococcus, coupled with a decreased percentage of Blautia, Eubacterium_hallii_group, Subdoligranulum, Dorea, Faecalibacterium, Ruminococcus, and Collinsella. Furthermore, Escherichia-Shigella, Enterococcus, Blautia, Eubacterium_hallii_group and Faecalibacterium showed predictive value for 3-month poor prognosis in patients. Compared with mice inoculated with the NCIS gut microbiota, mice inoculated with the CIS gut microbiota showed more severe brain damage, impaired intestinal barrier function, and higher levels of inflammatory factors after the stroke model was established.

CONCLUSIONS: Our study indicates that cold-season-related gut dysbiosis may be linked to stroke severity and poor prognosis in AIS patients, suggesting that modulation of gut microbiota could represent a potential avenue for therapeutic intervention.

SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12866-026-05013-8.},
}

@article {pmid42148776,
year = {2026},
author = {Guo, J and Xiang, Z-w and Hu, F-f and Zhang, S-x and Han, W-j and Ding, X and Wang, X and Ye, M-l and Chen, J-h and Rao, T and Wu, L-l and Lian, G-h and Zhang, W and Huang, Y and Chen, Y},
title = {Turicibacter sanguinis is a candidate gut microbial pathobiont that promotes metabolic dysfunction-associated steatohepatitis.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0029226},
doi = {10.1128/msystems.00292-26},
pmid = {42148776},
issn = {2379-5077},
abstract = {UNLABELLED: Emerging evidence points to the gut microbiota's involvement in metabolic dysfunction-associated steatohepatitis (MASH), yet the specific causative microbes remain largely unidentified. This study aimed to identify and functionally characterize candidate microbial pathobionts to MASH progression. Differentially abundant microbes were identified by 16S rRNA sequencing in a choline-deficient, L-amino acid-defined, high-fat diet MASH model, validated in other animal MASH models and in public clinical metagenomic data sets, then screened for consistently altered gut taxa. A candidate underwent functional validation via directed oral administration in mice. Mechanisms were explored through bile acid profiling by UHPLC-MS/MS and FXR signaling analysis by qPCR and immunohistochemistry. Additionally, fecal samples from MASH patients before and after treatment were analyzed to correlate microbial abundance with treatment response. Turicibacter sanguinis was consistently enriched in all MASH models and public data sets, with abundance correlating positively with liver injury markers. Its increased abundance exacerbated steatosis, inflammation, and fibrosis in healthy and diseased mice. Mechanistically, Turicibacter sanguinis altered bile acid composition, thereby increasing conjugated and decreasing unconjugated species, and inhibited hepatic FXR signaling, accompanied by suppressed SHP and elevated CYP7A1 and SREBP1c expression, which is consistent with enhanced bile acid synthesis and lipid accumulation. Futhermore, after pharmacotherapy, reduced Turicibater sanguinis levels correlated positively with alanine aminotransferase (ALT) and aspartate aminotransferase (AST) improvements. In conclusion, Turicibacter sanguinis is a clinically relevant microbial pathogen that exacerbated MASH by inducing bile acid dysregulation and suppressing FXR signaling, highlighting its potential as a candidate biomarker for disease monitoring and motivating future evaluation of targeted microbiome interventions.

IMPORTANCE: Metabolic dysfunction-associated steatohepatitis (MASH) is a growing global health problem with limited treatment options. Although the gut microbiome has been implicated in MASH, the specific bacterial strains that directly drive disease progression remain largely unknown. This study identified Turicibacter sanguinis as a candidate gut microbial pathobiont that promotes MASH, demonstrating its significant enrichment in both animal models and patient samples. By disrupting hepatic metabolic signaling, this bacterium promotes bile acid synthesis and exacerbates liver fat accumulation, inflammation, and fibrosis. Following effective treatment, its abundance decreased significantly in patients. These findings indicate that Turicibacter sanguinis holds promise as a potential target for developing novel microbiome-based diagnostic and therapeutic approaches for MASH.},
}

@article {pmid42149263,
year = {2026},
author = {Sorensen, N and Buntzen, S and Pedersen, L and Thorlacius-Ussing, O},
title = {Efficacy and safety of freshly collected autologous adipose tissue for complex anal fistulas in non-IBD patients: a prospective cohort study.},
journal = {Techniques in coloproctology},
volume = {},
number = {},
pages = {},
doi = {10.1007/s10151-026-03297-6},
pmid = {42149263},
issn = {1128-045X},
abstract = {BACKGROUND: Complex cryptoglandular anal fistulas present a treatment challenge, with many surgical options associated with recurrence, variable healing rates, and risk of incontinence. Freshly collected autologous adipose tissue (FCAAT) has been proposed as a minimally invasive, one-step alternative. This study aimed to assess clinical healing and clinical improvement and to evaluate the safety of the procedure.

METHODS: This prospective cohort study included 31 patients without inflammatory bowel disease (IBD) with complex single-tract cryptoglandular anal fistulas treated with FCAAT between May 2019 and December 2023 and followed until August 2024. The surgical procedure involved liposuction, processing of adipose tissue, closure of the internal opening, and local injection along the fistula tract in a one-step procedure. Primary outcomes were clinical healing and clinical improvement; secondary outcomes were adverse events.

RESULTS: The patient cohort presented with advanced disease. Median disease duration was 20 months, and one-third of patients had undergone previous attempts at surgical closure. Clinical healing was achieved in 23 patients (74%), with an additional four patients (13%) demonstrating clinical improvement. Five of 27 responders (19%) healed more than 3 months post-procedure. Common adverse events included proctalgia in 8 patients (22%), donor site pain 5 (14%), and minor graft site hematomas in 4 (11%). One Clavien-Dindo IIIa event (graft site bleeding) was managed with a single suture; all other complications were minor and resolved conservatively.

CONCLUSION: FCAAT is a safe and effective one-step treatment for complex anal fistulas in non-IBD patients, offering a high healing rate with predominantly minor complications. A delayed effect was observed in some patients.},
}

@article {pmid42151161,
year = {2026},
author = {Wang, Y and Hou, Q and Lv, X and Liu, J and Wang, H and Zhao, Y and Tong, H and Liu, Y and Du, J and Yang, X and Wu, S and He, S and Yang, X},
title = {Inorganic nitrogen metabolic reprogramming of the gut microbiome drives fecal microbiota transplantation in ulcerative colitis.},
journal = {Nature communications},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41467-026-73290-y},
pmid = {42151161},
issn = {2041-1723},
support = {32172776//National Natural Science Foundation of China (National Science Foundation of China)/ ; },
abstract = {Although fecal microbiota transplantation (FMT) shows promise for ulcerative colitis (UC), its clinical success appears to be contingent upon the degree of donor microbiota engraftment. Using an LD50-based ecological model, our study reveals that inorganic nitrogen utilization capacity (IN-uc) critically determines gut microbial assembly in high oxidative stress environments, which significantly influences microbial engraftment outcomes. Building on this mechanistic insight, we engineer a probiotic-metabolite consortia designed to synergistically increase IN-uc in the gut ecosystem. We find that PM-mix14 alleviates oxidative stress-mediated colonization barriers of donor microbiota by catalyzing the conversion of excess reactive nitrogen species through multi-step reactions, promotes L-glutamate biosynthesis and ATP production, thereby ensuring greater similarity in the structure and function of the recipient microbiota to those of the donor. In multiple male murine models of colitis, PM-mix14 supplementation during FMT significantly improves microbial engraftment fidelity, which is correlated with increased anti-inflammatory responses and attenuated colonic pathology. Network meta-analysis of multiple clinical datasets further substantiates the prognostic value of donor gut microbial IN-uc in UC remission. Our findings establish the gut microbial IN-uc as an ecological driver of microbiota engraftment and present a rationally designed microbial therapy that optimizes FMT efficacy through targeted metabolic reprogramming.},
}

@article {pmid42152659,
year = {2026},
author = {He, L and Huang, Y and Feng, S and Li, H and Zhang, Z and Wu, J and Huang, S and Fong, LM and Wu, K and Li, Z and Wu, F},
title = {Gut Microbiota-Targeted Therapies for Major Depressive Disorder: Mechanisms, Clinical Evidence, and Future Directions.},
journal = {Current neuropharmacology},
volume = {},
number = {},
pages = {},
doi = {10.2174/011570159X432808251117075147},
pmid = {42152659},
issn = {1875-6190},
abstract = {Major Depressive Disorder (MDD) severely impairs individuals' physical and mental health, imposing substantial burdens on families and society. The pathogenesis of MDD remains elusive, but it is hypothesized to involve genetics, central neurotransmitter imbalance, hypothalamic- pituitary-adrenal (HPA) axis hyperactivity, and gut microbiota dysbiosis, among other factors. Antidepressants, which primarily address central neurotransmitter imbalances, are the first-line treatment; however, approximately half of patients exhibit suboptimal responses to conventional therapies. In recent years, attention has been drawn to specific alterations in gut microbiota composition observed in patients with severe depression. Animal studies have demonstrated that fecal transplantation from MDD patients to rodents can induce depressive-like behaviors, whereas fecal transplantation from healthy individuals may reverse such changes. Based on these findings, gut microbiota-targeted interventions have been progressively investigated in subclinical and clinical settings, including probiotic supplementation, fecal microbiota transplantation, and dietary modifications (such as the Mediterranean diet and ketogenic diet). These interventions may offer significant therapeutic effects with minimal side effects and high acceptability, providing new hope for patients with treatment-resistant depression. However, critical parameters such as optimal treatment regimens, dosages, and intervention durations remain unstandardized, and their underlying mechanisms and specific efficacy are still unclear. This review comprehensively evaluates existing clinical studies, focusing on the design of intervention protocols, therapeutic outcomes, adverse effects, and potential mechanisms of action, with the aim of providing guidance for future research.},
}

@article {pmid42152807,
year = {2026},
author = {Jing, M and Chen, X and Jiang, M and Fang, H and Zhu, X and Jin, X and Jiao, Y and Hou, N and Gong, W and Liu, A},
title = {Microbial and Metabolic Correlates of Endometrial Dysfunction in Polycystic Ovary Syndrome: A Translational Study.},
journal = {BJOG : an international journal of obstetrics and gynaecology},
volume = {},
number = {},
pages = {},
doi = {10.1111/1471-0528.70266},
pmid = {42152807},
issn = {1471-0528},
support = {//Hangzhou Joint Fund of the Zhejiang Provincial Natural Science Foundation of China/ ; //Natural Science Foundation of Xinjiang Uygur Autonomous Region/ ; },
abstract = {OBJECTIVE: Women with polycystic ovary syndrome (PCOS) exhibit a substantially increased risk of miscarriage, yet the underlying mechanisms remain inadequately understood. This study aimed to investigate whether specific gut microbial dysbiosis and metabolic disturbance are associated with and may potentially contribute to endometrial dysfunction and adverse pregnancy outcomes in women with PCOS.

DESIGN: Prospective cohort study integrated with mechanistic experiments.

SETTING: Women's Hospital, School of Medicine, Zhejiang University, China (2022-2024).

POPULATION: A total of 110 women with PCOS and 110 age- and body mass index-matched controls were enrolled.

METHODS: We performed 16S rRNA and metagenomic sequencing of gut microbiota, with untargeted and targeted serum metabolomics. Functional validation was conducted using primary human endometrial stromal cells and a PCOS rat model intervened with Parabacteroides merdae (P. merdae) supplementation or faecal microbiota transplantation.

MAIN OUTCOME MEASURES: Gut microbiota composition, serum metabolites, endometrial senescence markers, and pregnancy outcomes.

RESULTS: Women with PCOS exhibited significantly higher miscarriage rates than controls, accompanied by a marked depletion of P. merdae abundance and elevated serum levels of branched-chain amino acids, particularly isoleucine. Exogenous isoleucine induced cellular senescence in human endometrial stromal cells in a dose-dependent manner. Restoration of P. merdae levels in the PCOS rat model resulted in decreased serum isoleucine levels, amelioration of the senescent endometrial phenotype, and reduction in the fetal resorption rate.

CONCLUSIONS: These findings suggest that P. merdae depletion and the concurrent accumulation of isoleucine may be associated with endometrial senescence and elevated risk of miscarriage, suggesting the possible involvement of a gut microbiota-metabolite pathway in PCOS-related reproductive dysfunction. These results also provide a mechanistic basis for future translational investigations.},
}

@article {pmid42154122,
year = {2026},
author = {Desai, V and Ancil, S and Gupta, R and Kang, M and Bhadada, SK and Sharma, AK and Jearth, V and Rana, SS},
title = {Incidence and Determinants of Pancreatic Insufficiency After Acute Necrotizing Pancreatitis: A Prospective Study.},
journal = {Digestive diseases and sciences},
volume = {},
number = {},
pages = {},
pmid = {42154122},
issn = {1573-2568},
abstract = {BACKGROUND AND AIM: Acute necrotizing pancreatitis (ANP) is associated with pancreatic parenchymal necrosis and may lead to exocrine and endocrine dysfunction. However, the natural course and determinants of pancreatic functional impairment remain incompletely defined. We prospectively evaluated the pancreatic exocrine and endocrine function in patients with ANP and attempted to identify associated risk factors.

METHODS: Patients aged 18-80 years with ANP defined by the Revised Atlanta Classification were enrolled and prospectively followed for 6 months. Exocrine function was assessed using fecal elastase-1 (FE-1), and endocrine function was evaluated using fasting glucose, postprandial glucose, HbA1c, and homeostatic model assessment of insulin resistance (HOMA-IR). Clinical severity, etiology, anatomic distribution of necrosis, infected necrosis, and interventions were analyzed as predictors of dysfunction.

RESULTS: Thirty patients completed 6-month follow-up. At 6 months, exocrine insufficiency occurred in 40% of patients (mild 16.7%, severe 23.3%). Endocrine dysfunction was observed in 30% of patients, including diabetes mellitus (6.7%) and prediabetes (23.3%). Necrosis involving the pancreatic head was significantly associated with exocrine insufficiency (p = 0.003). Moderately severe acute pancreatitis independently predicted exocrine dysfunction (p = 0.01). No clinical or radiologic factor predicted endocrine insufficiency.

CONCLUSION: Exocrine insufficiency appears to be relatively common following ANP, with a possible association observed in patients with moderately severe disease and head-dominant necrosis; however, these findings require further validation. Endocrine dysfunction was observed in approximately one-third of patients, but no consistent predictors were identified in this cohort.},
}

@article {pmid42138826,
year = {2026},
author = {Chen, X and Shen, M and Zhang, R and Huang, Z and Niu, H and Yu, Q and Chen, Y and Pan, X and Rong, L and Wen, H and Yang, J and Xie, J},
title = {Sulfated Cyclocarya Paliurus Polysaccharide Sorchestrates the Gut Microbiome to Mobilize a Host-Derived 12-HEPE Against Ulcerative Colitis.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e75681},
doi = {10.1002/advs.75681},
pmid = {42138826},
issn = {2198-3844},
support = {2023YFF1104001//National Key Research and Development Program of China/ ; 82460642//National Natural Science Foundation of China/ ; },
abstract = {Despite extensive evidence supporting the therapeutic potential of natural product-derived compounds in Ulcerative colitis (UC), their precise mechanisms have yet to be fully elucidated. In this study, structurally modified Cyclocarya paliurus polysaccharide (CP) derivatives were evaluated in a dextran sulfate sodium (DSS)-induced UC mouse model. Among the variants tested, sulfated Cyclocarya paliurus polysaccharide (SCP) emerged as the most therapeutically potent. SCP administration markedly attenuated colitis severity, as evidenced by relieved disease symptoms and reinforced intestinal barrier function. Mechanistically, SCP restored gut microbial homeostasis by enriching beneficial Bacteroidetes and enhancing short-chain fatty acids (SCFAs) production. This remodeled microbial ecosystem orchestrates the upregulation of host-derived 12-hydroxyeicosapentaenoic acid (12-HEPE), which exerts anti-inflammatory effects via direct inhibition of Toll-like receptor 4 (TLR4) signaling. The gut microbiota's functional relevance was substantiated by fecal microbiota transplantation and antibiotic-mediated exhaustion studies. Notably, the therapeutic benefits of 12-HEPE were abrogated upon co-administration of a TLR4 agonist, confirming its target specificity. Elevated serum 12-HEPE levels were observed in a human UC cohort, implying a potential compensatory immunoregulatory response. Our findings elucidate a novel microbiota-host interaction axis wherein SCP alleviates UC by modulating the gut microbiota to enhance endogenous 12-HEPE production, thereby suppressing TLR4-mediated inflammation.},
}

@article {pmid42140492,
year = {2026},
author = {Corcione, S and Benech, N and Kuijper, E and , },
title = {Microbiome science at a turning point: from descriptive ecology to clinical decision-making in infectious diseases.},
journal = {Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cmi.2026.05.017},
pmid = {42140492},
issn = {1469-0691},
}

@article {pmid42141775,
year = {2026},
author = {Zhou, F and Wang, L and Zhao, Y and Hu, C and Meng, Y and Fan, J and Fraser, WD and Baillargeon, JP and Ouyang, F and Lye, SJ and Dennis, CL and Shen, J and Wu, Y and Huang, H},
title = {Antenatal depressive symptoms impair offspring neurodevelopment by inducing maternal gut microbiota dysbiosis during pregnancy.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2672188},
doi = {10.1080/19490976.2026.2672188},
pmid = {42141775},
issn = {1949-0984},
mesh = {Female ; Pregnancy ; Humans ; *Gastrointestinal Microbiome/physiology ; *Dysbiosis/microbiology ; *Depression/microbiology/complications ; Fecal Microbiota Transplantation ; Adult ; Case-Control Studies ; *Pregnancy Complications/microbiology/psychology ; Prospective Studies ; Butyrates/metabolism ; Bacteria/classification/genetics/isolation & purification/metabolism ; *Prenatal Exposure Delayed Effects ; Feces/microbiology ; Infant ; Brain/growth & development/metabolism ; *Neurodevelopmental Disorders/etiology ; RNA, Ribosomal, 16S/genetics ; },
abstract = {The effects of maternal antenatal depression (AND) across different stages of pregnancy on offspring neurodevelopment remain poorly understood, and the underlying microbiota-related mechanisms are largely unknown. In a multicenter prospective cohort of 2053 pregnant women, we found that elevated depressive symptoms at any trimester were significantly associated with delayed infant neurodevelopment. Using a nested case‒control design with 16S rRNA sequencing of 504 maternal fecal samples, we identified a consistent reduction of butyrate-producing bacteria and disruption of amino acid metabolism in women with AND symptoms - features that correlated with poorer infant cognitive outcomes. To establish causality, fecal microbiota transplantation (FMT) from women with AND symptoms was administered to germ-free dams, resulting in impaired intestinal barrier integrity, heightened neuroinflammatory signaling, and altered polyunsaturated fatty acid and amino acid metabolism in fetal brains at E18.5, leading to postnatal cognitive deficits in the offspring. Remarkably, maternal butyrate supplementation partially rescued these molecular and neurodevelopmental abnormalities. Together, these findings reveal a mechanistic link between maternal mood, gut microbial ecology, and fetal brain development, and identify the maternal gut microbiota and its metabolites as potential therapeutic targets to prevent the intergenerational effects of antenatal depression.},
}

Female
Pregnancy
Humans
*Gastrointestinal Microbiome/physiology
*Dysbiosis/microbiology
*Depression/microbiology/complications
Fecal Microbiota Transplantation
Adult
Case-Control Studies
*Pregnancy Complications/microbiology/psychology
Prospective Studies
Butyrates/metabolism
Bacteria/classification/genetics/isolation & purification/metabolism
*Prenatal Exposure Delayed Effects
Feces/microbiology
Infant
Brain/growth & development/metabolism
*Neurodevelopmental Disorders/etiology
RNA, Ribosomal, 16S/genetics

@article {pmid42145753,
year = {2026},
author = {Wu, Y and Yan, H and Li, P and Liu, Y and Leng, J and Cui, Y and Lv, X and Pang, L and Zang, N},
title = {Bridging the gaps: the gut-lung axis and microbial metabolites in the pathogenesis and treatment of pulmonary fibrosis.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1817835},
pmid = {42145753},
issn = {2296-858X},
abstract = {Pulmonary fibrosis (PF) is a chronic interstitial lung disease characterized by structural damage to the lung parenchyma, excessive deposition of extracellular matrix (ECM), and irreversible decline in lung function. Current pharmacological treatments cannot effectively reverse fibrosis, highlighting an urgent need for novel therapeutic targets. Recently, the gut-lung axis and its bidirectional communication have received increasing attention for their roles in PF progression. Metabolites derived from gut microbiota, including short-chain fatty acids (SCFAs), bile acids, tryptophan metabolites, lipopolysaccharides (LPS), and trimethylamine N-oxide, regulate immune responses, modulate signaling pathways, influence epigenetic modifications, and maintain intestinal barrier integrity, thereby exerting bidirectional effects on PF. Protective metabolites primarily inhibit fibroblast activation and collagen deposition, whereas pathological metabolites promote fibrosis by inducing inflammatory responses and oxidative stress. Potential therapeutic strategies targeting the gut-lung axis include fecal microbiota transplantation (FMT), probiotic and dietary interventions, and Traditional Chinese Medicine (TCM). However, clinical applications face challenges such as donor standardization, immunological safety, and consistency of therapeutic efficacy. Critical limitations remain, including reliance on acute-injury animal models that inadequately represent the chronic, irreversible nature of human PF. Translating findings across distinct PF subtypes requires caution, as their genetic architectures, immune landscapes, and microbiome interactions may differ considerably. Additionally, the causal relationship between microbial dysbiosis and fibrosis remains unclear, and clinical translation currently lacks stratified intervention strategies based on biomarkers. Future research should prioritize large-scale longitudinal cohort studies, integrated multi-omics analyses, organoid models, and gut-lung chip platforms to identify key effector molecules and therapeutic targets, ultimately facilitating precise clinical interventions targeting the gut-lung axis.},
}

@article {pmid42146050,
year = {2026},
author = {Huang, X and Yang, X and Yu, Y and Huang, J and Tao, W and Yu, R},
title = {Bibliometric analysis of human microbiota-associated animal model (2005-2025).},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1777297},
pmid = {42146050},
issn = {1664-302X},
abstract = {BACKGROUND: The research on human microbiota-associated (HMA) animal models is an important tool for studying the human microbiome and holds great potential for elucidating disease mechanisms and microbe-based therapeutic interactions. However, a systematic bibliometric assessment of this field has been limited.

METHODS: This study employed bibliometric methods, retrieving relevant publications published between 2005 and 2025 from the Web of Science Core Collection, Scopus, and PubMed, and visualizing the data with VOSviewer and CiteSpace.

RESULTS: The analysis revealed a continuous upward trend in the number of publications on this topic. The United States and its research institutions contributed the most and maintained close collaborations with multiple countries. The majority of the articles appeared in journals such as Gut Microbes, Microbiome, and Proceedings of the National Academy of Sciences of the United States of America (PNAS). Keyword and highly-cited reference analyses focused on the application of these models in investigating disease mechanisms and therapeutic exploration, particularly for metabolic, gastrointestinal, oncological, and neurodegenerative diseases. In addition, the impact of modeling factors such as diet and host genetics on the models has also attracted attention.

CONCLUSION: HMA animal models have become a core platform linking clinical and basic microbiology research, demonstrating unique advantages in recapitulating disease-associated microbial features and phenotypes. Nevertheless, because these models are essential for testing causal links between microbiota and disease, methodological standardization and procedural refinement are needed to enhance reproducibility and clinical applicability.},
}

@article {pmid42146068,
year = {2026},
author = {Xie, X and Yan, W and Gan, C and Xiong, W and Huang, Y and Lin, L and Lei, X and Ke, W and Chai, Y and Tang, H and Zhu, H},
title = {Tongxie Yaofang ameliorates IBS-D by targeting the gut microbiota-derived tryptophan metabolites and AhR signaling axis.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1786701},
pmid = {42146068},
issn = {1664-302X},
abstract = {BACKGROUND AND AIMS: Tongxie Yaofang (TXYF) is a classic prescription for IBS-D with liver depression and spleen deficiency, with its therapeutic mechanisms requiring further elucidation. This study investigated the modulatory effects of TXYF on the gut microbiota and microbiota-derived metabolism in an IBS-D rat model to elucidate the underlying mechanisms.

METHODS: HPLC was employed to identify the main components of TXYF. An IBS-D rat model was replicated using a triple-factor approach that combined neonatal maternal separation, chronic restraint stress, and oral gavage of Sennae folium decoction. To elucidate the mechanisms underlying the effects of TXYF on IBS-D, the gut microbiota was assessed by 16S rRNA sequencing, and microbial metabolites were profiled via untargeted metabolomics. Furthermore, key regulatory factors were examined by immunohistochemistry (IHC), reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and western blotting. Finally, fecal microbiota transplantation (FMT) was performed to validate the pathogenic role of the microbiota and the therapeutic potential of TXYF.

RESULTS: TXYF significantly alleviated IBS-D symptoms in rats, including diarrhea and abdominal pain, and improved both depressive-like behavior and intestinal barrier function. Treatment with TXYF increased the abundance of Bifidobacterium in the gut microbiota and promoted the microbial-related metabolic conversion of tryptophan (TRP) to 5-hydroxyindoleacetic acid (5-HIAA), indole-3-acetic acid (IAA), tryptamine, 5-hydroxytryptamine (5-HT), and 2-oxindole. These metabolites activated the aryl hydrocarbon receptor (AhR) signaling pathway, thereby inhibiting MLC phosphorylation and decreasing MLCK expression, and ultimately restoring intestinal barrier function. Furthermore, the FMT experiment demonstrated that the microbiota from TXYF-treated rats significantly ameliorated IBS-D by activating the AhR signaling pathway.

CONCLUSION: TXYF may alleviate IBS-D symptoms and restore barrier function by increasing the abundance of Bifidobacterium, restoring tryptophan metabolism, and activating the AhR pathway.},
}

@article {pmid42148715,
year = {2026},
author = {Li, ZP and Hu, Y and Chen, L and Cheng, J and Huang, YF and Huang, WF and Yi, LT},
title = {Fungicide Chlorothalonil Exposure Induced Intestinal Impairment via the Microbiota/Sphinganine/Ferroptosis Axis.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.6c01962},
pmid = {42148715},
issn = {1520-5118},
abstract = {Chlorothalonil is linked to gastrointestinal toxicity, but its underlying mechanisms remain unclear. This study investigated the chlorothalonil-induced intestinal injury in mice. Histological analysis showed epithelial damage and goblet cell depletion. Chlorothalonil disrupted the gut microbiota, including the depletion of Lactobacillus and the enrichment of Enterococcus. Untargeted metabolomics revealed a reduction in sphinganine, which is associated with oxidative stress and ferroptosis. Molecular analysis indicated ferroptosis activation via the Keap1/Nrf2 pathway, evidenced by decreased glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11) expression. Prussian blue staining and transmission electron microscopy confirmed iron deposition and mitochondrial injury, hallmark features of ferroptosis. Fecal microbiota transplantation confirmed dysbiosis as a driver of injury, while ferrostatin-1 treatment partially rescued the pathological phenotype. These findings demonstrate that chlorothalonil causes microbiota dysbiosis and decreases sphinganine, which inactivates Nrf2 signaling and results in ferroptosis. Our study provides new mechanistic insights into the toxicological mechanisms of chlorothalonil.},
}

@article {pmid41881081,
year = {2026},
author = {Ren, J and Perhat, SH and Gao, M and Hao, C and Nuertai, M and Li, Y},
title = {Characterized polyphenols from Prunus cerasifera alleviated HFD-induced intestinal inflammation and barrier dysfunction in obese mice by remodeling the gut microbiota and short-chain fatty acid profile.},
journal = {Fitoterapia},
volume = {191},
number = {},
pages = {107203},
doi = {10.1016/j.fitote.2026.107203},
pmid = {41881081},
issn = {1873-6971},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Fatty Acids, Volatile/metabolism ; Mice ; Mice, Inbred C57BL ; Male ; *Obesity/drug therapy ; Diet, High-Fat/adverse effects ; *Polyphenols/pharmacology ; Mice, Obese ; Inflammation/drug therapy ; Fecal Microbiota Transplantation ; },
abstract = {Our previous study demonstrated that PPE alleviates NAFLD by modulating cholesterol and bile acid metabolism; to further investigate whether additional mechanisms are involved in PPE intervention of ameliorated obesity-associated intestinal inflammation and barrier dysfunction, particularly via the gut microbiota - SCFA axis, we conducted this study. PPE significantly reduced weight gain in HFD-induced obese mice, alleviated dyslipidemia and liver function impairment, and decreased ectopic fat deposition, with H-PPE showing superior efficacy to L-PPE. Moreover, H-PPE outperformed L-PPE in mitigating obesity-related intestinal inflammation and barrier integrity, shown by decreased expression of inflammatory cytokines and enhanced expression of tight junction proteins. Targeted SCFAs analysis demonstrated that H-PPE normalized the disrupted SCFA profile in obese mice, with marked decreases in T-SCFAs, acetate, isobutyrate, and isovalerate levels. The H-PPE supplementation induced a favorable microbiota shift in obese mice, characterized by expansion of SCFA producers (Lactobacillus, Alistipes, Candidatus Saccharimonas) and a promoter of gut barrier integrity (Akkermansia). Finally, FMT revealed that PPE attenuates obesity-associated intestinal inflammation via gut microbiota remodeling and SCFA modulation. Thus, PPE, particularly H-PPE, mitigates obesity-related intestinal inflammation and barrier dysfunction by restructuring the gut microbiota in obese mice, an effect that leads to suppressed intestinal production of acetate, isobutyrate, and isovalerate.},
}

Animals
*Gastrointestinal Microbiome/drug effects
*Fatty Acids, Volatile/metabolism
Mice
Mice, Inbred C57BL
Male
*Obesity/drug therapy
Diet, High-Fat/adverse effects
*Polyphenols/pharmacology
Mice, Obese
Inflammation/drug therapy
Fecal Microbiota Transplantation

@article {pmid42138670,
year = {2026},
author = {Khanna, S and Allegretti, JR and Hashash, JG and Feuerstadt, P},
title = {AGA Clinical Practice Update on Management of Clostridioides difficile Infection in Inflammatory Bowel Disease: Expert Review.},
journal = {Gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.1053/j.gastro.2026.03.008},
pmid = {42138670},
issn = {1528-0012},
abstract = {DESCRIPTION: Clostridioides difficile infection (CDI) remains a significant driver of disease flares and poor outcomes in patients with inflammatory bowel disease (IBD), leading to increased hospitalization, intensified or failed therapy, and higher surgical rates. Compared with the non-IBD population, patients with IBD face greater CDI risk and severity and higher recurrence risk, creating clinical dilemmas when considering antibiotic selection and the timing or necessity of IBD-related therapy adjustments. Emerging evidence highlights microbiota-based therapies such as unapproved fecal microbiota transplantation or US Food and Drug Administration-approved donor-derived therapies as a promising therapeutic avenue for recurrent CDI in patients with IBD, reflecting a growing emphasis on microbiome-directed interventions. This review examines the evolving literature, considering the diagnosis and management strategies and offering pragmatic guidance to optimize outcomes for patients with IBD challenged by concomitant CDI and recurrent CDI.

METHODS: This Expert Review was commissioned and approved by the American Gastroenterological Association (AGA) Institute Clinical Practice Updates Committee and the AGA Governing Board to provide timely guidance on a topic of high clinical importance to the AGA membership and underwent internal peer review by the Clinical Practice Updates Committee and external peer review through standard procedures of Gastroenterology. These practical Best Practice Advice statements were drawn from a review of the best available published evidence, including existing clinical studies, systematic reviews and practice guidelines, and expert opinion. Because a formal systematic review was not performed, these Best Practice Advice statements do not carry formal ratings of the quality of evidence or strength of the presented considerations. The focus is on the management of both CDI and IBD in patients with underlying IBD who develop CDI. Best Practice Advice Statements BEST PRACTICE ADVICE 1: In patients with IBD who have new or worsening diarrhea, CDI should be excluded, especially among those with colonic involvement, as they are at increased risk of CDI. Clinicians should consider and treat CDI in patients with end ileostomy or ileo-anal pouch anastomosis with worsening diarrhea. BEST PRACTICE ADVICE 2: In patients with IBD and suspected CDI, a multistep toxin-based assay should be used for diagnostic evaluation. BEST PRACTICE ADVICE 3: In patients with IBD and recent CDI who have been treated successfully with antibiotics, recurrent diarrhea should prompt retesting for CDI. BEST PRACTICE ADVICE 4: In patients with IBD who develop an initial episode of CDI, clinicians should preferentially use fidaxomicin or use vancomycin if fidaxomicin is unavailable or cost-prohibitive. Metronidazole should not be used. BEST PRACTICE ADVICE 5: Clinicians should strongly consider hospitalization for patients with IBD and CDI who demonstrate features of severe colitis or systemic toxicity (eg, more than 6 bowel movements per day, severe abdominal pain, marked leukocytosis, hemodynamic instability, or other evidence of sepsis). BEST PRACTICE ADVICE 6: When selecting an immunosuppressive therapy to treat IBD, no class or mechanism of action has a differential risk of CDI and, therefore, clinicians should choose the therapy that is best to treat the IBD. BEST PRACTICE ADVICE 7: In patients with IBD and acute CDI, concurrent treatment of IBD is critical and clinicians should continue therapy with the required immunosuppressive therapies (ie, immunomodulators, biologics, or small molecules). Steroids can also be used if deemed necessary while CDI is treated with antibiotics. BEST PRACTICE ADVICE 8: Clinicians should consider endoscopic evaluation for IBD activity and exclusion of concomitant cytomegalovirus infection if symptoms persist 48-72 hours after initiation of treatment for CDI. BEST PRACTICE ADVICE 9: Clinicians may consider loperamide in patients with improving inflammation and infection but ongoing diarrhea. BEST PRACTICE ADVICE 10: Clinicians should offer microbiome-based therapies (eg, fecal microbiota, live-jslm, fecal microbiota spores, live-brpk, or unapproved fecal microbiota transplantation) to patients with IBD with at least 1 recurrence of CDI to prevent future infection. BEST PRACTICE ADVICE 11: In patients with IBD, clinicians should not advise probiotics for primary or secondary prevention of CDI. BEST PRACTICE ADVICE 12: In patients with IBD and a history of CDI who are receiving systemic antibiotics, clinicians may consider oral vancomycin prophylaxis as secondary prevention.},
}

@article {pmid42132696,
year = {2026},
author = {Zhou, Z and Pan, X and Ni, J and Lou, Z and Shen, Y and Jiang, S and Dong, X and Wang, F and Chen, Y and Li, L},
title = {Akkermansia muciniphila ameliorates acute liver injury aggravated by MASLD-associated dysbiosis via daidzein/PPAR-α/NF-κB signaling.},
journal = {Food & function},
volume = {},
number = {},
pages = {},
doi = {10.1039/d6fo01338d},
pmid = {42132696},
issn = {2042-650X},
abstract = {Existing evidence indicates that pre-existing metabolic dysfunction-associated steatotic liver disease (MASLD) confers susceptibility to acute liver injury (ALI). Nevertheless, the underlying mechanism prompting ALI risk in such a condition is not fully uncovered yet. Gut dysbiosis has been well-documented in MASLD patients which prompts us to hypothesize that gut dysbiosis may serve as a contributing factor and a regulatory target to ALI susceptibility. A case-control study was performed and the increased risk of ALI in MASLD patients was verified. Mice pretreated with MASLD mouse/patient-derived fecal microbiota transplantation (FMT) demonstrated worsened ALI after D-GalN/LPS injection. We identified significant gut dysbiosis with decreased microbial α-diversity, beneficial genus Lactobacillus, and increased potentially harmful bacteria Campylobacter and Helicobacter. Probiotic Akkermansia muciniphila (A. muciniphila) was reported to improve gut dysbiosis. Thus, we tested the effect of A. muciniphila on ALI mice pretreated with MASLD mouse-derived FMT. A. muciniphila significantly ameliorated the worsened ALI and improved gut dysbiosis. Transcriptomic analysis revealed that A. muciniphila restored the impaired liver PPAR-α signaling, alleviating the aggravated NF-κB signaling and downstream inflammation response in the liver. Specifically, A. muciniphila restored the decreased abundance of the PPAR-α agonist daidzein in the colon, thereby restoring PPAR-α activation and inhibiting NF-κB signaling in the liver. Daidzein is also capable of ameliorating ALI aggravated by MASLD-associated dysbiosis, accompanied by PPAR-α activation and NF-κB inhibition. Our findings revealed that gut dysbiosis in MASLD increased the risk of ALI. A. muciniphila exhibited preventive potential for MASLD patients to reduce ALI risk. Daidzein/PPAR-α/NF-κB signaling is important to maintain host resistance to hepatoxic challenge.},
}

@article {pmid42134452,
year = {2026},
author = {Sharma, AK and Akhtar, MS and Orayj, K and Farooqui, S and Khan, A and Sharma, G},
title = {Microbial dysbiosis in metabolic disorders: linking epigenomic regulation and pathological mechanisms.},
journal = {Drug discovery today},
volume = {},
number = {},
pages = {104698},
doi = {10.1016/j.drudis.2026.104698},
pmid = {42134452},
issn = {1878-5832},
abstract = {Microbial dysbiosis critically contributes to metabolic disorders by altering host-microbiome interactions and disrupting metabolic homeostasis. This review highlights how dysbiosis-derived metabolites, including short-chain fatty acids (SCFA) and trimethylamine-N-oxide (TMAO), modulate epigenetic mechanisms such as DNA methylation, histone modification, and non-coding RNA expression in key metabolic tissues. These epigenomic changes impair insulin signaling, lipid metabolism, and inflammatory responses. We further explore the potential of microbial-epigenetic biomarkers for early diagnosis of metabolic disease. Moreover, we assess emerging microbiome-based therapies including prebiotics, SCFA supplementation, and fecal microbiota transplantation for their ability to reverse epigenetic dysregulation. Understanding the microbiome-epigenome-metabolism axis may enable precision diagnostics and targeted interventions for obesity, type 2 diabetes, and related disorders.},
}

@article {pmid42134502,
year = {2026},
author = {Li, T and Jiang, M and Chen, L and Dong, H and Yu, J and Chen, J and Wang, X},
title = {A neutral polysaccharide from the pulp of Trichosanthes kirilowii Maxim mitigates constipation through microbiota-dependent activation of brain-gut axis.},
journal = {Journal of ethnopharmacology},
volume = {},
number = {},
pages = {121845},
doi = {10.1016/j.jep.2026.121845},
pmid = {42134502},
issn = {1872-7573},
abstract = {Trichosanthes kirilowii Maxim, known as "Gualou" in traditional Chinese medicine, has been extensively utilized to cure various diseases. Nevertheless, the precise mechanism through which TKPW, a neutral polysaccharide isolated from the pulp of Trichosanthes kirilowii Maxim by water elution, alleviates constipation remains to be fully elucidated.

AIM OF THE STUDY: To investigate the efficacy of TKPW in alleviating constipation in mice and to clarify the mechanisms.

MATERIALS AND METHODS: TKPW was isolated, structurally characterized, and evaluated for its anti-constipation effect in diphenoxylate-induced mice. Fecal parameters, biochemical markers, gut microbiota were analyzed, and the microbiota's role was substantiated using a fecal microbiota transplantation (FMT) trial.

RESULTS: TKPW was characterized as a heteropolysaccharide with average molecular weight of 12.431 kDa, featuring a backbone of α-D-Glcp-(1→5)-Araf-(1→6)-α-D-Galp-(1→ 6)-α-D-Glcp-(1→. High-dose TKPW (TKPW-H) treatment significantly improved fecal output, gastrointestinal transit rate, and colonic morphology in constipated mice. Concurrently, pro-inflammatory cytokine levels were markedly diminished by TKPW-H, alongside a significant increase in tight-junction protein expression. Additionally, TKPW-H selectively promoted excitatory enteric neurotransmitters and suppressed inhibitory ones. TKPW-H resulted in a significant suppression of colonic vasoactive intestinal peptide receptor 1 (VIPR1) expression, accompanied by a concurrent upregulation of 5-hydroxytryptamine receptor 4 (HTR4). Importantly, TKPW-H enhanced the relative abundance of beneficial bacteria, elevated the fecal concentrations of short-chain fatty acids (SCFAs), and activated the cerebral receptors (GPR41, GPR43 and GPR109a). FMT from TKPW-treated donors reproduced the anti-constipation effects.

CONCLUSION: TKPW supplementation alleviates constipation through modulation of the microbiota-brain-gut axis, underscoring its potential as a prebiotic therapeutic agent.},
}

@article {pmid42135927,
year = {2026},
author = {Li, Z and Li, P and Peng, T and Zhou, X and Liu, Y and Ai, C and Xiao, N and Song, S and Lei, X and Liu, J and Wang, W and Zhou, P and Li, Z and Liu, Z and Dai, X and Zhang, Z and Li, T},
title = {Indole-3-carboxaldehyde from Limosilactobacillus reuteri targets the DUSP1/ERK/NOX2/ROS axis to enhance the bactericidal activity of macrophages and protects against sepsis.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2671382},
doi = {10.1080/19490976.2026.2671382},
pmid = {42135927},
issn = {1949-0984},
mesh = {*Limosilactobacillus reuteri/metabolism/chemistry ; Animals ; *Macrophages/drug effects/immunology/metabolism/microbiology ; Humans ; *Sepsis/microbiology/prevention & control/immunology/metabolism ; Mice ; *Dual Specificity Phosphatase 1/metabolism/genetics ; Male ; Reactive Oxygen Species/metabolism ; *Indoles/pharmacology/metabolism ; *NADPH Oxidase 2/metabolism/genetics ; Female ; Disease Models, Animal ; Gastrointestinal Microbiome ; Mice, Inbred C57BL ; Middle Aged ; },
abstract = {The gut microbiota plays a critical regulatory role in the pathogenesis of sepsis, yet the immunomodulatory mechanisms of Limosilactobacillus reuteri (L. reuteri) and its metabolites in sepsis remain to be fully elucidated. This study found that the abundance of intestinal L. reuteri was significantly reduced in patients with bacterial sepsis and showed a negative correlation with disease severity. In a mouse model of sepsis induced by cecal ligation and puncture, fecal microbiota transplantation and live bacterial supplementation further confirmed that live L. reuteri effectively attenuated sepsis progression. Integrated metabolomic and network pharmacological analysis identified indole-3-carboxaldehyde (IAld), a metabolite derived from L. reuteri, which enhances macrophage bactericidal function and alleviates sepsis-associated organ damage. Mechanistically, IAld directly targets DUSP1 in macrophages, inhibits its phosphatase activity, thereby promoting ERK phosphorylation, upregulating NOX2 expression, stimulating reactive oxygen species production, and ultimately enhancing bacterial clearance. Notably, circulating IAld levels in septic patients were significantly inversely correlated with SOFA score, APACHE II score, and arterial lactate levels, and IAld safely enhanced the bactericidal function of human macrophages in vitro. This study is the first to systematically demonstrate that L. reuteri and its metabolite IAld exert a protective effect against sepsis through the DUSP1/ERK/NOX2/ROS axis, providing novel mechanistic insights and potential therapeutic targets for immunometabolic intervention in sepsis.},
}

*Limosilactobacillus reuteri/metabolism/chemistry
Animals
*Macrophages/drug effects/immunology/metabolism/microbiology
Humans
*Sepsis/microbiology/prevention & control/immunology/metabolism
Mice
*Dual Specificity Phosphatase 1/metabolism/genetics
Male
Reactive Oxygen Species/metabolism
*Indoles/pharmacology/metabolism
*NADPH Oxidase 2/metabolism/genetics
Female
Disease Models, Animal
Gastrointestinal Microbiome
Mice, Inbred C57BL
Middle Aged

@article {pmid42136241,
year = {2026},
author = {Singh, R and Monika, and Mazumder, R and Mazumder, A and Singh, M and Majee, C and Padhi, S and Das, S},
title = {Chronic Inflammation (A Silent Killer) - Molecular Mechanisms and Emerging Therapeutic Approaches.},
journal = {Current drug targets},
volume = {},
number = {},
pages = {},
doi = {10.2174/0113894501450885260409050432},
pmid = {42136241},
issn = {1873-5592},
abstract = {Chronic inflammation is a dysregulated and persistent immune response that underlies numerous serious health conditions, like heart problems, diabetes, nerve damage, cancer, or conditions where the body attacks itself. Recently, scientists have gained a better understanding of how molecules such as cytokines and chemokines, along with dysregulated immune cells, contribute to excessive oxidative stress and impaired healing processes. New tools now help identify this condition as early as possible through biomarkers, advanced laboratory techniques, integrated data approaches, and smart sensors that track biological changes in real time. However, despite this knowledge, effective strategies for early prevention and long-term treatment remain limited. Daily habits, particularly anti-inflammatory dietary patterns, regular physical activity, and stress management, play a critical role in reducing the risk of disease. Emerging therapies, including inflammasome inhibitors, cytokine-targeted biologics, immunometabolic modulators, and specialized pro-resolving mediators, may restore immune homeostasis rather than merely suppressing symptoms. Additionally, microbiome-targeted interventions-such as probiotics, prebiotics, bacteriophage therapy, and fecal microbiota transplantation-are increasingly being recognized as potential strategies to modulate systemic inflammation. Daily habits, especially eating patterns that fight inflammation, walking regularly, or handling stress, are critically important for lowering the chances of illness. Chronic inflammation is a complex, multifactorial process; therefore, its effective management requires integrated efforts in basic research, therapeutic innovation, and population- level healthcare strategies. Innovations in personalized medicine, AI-based analytics, digital health technologies, and microbiome science are poised to significantly enhance diagnostic and therapeutic approaches. Sustained cross-disciplinary collaboration will be critical in mitigating the worldwide impact of chronic inflammatory disorders and improving long-term health outcomes.},
}

@article {pmid42136267,
year = {2026},
author = {Saraswati, BD and Wicaksono, AW and Valles, SL and Poeggeler, B and Singh, SK},
title = {Exploring the Gut Microbiome as a Promising Frontier in Alzheimer's Disease Therapy.},
journal = {Current neuropharmacology},
volume = {},
number = {},
pages = {},
doi = {10.2174/011570159X444975260408044214},
pmid = {42136267},
issn = {1875-6190},
abstract = {Alzheimer's Disease (AD) is a major global health challenge, particularly in ageing populations, and current therapies offer limited modification of disease progression. Emerging evidence indicates that the gut microbiome contributes to AD pathogenesis through metabolic, immune, and neuroendocrine mechanisms. Microbial metabolites, including Short-Chain Fatty Acids (SCFAs), bile acids, and trimethylamine-N-oxide (TMAO), regulate neuronal signalling and blood-brain barrier integrity, and dysbiosis has been linked to amyloid-β (Aβ) accumulation, tau hyperphosphorylation, chronic neuroinflammation, oxidative stress, and synaptic dysfunction. Host genetic factors, particularly APOE ε4 and immune-regulatory variants such as TREM2 and CD33, further influence microbial composition and susceptibility to metabolite-driven pathology. This review provides a deeper synthesis of current evidence by integrating findings across multi-omics studies and identifying key unresolved issues in the microbiome-AD field. The discussion evaluates whether microbiome alterations act as early initiators or downstream consequences of neurodegeneration, examines sources of heterogeneity in microbiome-targeted interventions, and considers how inter-individual variability in host genetics and microbial ecology may inform precision therapeutics. Conceptual frameworks presented here, including a two-phase dysbiosis trajectory and a metabolite "tipping-point" network, aim to reconcile conflicting results and support the development of testable mechanistic hypotheses. Microbiome-directed strategies, such as probiotics, prebiotics, dietary modulation, faecal microbiota transplantation, and antiviral therapies, demonstrate promise but require rigorous mechanistic validation and methodological standardisation. Continued advancement in longitudinal, genotype-stratified, and multi-omics research will be essential for translating microbiome science into clinically actionable approaches. Overall, current evidence positions the gut microbiome as a compelling frontier for the development of personalised, diseasemodifying strategies in AD.},
}

@article {pmid42136277,
year = {2026},
author = {Saxena, V and Singh, V and Sanskriti, },
title = {Translational Perspectives on Anti-Inflammatory Interventions for Neurodegenerative Disorders: Evidence from Gut-Brain Axis.},
journal = {Central nervous system agents in medicinal chemistry},
volume = {},
number = {},
pages = {},
doi = {10.2174/0118715249430752260407050033},
pmid = {42136277},
issn = {1875-6166},
abstract = {The Gut-Brain Axis (GBA) has a complex role in chronic neuroinflammation, which is increasingly connected to neurodegenerative diseases (NDDs) such as Multiple Sclerosis (MS), Parkinson's Disease (PD), and Alzheimer's Disease (AD). Through neuronal, endocrine, and immunological pathways, the GBA enables twoway communication between the gastrointestinal tract and the central nervous system. According to recent research, the pathophysiology of neuroinflammatory responses in NDDs may be significantly influenced by gut dysbiosis, increased intestinal permeability, and modified microbial metabolites, such as Short-Chain Fatty Acids (SCFAs) and polyphenols. This study summarizes preclinical and clinical data supporting several anti- inflammatory approaches targeting GBA. Probiotics and fecal microbiota transplantation are two examples of microbiota-based treatments that have demonstrated promise in reducing neuroinflammatory responses and enhancing cognitive performance. Mediterranean and polyphenol-rich diets are among the dietary therapies that show promise in modifying the composition of microorganisms, lowering pro-inflammatory signaling, and enhancing neuroprotection. Through microbiota regulation, pharmacological substances such as curcumin, resveratrol, and SCFA mimetics also have anti-neuroinflammatory benefits. However, a number of translational challenges still exist, including limitations in animal models, a lack of standardized therapies, and inter-individual microbiome heterogeneity. In order to provide precise, GBA-targeted therapies, future views place a strong emphasis on integrating multi-omics, artificial intelligence, and personalized medicine. This study highlights a new therapeutic approach to treating neurodegeneration by examining the translational potential of anti- inflammatory therapies targeting GBA. It also emphasizes the necessity of strong clinical studies to confirm these findings.},
}