@article {pmid42599328,
year = {2026},
author = {Mengistu, DA and Mekasha, YT and Molla, FW},
title = {Non-Drug therapeutic strategies to combat antimicrobial resistance in livestock: a review.},
journal = {Molecular biology reports},
volume = {53},
number = {1},
pages = {},
pmid = {42599328},
issn = {1573-4978},
mesh = {Animals ; *Livestock/microbiology/genetics ; Humans ; Probiotics/therapeutic use ; Phage Therapy ; CRISPR-Cas Systems ; *Drug Resistance, Microbial ; Anti-Infective Agents ; Fecal Microbiota Transplantation ; Anti-Bacterial Agents ; Genetic Engineering/methods ; },
abstract = {BACKGROUND: Antimicrobial resistance (AMR) represents an escalating global public health crisis, projected to cause 10 million deaths annually by 2050. Pathogens such as bacteria, viruses, fungi, and parasites evade treatments in animals and humans due to overuse and misuse of antimicrobials, particularly antibiotics, in medical and veterinary practices. This drives a worldwide surge in resistant infections, disproportionately burdening livestock health and productivity.

OBJECTIVES: This review examines the global rise of AMR and its impacts on livestock and public health, underscoring the need for non-drug therapeutic alternatives.

CONCLUSION: Promising alternatives include genetic engineering and CRISPR-Cas systems, phage therapy, probiotics, antimicrobial peptides, fecal microbiota transplantation, phytotherapy and essential oils, immunomodulators, nanotechnology, biofilm disruptors, acidifiers, vaccination strategies, and precision livestock farming. These approaches target resistance mechanisms without relying on conventional drugs. Despite challenges like knowledge gaps, regulatory barriers, financial limitations, and policy gaps, stakeholders must prioritize accelerated research, regulatory reforms, investments, and international collaboration. Rapid integration of these technologies into human and veterinary medicine is vital to mitigate AMR's health, economic, and social impacts.},
}

Animals
*Livestock/microbiology/genetics
Humans
Probiotics/therapeutic use
Phage Therapy
CRISPR-Cas Systems
*Drug Resistance, Microbial
Anti-Infective Agents
Fecal Microbiota Transplantation
Anti-Bacterial Agents
Genetic Engineering/methods

@article {pmid42600364,
year = {2026},
author = {Liu, C and Zhang, H and Zhang, H and Zhao, Y and Wu, C and Lin, Q and Luo, Y and Wei, L and Chen, J and Rao, X and Xiong, S and Shen, H and Hong, S and Shi, Z and Yin, S and Lan, Z and Chen, L},
title = {Triphala ameliorates hyperuricemia-associated nephropathy by modulating the gut microbiota-glycerophospholipid-TLR4 axis.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {160},
number = {},
pages = {158694},
doi = {10.1016/j.phymed.2026.158694},
pmid = {42600364},
issn = {1618-095X},
abstract = {BACKGROUND: Hyperuricemia (HUA) is a metabolic disorder with an escalating global prevalence, and its progression to HUA-associated nephropathy represents an important contributor to chronic kidney injury. Emerging evidence highlights a bidirectional relationship between uric acid and lipid metabolism, with dyslipidemia contributing to the pathological progression of HUA-related complications. Triphala (TRP), a classic Tibetan herbal formula with broad metabolic regulatory properties, was selected as a potential intervention for the complex metabolic disturbances associated with HUA. However, its therapeutic efficacy and the precise molecular mechanisms underlying its effects in HUA remain to be fully elucidated.

PURPOSE: This study aimed to investigate the protective effects of TRP on hyperuricemia-associated nephropathy and to elucidate the underlying mechanisms.

METHODS: High-performance liquid chromatography (HPLC) was first employed to identify and quantify seven representative constituents in the TRP aqueous extract. To evaluate the efficacy of TRP, an HUA mouse model was established through the combined administration of intraperitoneal potassium oxonate injections and a yeast-containing diet. A multi-omics strategy integrating 16S rRNA sequencing, metabolomics and lipidomics elucidated TRP's impact on the gut microbiota and host metabolism. Critically, fecal microbiota transplantation (FMT), TLR4 blockade experiments, and in vitro assays were employed to evaluate the contribution of TRP-modulated microbiota and the LPC-TLR4 pathway to the protective effects of TRP.

RESULTS: HPLC identified chebulic acid, gallic acid, and corilagin as the major representative constituents of TRP aqueous extract. TRP dose-dependently reduced serum uric acid, improved renal function by lowering serum creatinine (Cr) and blood urea nitrogen (BUN) levels, increased the fractional excretion of uric acid (FEUA), and alleviated tubular injury and fibrosis. These improvements were accompanied by normalized urate transporters (downregulated URAT1/GLUT9; restored OAT1/OAT3) and suppressed renal inflammatory cytokines. Multi-omics analysis revealed that TRP reversed HUA-induced dysbiosis by suppressing opportunistic pathogens (e.g., Parasutterella, Allobaculum) and enriching beneficial genera (e.g., Bifidobacterium, Akkermansia), specifically reducing pro-inflammatory LPC (e.g., LPC16:0, LPC18:1). TRP and FMT effectively inhibited the TLR4/MyD88/NF-κB signaling axis and reduced LPC accumulation within the kidney. In vitro experiments validated that these specific LPC directly trigger TLR4 expression and TNF-α release, confirming the potential role of the microbiota-driven lysophospholipid-TLR4 pathway in HUA-associated chronic renal inflammation.

CONCLUSION: TRP ameliorates HUA and renal inflammation by remodeling the gut microbiota to suppress the aberrant accumulation of pro-inflammatory lysophospholipids, thereby deactivating the TLR4-mediated inflammatory cascade. These findings establish the gut microbiota-glycerophospholipid metabolism-renal inflammation axis as a potential therapeutic target and validate TRP as a relevant strategy for targeting the gut microbiome to treat systemic metabolic disease.},
}

@article {pmid42602177,
year = {2026},
author = {Azimzadeh, M and Ababzadeh, S and Kahaki, AG and Babaei, SMH and Seyedebrahimi, R and Farsani, ME},
title = {The Gut-Brain Axis in Neurodegeneration: Mechanistic Links Between Dysbiosis and Neuropathology.},
journal = {Iranian journal of pathology},
volume = {21},
number = {4},
pages = {507-522},
pmid = {42602177},
issn = {1735-5303},
abstract = {BACKGROUND & OBJECTIVE: The gut-brain axis is essentially a two-way communication system that physically connects the brain and the intestinal tract. The connection is mediated through a series of pathways, including neural, endocrine, and immune pathways. Gut dysbiosis, which is explained as an imbalance in the microbial community, has been linked to the causation of various neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis. However, the pathological mechanisms in the brain are only partially known. The present review outlines the process of gut dysbiosis and neurodegeneration, detailing the roles of protein aggregation, neuroinflammation, barrier disruption, and neuroglial dysfunction. Then, extending the comparison to a range of neurodegenerative diseases, we discuss the possibility of common pathway therapeutics and actual microbiome-based treatment options planning from the standpoint of microbiome-directed interventions.

CONTENT/FINDINGS: Gut dysbiosis triggers a definable cascade, starting with the disruption of the intestinal barrier and increased permeability (leaky gut), which allows bacterial products (lipopolysaccharides, bacterial amyloids) and pro-inflammatory cytokines to enter systemic circulation. Such peripheral changes weaken the blood-brain barrier and thus allow these factors to access the CNS, where they lead to neuroglial dysfunction (microglial priming, astrocytic reactivity, and oligodendrocyte injury) by disruption of glial homeostasis. CNS glial cell malfunction leads to the development of proteinopathies characteristic of each disease: amyloid and tau hyperphosphorylation in Alzheimer's disease through BACE1 upregulation and kinase activation; synuclein in Parkinson's disease via molecular mimicry, oxidative stress, and impaired clearance; and demyelination in multiple sclerosis through oligodendrocyte apoptosis. Oral bacteria such as Porphyromonas gingivalis aggravate this inflammatory loop through the direct invasion of the CNS and proteolytic cleavage of amyloid and tau. The vagus nerve is yet another pathway through which gut-derived inflammatory signals and pathological synuclein can be transmitted to the brain.

CONCLUSION: The gut microbiome is more than just a correlate of neurodegeneration; it actively promotes neurodegenerative diseases through pathways that can be mechanistically defined. Microbiome-targeted interventions such as dietary changes, precision probiotics, fecal microbiota transplantation, and anti-inflammatory agents offer a measure of hope for changing these pathological processes. Future studies need to be directed at determining the time sequence of cause and effect, finding dependable microbiota-based biomarkers, and formulating tailored strategies that can account for individual microbial composition variability, genetic susceptibility, and environmental exposures. A deeper understanding of the gut-brain axis from this mechanistic perspective could eventually lead to the prevention or postponement of neurodegeneration.},
}

@article {pmid42602314,
year = {2026},
author = {Wang, R and Li, H and Ge, R and Pan, Y and He, Z},
title = {Correlative study of Parnassia palustris extract on orthotopic glioma suppression and gut microbiota modulation in mice.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1843204},
pmid = {42602314},
issn = {1664-302X},
abstract = {OBJECTIVE: The gut microbiota is associated with brain tumor development and prognosis. Natural products are increasingly recognized for their therapeutic potential. Based on previously observed anti-glioma effects of Parnassia palustris (MHC) in vitro, this study evaluates the efficacy of its oral extract in an orthotopic glioma model and explores the correlative relationship between its antitumor activity and alterations in gut microbiota composition, without inferring causation.

METHODS: Four-week-old female Balb/c nude mice underwent intracranial implantation of RFP-U87 MG or U87 MG cells. Mice received intragastric administration of MHC extract (25 mg/kg every other day from day 6 to 24 post-implantation, n = 7) or PBS (n = 7). Untreated healthy mice served as controls (n = 6). Tumor growth was monitored via in vivo fluorescence imaging. Brain tissues and gliomas were collected for weighing, H&E, and IHC staining. Fecal samples were collected for gut microbiota analysis using Illumina high-throughput sequencing.

RESULTS: In vivo imaging and tumor weight measurements demonstrated that MHC significantly suppressed orthotopic glioma proliferation. H&E staining showed reduced tumor cell density, normalized nuclear-to-cytoplasmic ratio, and decreased nuclear atypia in the MHC group. IHC indicated that MHC inhibited the PI3K/Akt pathway, leading to decreased KI67 and increased p53 expression. MHC did not alter α-diversity but modulated the abundance of specific bacterial taxa, notably increasing Muribaculum intestinale, Bacteroides faecichinchillae, and Klebsiella oxytoca, while decreasing Lachnospiraceae bacterium A4 and Helicobacter japonicus. Compared to healthy controls, tumor-bearing mice exhibited distinct microbial profiles.

CONCLUSION: MHC extract significantly inhibits orthotopic glioma growth and is associated with compositional changes in the gut microbiota, including enrichment of Muribaculum intestinale and Bacteroides faecichinchillae. These correlational findings indicate a potential link between microbial shifts and anti-glioma effects; however, causality remains to be established. Future studies employing fecal microbiota transplantation, antibiotic depletion, or germ-free models are required to determine whether microbiota modulation directly mediates MHC's antitumor activity.},
}

@article {pmid42602359,
year = {2026},
author = {Fan, YM and Li, Y and Bi, HY and Ding, Y and Lyu, L and Geng, Y and Fu, W},
title = {Application and prospects of fecal microbiota transplantation in cancer therapy.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1880573},
pmid = {42602359},
issn = {2235-2988},
mesh = {*Fecal Microbiota Transplantation/methods/adverse effects ; Humans ; *Neoplasms/therapy ; Gastrointestinal Microbiome ; Tumor Microenvironment ; Animals ; Immunotherapy/methods ; },
abstract = {As the largest community of commensal microorganisms in the human body, the gut microbiota-through its structural and functional imbalances-participates in the entire process of tumor initiation and progression, and profoundly influences the efficacy and safety of conventional anticancer regimens, including chemotherapy and immunotherapy. Fecal microbiota transplantation (FMT) offers a novel biological strategy for cancer treatment by reestablishing the ecological balance of the host gut microbiota. This review systematically integrates the basic theory, clinical practice, technical optimization, epidemiological features, current challenges, and future directions of FMT in oncology. It elaborates on how FMT modulates the tumor microenvironment via core mechanisms such as immune regulation, metabolic reprogramming, and intestinal barrier repair, and shows potential value in enhancing immunotherapy responses, improving chemotherapy tolerance, and alleviating treatment-related complications across various malignancies, including colorectal cancer, liver cancer, and melanoma. Meanwhile, the article outlines practical difficulties regarding donor screening, formulation standardization, ethical oversight, and long-term safety evaluation of FMT, and looks ahead to the development of precision FMT, synthetic microbial consortia, integration of multi-omics technologies, and combination treatment paradigms. The aim is to provide a comprehensive, systematic, and academically in-depth reference for the translational and basic research of FMT in precision cancer therapy.},
}

*Fecal Microbiota Transplantation/methods/adverse effects
Humans
*Neoplasms/therapy
Gastrointestinal Microbiome
Tumor Microenvironment
Animals
Immunotherapy/methods

@article {pmid42602487,
year = {2026},
author = {Niu, M and Li, F and Hao, Z and Dou, J and Xu, Z and Jia, K},
title = {Research progress on the mechanisms and intervention strategies of microbiota-gut-brain axis dysfunction under heat stress.},
journal = {Frontiers in physiology},
volume = {17},
number = {},
pages = {1897985},
pmid = {42602487},
issn = {1664-042X},
abstract = {Heat stress (HS), as an important environmental stressor in the context of global warming, profoundly affects body health by disrupting the Microbiota-Gut-Brain Axis (MGBA). This review provides a critical synthesis of the mechanisms underlying MGBA disruption under HS. HS initially induces gut microbiota imbalance, which subsequently disrupts the intestinal mechanical and immune barriers, thereby interfering with the bidirectional gut-brain signaling mediated by pathways such as the vagus nerve. Based on the above mechanisms, this review further explores MGBA-centered therapeutic strategies, including microbiota-oriented therapies such as probiotics, prebiotics, synbiotics, postbiotics, and fecal microbiota transplantation to reshape gut ecology, as well as the use of metabolites for targeted therapy. Finally, this article looks forward to future research directions in this field, emphasizing the exploration of molecular mechanisms and the search for key targets.},
}

@article {pmid42603146,
year = {2026},
author = {Zhang, R and Li, H and Wang, C and Yang, G},
title = {Synthetic microbial communities: emerging live biotherapeutics for targeted gut microbiome modulation.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2719056},
doi = {10.1080/19490976.2026.2719056},
pmid = {42603146},
issn = {1949-0984},
mesh = {Humans ; Animals ; Fecal Microbiota Transplantation/methods ; *Gastrointestinal Microbiome ; Inflammatory Bowel Diseases/therapy/microbiology ; *Biological Therapy/methods ; *Dysbiosis/therapy/microbiology ; Clostridium Infections/therapy/microbiology ; Colorectal Neoplasms/therapy/microbiology ; Clostridioides difficile ; },
abstract = {Gut microbiome dysbiosis causes various intestinal diseases. However, an undefined composition and potential biosafety risks limit the applicability of traditional fecal microbiota transplantation (FMT). Synthetic microbial communities (SynComs), which are compositionally defined and rationally designed emerging live biotherapeutics, offer a novel alternative to FMT. This review establishes strict boundaries between SynComs and traditional donor-derived preparations, comparatively evaluating "top-down" and "bottom-up" construction strategies. We explored the mechanisms underlying the SynComs-mediated synergistic restoration of intestinal homeostasis via direct targeted antagonism and modulation of the host immune network. Moreover, we systematically evaluated the current research landscape of SynComs in Clostridioides difficile infection, inflammatory bowel disease, and colorectal cancer. This review examines fundamental challenges, including host colonization resistance, chemistry, manufacturing, and control barriers, biosafety risks, and microbiokinetic regulatory frameworks, thereby addressing the translational gap. Our analysis of current literature provides a theoretical basis for the clinical translation of SynComs as emerging live biotherapeutics.},
}

Humans
Animals
Fecal Microbiota Transplantation/methods
*Gastrointestinal Microbiome
Inflammatory Bowel Diseases/therapy/microbiology
*Biological Therapy/methods
*Dysbiosis/therapy/microbiology
Clostridium Infections/therapy/microbiology
Colorectal Neoplasms/therapy/microbiology
Clostridioides difficile

@article {pmid42589563,
year = {2026},
author = {Shimizu, S and Tanaka, M and Tominaga, N and Fujinami, K and Takanashi, K and Dan, K},
title = {Generation and Application of Ultra-Fine, Long-Term Stable Nanobubble Water: An Evaluation of Inclusion Effects on Aromatic Components and Antimicrobial Activity.},
journal = {International journal of molecular sciences},
volume = {27},
number = {15},
pages = {},
pmid = {42589563},
issn = {1422-0067},
support = {#R2271U00606//New Energy and Industrial Technology Development Organization/ ; #1201002//Business Restructuring Grant/ ; },
mesh = {*Water/chemistry ; Ozone/chemistry/pharmacology ; Hydrogen/chemistry/pharmacology ; *Anti-Bacterial Agents/pharmacology/chemistry ; *Anti-Infective Agents/pharmacology/chemistry ; Fecal Microbiota Transplantation/methods ; Humans ; Microbial Sensitivity Tests ; },
abstract = {Nano- and pico-bubble water (NPB), containing hydrogen or ozone, is widely used as a cleaning agent due to its bactericidal and antiviral properties. However, some products-such as certain hydrogen waters-contain only large bubbles or have an extremely low bubble count, making them sometimes indistinguishable from ordinary drinking water. To accurately evaluate NPB activity, we developed a method for producing ultra-nano-pico-bubble water (NanoGAS water [NGW]), an ultra-fine bubble water that is stable and non-volatile over extended periods. By combining a mixed gas-liquid fluid rotary mixer and a shear filter, we produced ultra-fine bubbles that could be sealed in water. This method produced bubbles that remained stable in water even after 10 years since production. NGW has been clinically evaluated as a solvent for fecal microbiota transplantation (FMT) and has been demonstrated to be effective at improving bacterial engraftment in the intestinal tract in patients with autism spectrum disorder (ASD). Furthermore, encapsulating specific gases (hydrogen and ozone) can achieve more diverse effects. In this study, we evaluated the aroma-encapsulating effects, as well as the strength and persistence of the antimicrobial activity, of novel NGW formulations (Air-NGW, H2-NGW, S-O3-NGW, and L-O3-NGW). Both H2-NGW and O3-NGW generated in this study demonstrated slight inclusion activity with volatile aromatic compounds (citral). Furthermore, both H2-NGW (at ≥10% dilution) and O3-NGW (even at a 1% dilution) exhibited sustained antibacterial efficacy against general viable bacteria for 24 weeks. Moreover, additive effects were observed when combined with antibacterial and antiviral compounds (polyoxometalates) developed by the authors. While further consideration, including cost-effectiveness, is needed to translate these findings into practical applications, they provide a fundamental framework for future research.},
}

*Water/chemistry
Ozone/chemistry/pharmacology
Hydrogen/chemistry/pharmacology
*Anti-Bacterial Agents/pharmacology/chemistry
*Anti-Infective Agents/pharmacology/chemistry
Fecal Microbiota Transplantation/methods
Humans
Microbial Sensitivity Tests

@article {pmid42593554,
year = {2026},
author = {Xiao, J and Zha, Z and Liao, Z and Li, Z},
title = {Treatment with Roseburia intestinalis Relieves Symptoms of Chronic Kidney Disease (CKD) by Altering the Gut Microbiota and Increasing the Levels of Fecal SCFAs in Adriamycin-Induced CKD Rats.},
journal = {Current microbiology},
volume = {83},
number = {10},
pages = {},
pmid = {42593554},
issn = {1432-0991},
support = {82405007//the National Natural Science Foundation of China/ ; 20242BAB20468//The Foundation of the Jiangxi Province Department of Science and Technology Youth Project/ ; },
mesh = {Animals ; *Feces/chemistry/microbiology ; *Fatty Acids, Volatile/analysis/metabolism ; Rats ; *Gastrointestinal Microbiome/drug effects ; Male ; *Renal Insufficiency, Chronic/therapy/chemically induced/microbiology/drug therapy ; Doxorubicin/adverse effects ; *Probiotics/administration & dosage ; Fecal Microbiota Transplantation ; Disease Models, Animal ; Rats, Sprague-Dawley ; Kidney/pathology ; RNA, Ribosomal, 16S/genetics ; },
abstract = {This study investigated the therapeutic potential of the probiotic Roseburia intestinalis (R. intestinalis) in alleviating chronic kidney disease (CKD) symptoms and explored whether these effects are mediated through the modulation of the gut microbiota and fecal short-chain fatty acids (SCFAs). An Adriamycin (ADR)-induced CKD rat model was established, and the rats were treated with R. intestinalis via oral gavage for 8 weeks. Renal function, histopathology, and inflammatory markers were assessed. The gut microbiota composition was analyzed using 16 S rRNA sequencing, and SCFA levels were quantified by gas chromatography. To verify the underlying mechanism, fecal microbiota transplantation (FMT) was performed in germ-free CKD rats. The results demonstrate that R. intestinalis significantly mitigated CKD symptoms, including reduced proteinuria, serum creatinine, and renal inflammation, while reversing weight loss. The treatment restored gut microbial diversity, specifically by increasing the abundance of Firmicutes and fecal SCFA levels (acetate, propionate, and butyrate). Importantly, FMT from R. intestinalis-treated rats into germ-free CKD rats reversed these beneficial effects, whereas R. intestinalis alone under germ-free conditions was less effective, suggesting the need for a complex microbiome for full efficacy. These findings indicate that R. intestinalis is associated with alleviation of CKD symptoms by modulating the gut microbiota and enhancing fecal SCFA production, highlighting its potential as a promising probiotic intervention for CKD management and underscoring the role of the gut-kidney axis as a therapeutic target.},
}

Animals
*Feces/chemistry/microbiology
*Fatty Acids, Volatile/analysis/metabolism
Rats
*Gastrointestinal Microbiome/drug effects
Male
*Renal Insufficiency, Chronic/therapy/chemically induced/microbiology/drug therapy
Doxorubicin/adverse effects
*Probiotics/administration & dosage
Fecal Microbiota Transplantation
Disease Models, Animal
Rats, Sprague-Dawley
Kidney/pathology
RNA, Ribosomal, 16S/genetics

@article {pmid42596514,
year = {2026},
author = {Xu, J and Diao, A and Ai, R and Wu, X and Wen, Q and Xiao, Y and He, X and Yu, Y and Zhang, Z and Wang, Y and Zhang, Z and Zhang, F and Cui, B},
title = {Feasibility and Safety of Washed Microbiota Transplantation as Salvage Therapy for Refractory Non-CDI Gut Pathogens in Critically Ill Patients.},
journal = {Microbial biotechnology},
volume = {19},
number = {8},
pages = {e70431},
doi = {10.1111/1751-7915.70431},
pmid = {42596514},
issn = {1751-7915},
support = {BK20251961//Natural Science Foundation of Jiangsu Province/ ; K2023011//Jiangsu Provincial Health Commission/ ; },
mesh = {Humans ; *Salvage Therapy/methods/adverse effects ; *Fecal Microbiota Transplantation/methods/adverse effects ; *Critical Illness/therapy ; Female ; Retrospective Studies ; Male ; Middle Aged ; Treatment Outcome ; Aged ; Feasibility Studies ; Adult ; Feces/microbiology ; },
abstract = {Limited treatment options exist for refractory non-Clostridioides difficile infection (non-CDI) of the gut in critically ill patients; whether washed microbiota transplantation (WMT) is feasible and safe in this heterogeneous population is unknown. We retrospectively analysed prospectively registered consecutive cases (NCT03895593) between September 2015 and August 2022, in which severe non-CDI gut pathogens were identified, and rescue WMT was administered after standard treatment failure. Primary outcomes were the clinical outcome and adverse events graded by CTCAE v5.0. Secondary descriptive outcomes were the change in total abdominal symptom score (TASS) on day 7, microbiological clearance, and 12-week survival. Ten patients underwent 29 WMT infusions. Fifty percentage of patients (5/10) obtained clinical cure after WMT. Twenty percentage of patients (2/10) achieved clinical improvement and 30% (3/10) showed no response 7 days after WMT. One transient WMT-related fever occurred (1/29, 3.45%). No serious WMT-attributed events were observed. TASS decreased significantly (p = 0.007). Microbiological clearance was documented in 3 of 4 patients with available post-WMT stool bacteriological test results. This case series provides preliminary evidence supporting the feasibility and potential efficacy of WMT for refractory non-CDI gut pathogens.},
}

Humans
*Salvage Therapy/methods/adverse effects
*Fecal Microbiota Transplantation/methods/adverse effects
*Critical Illness/therapy
Female
Retrospective Studies
Male
Middle Aged
Treatment Outcome
Aged
Feasibility Studies
Adult
Feces/microbiology

@article {pmid42596535,
year = {2026},
author = {Chaki, T and Maruyama, D and Doan, TNM and Tian, X and Prakash, A},
title = {Dietary tryptophan mitigates lung ischemia-reperfusion injury in association with increased indole-3-propionate and aryl hydrocarbon receptor signaling.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2715839},
doi = {10.1080/19490976.2026.2715839},
pmid = {42596535},
issn = {1949-0984},
mesh = {Animals ; *Receptors, Aryl Hydrocarbon/metabolism/genetics ; *Tryptophan/metabolism/administration & dosage ; *Reperfusion Injury/metabolism/diet therapy/microbiology ; *Indoles/metabolism ; Mice, Inbred C57BL ; Mice ; Signal Transduction ; Humans ; Male ; Gastrointestinal Microbiome ; Lung/metabolism ; Diet ; Macrophages, Alveolar/immunology/metabolism ; *Lung Injury/metabolism ; Cytokines/metabolism ; },
abstract = {BACKGROUND: Lung ischemia-reperfusion (IR) injury drives early morbidity after lung transplantation and cardiothoracic surgery, yet targeted preventive therapies are lacking. The gut-lung axis and microbiota-derived tryptophan metabolites, including indole-3-propionate (IPA), may regulate pulmonary immunity and inflammation. We investigated whether a tryptophan-rich (Trp-Rich) diet attenuates sterile lung IR injury by increasing microbiota-derived indole metabolites and reprogramming alveolar macrophage (AM) inflammatory responses.

METHODS: C57BL/6 mice receiving isocaloric tryptophan-standard (Trp-Std) or tryptophan-rich (Trp-Rich) diets underwent lung IR injury. Oxygen saturation, lung cytokines, and aryl hydrocarbon receptor (AhR) signaling readouts were evaluated. Gut microbiota was profiled by 16S rRNA sequencing, and targeted metabolomics quantified tryptophan metabolites in feces, portal vein (PV) plasma, and lung tissue. To further assess inflammatory priming in vivo, mice were additionally challenged with intratracheal lipopolysaccharide (LPS). Mechanistic studies compared IPA with related indoles in cell lines and primary human AMs, including ex vivo nutritional IR, LPS stimulation, and AhR stimulation and blockade using synthetic agonists and antagonists.

RESULTS: Trp-Rich feeding improved post-IR oxygenation, reduced lung IL-1β, and increased pulmonary AhR-downstream gene expression. Trp-Rich diet remodeled gut microbiota, enriching for Bifidobacterium and Lactobacillus, and increasing IPA levels across feces, PV plasma, and lung tissue. In the LPS intratracheal challenge, Trp-Rich feeding reduced IL-6 levels in lung tissue and systemic plasma. Primary AMs isolated from Trp-Rich mice also showed reduced IL-1β and IL-6 release in an ex vivo nutritional IR model. Among the tested indole metabolites, IPA showed the strongest dose-dependent suppression of LPS-induced cytokines and chemokines, suppressed ex vivo nutritional IR injury, and its effects were attenuated by pharmacologic AhR blockade.

CONCLUSIONS: A Trp-Rich diet attenuated sterile lung IR injury, coinciding with gut microbiota remodeling, increased systemic and pulmonary IPA, reduced inflammatory priming, and reprogrammed AM responses. These data support diet- or microbiome-directed strategies targeting IPA-AhR signaling to mitigate perioperative lung IR injury.},
}

Animals
*Receptors, Aryl Hydrocarbon/metabolism/genetics
*Tryptophan/metabolism/administration & dosage
*Reperfusion Injury/metabolism/diet therapy/microbiology
*Indoles/metabolism
Mice, Inbred C57BL
Mice
Signal Transduction
Humans
Male
Gastrointestinal Microbiome
Lung/metabolism
Diet
Macrophages, Alveolar/immunology/metabolism
*Lung Injury/metabolism
Cytokines/metabolism

@article {pmid42597551,
year = {2026},
author = {Wen, Y and Peng, YM and Zhou, XY and Wu, HX and Tang, CY and Cheng, F and Han, YX and Jiang, HL and Gong, Z and Bu, YH and Li, L and Xiao, F and Cai, JM and Mo, YY and Yang, Q and Chen, HL and Zhan, CY and Zhou, HD},
title = {A novel solid beverage RLMCR prevents obesity-related metabolic disorders through the gut-adipose axis.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1895261},
pmid = {42597551},
issn = {2296-861X},
abstract = {BACKGROUND: The global obesity epidemic and associated metabolic comorbidities have imposed an insurmountable strain on healthcare systems, underscoring the urgent need for simple, early interventions to curb obesity at its onset. To address this problem, we developed a novel solid beverage RLMCR (Chinese National Invention Patent No. ZL 202410541939.2) and proved its therapeutic effects on established obesity, yet its preventive potential and underlying mechanisms remain unelucidated.

PURPOSE: This study aimed to further explore the preventive role of RLMCR on diet-induced obesity and elucidate its mechanism via the gut-adipose axis.

METHODS: Male C57BL/6J mice were given RLMCR throughout high-fat diet (HFD) feeding to assess its preventive efficacy against obesity. Post-intervention, key metabolic indices, including body weight, fat percentage, and glucose tolerance, were measured. Subsequently, energy expenditure was monitored, and cold tolerance assays, adipose histomorphology, and thermogenic gene expression analysis were conducted. To characterize the modulatory effects of RLMCR on gut microbiota, 16S rDNA sequencing and untargeted metabolomics analysis were performed. Fecal microbiota transplantation (FMT) was finally conducted to verify the mediating role of gut microbiota in the beneficial effects of RLMCR.

RESULTS: RLMCR markedly mitigated HFD-induced body weight gain and glucolipid metabolic disturbances, while significantly augmenting energy expenditure and cold tolerance. Besides, RLMCR facilitated white adipose tissue browning, as reflected by the emergence of multilocular adipocytes and the upregulation of core thermogenic genes including UCP1 and PGC-1α. Moreover, RLMCR effectively restored the HFD-induced gut microbial disruption and notably enriched the abundance of Akkermansia. FMT from RLMCR-treated donor mice recapitulated the enhanced adipose browning, thereby replicating the metabolic benefits of RLMCR in recipient mice.

CONCLUSION: RLMCR effectively prevented HFD-induced obesity and metabolic dysfunction via gut microbiota-mediated adipose browning. These findings offer a novel preventive strategy for obesity and support the development of RLMCR-based anti-obesity products.},
}

@article {pmid42597775,
year = {2026},
author = {Jiang, F and Zhu, JH and Liu, FJ and Chen, X and Zheng, L and Yu, JX and Chen, W},
title = {The interplay between gut microbiota and gestational diabetes mellitus: mechanisms, characteristics, and intervention strategies.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1789594},
pmid = {42597775},
issn = {1664-302X},
abstract = {Gestational diabetes mellitus (GDM) is a common metabolic complication during pregnancy that poses significant risks to maternal and infant health and is closely associated with gut microbiota dysbiosis. This review systematically summarizes the mechanisms, characteristic alterations, and intervention strategies related to the interplay between gut microbiota and GDM. Studies have shown that women with GDM exhibit distinct structural and compositional dysbiosis of the gut microbiota, such as an altered Firmicutes/Bacteroidetes ratio, reduced abundance of beneficial bacteria, and enrichment of pathogenic bacteria. This dysbiosis is associated with altered synthesis of metabolites such as short-chain fatty acids and bile acids, which may impair insulin signaling, compromise barrier function, and activate inflammatory responses, potentially playing a role in GDM pathogenesis. Furthermore, GDM-associated gut dysbiosis can be vertically transmitted to offspring, altering neonatal gut colonization and increasing long-term risks of metabolic and neurodevelopmental disorders. Diagnostic models based on gut microbiota features show promise for early GDM prediction. Interventions targeting the gut microbiota, including lifestyle modifications, probiotics/prebiotics supplementation, and fecal microbiota transplantation, have demonstrated potential in improving glucose metabolism by modulating microbial composition. However, current research faces challenges such as high heterogeneity, unclear causal mechanisms, and difficulties in clinical translation. Future studies should integrate multi-omics approaches and prospective cohorts to elucidate the core mechanisms of gut microbiota in GDM and advance personalized prevention and management strategies.},
}

@article {pmid42598446,
year = {2026},
author = {Cheng, H and Zhang, D and Wu, J and Feng, H and Zhou, Y and Wan, Y and Tan, Y and Feng, W and Peng, C},
title = {Chemical characterization of aconite polysaccharide and its ameliorative effect on ulcerative colitis by regulating gut microbiota and THDCA-driven TGR5/cAMP/PKA/NLRP3 pathway.},
journal = {Journal of pharmaceutical analysis},
volume = {16},
number = {8},
pages = {101642},
pmid = {42598446},
issn = {2214-0883},
abstract = {Aconite shows potential to improve ulcerative colitis (UC). However, the specific impact and mechanisms of aconite polysaccharides (APs) on UC remain poorly understood. This study aims to elucidate the chemical structures of APs, among which one was further evaluated for its effects on dextran sulfate sodium (DSS)-induced UC, and the underlying mechanism was explored with a focus on gut microbiota (GM). Four distinct APs were isolated, among which aconite polysaccharide A-1 (APA-1) was the predominant one. APA-1 is characterized as a glucan composed of →4)-α-glucose (Glc)-(1→, with residues such as →3, 4)-α-Glc-(1→, →2, 4)-α-Glc-(1→ and →4, 6)-α-Glc-(1→ functioning as branching points. APA-1 significantly ameliorated disease symptoms and colonic pathological alterations in UC mice. Furthermore, APA-1 restored GM diversity and richness, counteracting dysbiosis marked by a decrease in beneficial microorganisms such as Dubosiella and Lactobacillus, and an increase in potentially pathogenic ones including Proteobacteria and Escherichia-Shigella. Fecal microbiota transplantation (FMT) recapitulated the effects of APA-1 on UC mice, thereby confirming the role of APA-1-regulated GM in UC. Metabolomic analysis revealed that APA-1 may exert its effects by enhancing microbial metabolite taurohyodeoxycholic acid (THDCA). Oral administration of THDCA, in conjunction with transcriptomic and Western blotting (WB) analyses, demonstrated that both APA-1 and THDCA ameliorate UC by inhibiting the nucleotide-binding domain, leucine-rich-repeat-containing family, pyrin domain-containing 3 (NLRP3) inflammasome through the Takeda G protein-coupled receptor 5/cyclic adenosine monophosphate/protein kinase A (TGR5/cAMP/PKA) signaling pathway. In summary, APA-1 effectively mitigates UC by modulating GM and microbial metabolite THDCA, which subsequently targets the NLRP3 inflammasome via the TGR5/cAMP/PKA pathway.},
}

@article {pmid42599179,
year = {2026},
author = {Tang, A and Chen, Y and Ding, K and Zhang, J and Xu, L and Chen, W and Hu, S and Lai, J},
title = {IL-1β pathway-dependent regulation of glutamate receptor activity by gut microbiota in bipolar depression.},
journal = {Journal of Zhejiang University. Science. B},
volume = {27},
number = {8},
pages = {888-905},
doi = {10.1631/jzus.B2500219},
pmid = {42599179},
issn = {1862-1783},
support = {2023YFC2506200 and 2023YFC2506203//the National Key Research and Development Program of China/ ; 82571735 and 82471542//the National Natural Science Foundation of China/ ; 2024C03098 and 2025C02109//the Key R&D Program of Zhejiang Province/ ; JNL-2023001B//the Research Project of Jinan Microecological Biomedicine Shandong Laboratory/ ; 2023ZFJH01-01 and 2024ZFJH01-01//the Fundamental Research Funds for the Central Universities/ ; 2023316//the Major Science and Technology Plan Guidance Project of Xiaoshan District/ ; },
mesh = {Animals ; Male ; *Interleukin-1beta/physiology/metabolism ; *Bipolar Disorder/microbiology/metabolism ; Mice, Inbred C57BL ; *Gastrointestinal Microbiome ; Mice ; *Receptors, Glutamate/physiology/metabolism ; Signal Transduction ; Fecal Microbiota Transplantation ; Disease Models, Animal ; Receptors, N-Methyl-D-Aspartate/genetics/metabolism ; Microglia ; Interleukin 1 Receptor Antagonist Protein/pharmacology ; },
abstract = {OBJECTIVES: Neuroinflammation may disrupt neurotransmitter signaling. This study investigated whether gut microbiota-induced neuroinflammation can regulate glutamate pathways in bipolar disorder (BD).

METHODS: Fecal microbiota transplantation (FMT) was performed to observe behavioral changes in the antibiotic-treated C57BL/6J male mouse model of bipolar depression. Gut microbial structure, circulating, and prefrontal levels of inflammatory factors, microglial activation, and transcription levels of N-methyl- d-aspartate receptor (NMDAR) and α-amino-3-hydroxy-5-methyl-4 isoxazole receptor (AMPAR) genes were measured in the "BD" and control mice. Furthermore, the effects of interleukin-1 (IL-1) receptor antagonist (IL-1RA) on the glutamate pathways were assessed.

RESULTS: Compared with the control mice, "BD" mice displayed depression-like behaviors, with a lower diversity of gut bacteria and a decreased abundance of certain species. In addition, "BD" mice showed increased levels of inflammatory factors (e.g., IL-1β) in the serum and prefrontal cortex, microglial activation, and changes in the messenger RNA (mRNA) levels of NMDAR and AMPAR. Treatment with IL-1RA partially reversed the behavioral patterns, neuroinflammation, and transcription levels of glutamate receptors.

CONCLUSIONS: The findings suggest that gut microbiota may influence glutamate receptor gene expression via an IL-1β-dependent pathway in a mouse model of BD, potentially contributing to neuroinflammatory mechanisms relevant to this disorder.},
}

Animals
Male
*Interleukin-1beta/physiology/metabolism
*Bipolar Disorder/microbiology/metabolism
Mice, Inbred C57BL
*Gastrointestinal Microbiome
Mice
*Receptors, Glutamate/physiology/metabolism
Signal Transduction
Fecal Microbiota Transplantation
Disease Models, Animal
Receptors, N-Methyl-D-Aspartate/genetics/metabolism
Microglia
Interleukin 1 Receptor Antagonist Protein/pharmacology

@article {pmid42586732,
year = {2026},
author = {Große, K and Haedge, F and Fera, C and Hecker, J and Wienstroer, J and Tsakmaklis, A and Fichtner, A and Treichel, NS and Clavel, T and Wirtz, TH and Pabst, O and Schuckelt, R and Vehreschild, MJ and Bruns, T},
title = {Encapsulated faecal microbiota transfer to target immune activation in patients with cirrhosis and ascites (TransImmune): protocol for a randomised, double-blind, Phase IIa, placebo-controlled trial.},
journal = {BMJ open},
volume = {16},
number = {8},
pages = {e119299},
doi = {10.1136/bmjopen-2026-119299},
pmid = {42586732},
issn = {2044-6055},
mesh = {Humans ; Double-Blind Method ; *Liver Cirrhosis/therapy/immunology/complications ; *Fecal Microbiota Transplantation/methods ; *Ascites/therapy/immunology ; Clinical Trials, Phase II as Topic ; Randomized Controlled Trials as Topic ; Prospective Studies ; Pilot Projects ; *Dysbiosis/therapy ; },
abstract = {INTRODUCTION: Bacterial translocation and gut dysbiosis are key drivers of systemic immune activation in decompensated cirrhosis, precipitating inflammatory complications such as acute-on-chronic liver failure (ACLF). Currently, no licensed therapies effectively restore intestinal barrier function or reverse dysbiosis in this vulnerable population. While previous studies have suggested benefits of faecal microbiota transfer (FMT) in hepatic encephalopathy or alcohol-associated hepatitis, data on its safety and immunomodulatory effects in decompensated cirrhosis with ascites are lacking. This Phase IIa trial (TransImmune) aims to evaluate the safety and tolerability of encapsulated FMT. Furthermore, it will assess feasibility, microbial engraftment and downstream effects on intestinal barrier integrity, as well as systemic and peritoneal inflammation.

METHODS AND ANALYSIS: This is a prospective, single-centre, randomised, double-blind, placebo-controlled Phase IIa pilot study. A total of 24 patients with decompensated cirrhosis and ascites will be randomised in a 1:1 ratio to receive either encapsulated FMT or placebo over three consecutive days. The investigational product, INTESTIFIX 001, is an encapsulated FMT preparation derived from rigorously screened healthy donors and manufactured under Good Manufacturing Practice (GMP) conditions with predefined release specifications, including minimum alpha-diversity QC criteria, manufactured by the Cologne Microbiota Bank (CMB). The primary endpoints are the occurrence of serious adverse events (SAE) up to the end of study (EOS) and the occurrence and severity of treatment-emergent adverse events (TEAE). Secondary endpoints evaluate signals of clinical efficacy, specifically: (1) systemic inflammation (white blood cell count, C-reactive protein, procalcitonin and IL-6); (2) gut inflammation (faecal calprotectin); (3) organ dysfunction (Child-Pugh, MELD and CLIF-SOFA scores); (4) quality of life (EQ-5D-5L and CLDQ) and (5) the number of antibiotic-free days. Patients will be monitored across five study visits up to 90 days.

ETHICS AND DISSEMINATION: The study was approved by ethics committee review and the German Federal Institute for Drugs and Medical Devices (BfArM). The trial is registered under EU CT no. 2023-5 07 790-18-00. The results of the study will be disseminated via peer-reviewed publications and at international conferences.

TRIAL REGISTRATION NUMBER: EU Clinical Trials Register: 2023-507790-18-00. Registered on 8 August 2024.},
}

Humans
Double-Blind Method
*Liver Cirrhosis/therapy/immunology/complications
*Fecal Microbiota Transplantation/methods
*Ascites/therapy/immunology
Clinical Trials, Phase II as Topic
Randomized Controlled Trials as Topic
Prospective Studies
Pilot Projects
*Dysbiosis/therapy

@article {pmid42586870,
year = {2026},
author = {Feng, X and Pora, M and Ebert, M and Zimmermann, M and Zhan, T},
title = {The role of pharmacomicrobiomics in colorectal cancer therapy.},
journal = {Trends in molecular medicine},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.molmed.2026.07.006},
pmid = {42586870},
issn = {1471-499X},
abstract = {Interindividual variability in response to cancer therapy is a major challenge in the management of colorectal cancer (CRC). The gut microbiome contributes to differential therapeutic efficacy and toxicity by modifying the pharmacokinetics and pharmacodynamics of anticancer drugs. Furthermore, bacterial products interact with tumor and immune cells, altering therapeutic outcomes. This review focuses on the impact of pharmacomicrobiomics on CRC therapy. We describe how gut microbiota affects drug metabolism on a mechanistic level and outline the interactions of specific microbes and their products with chemo-, targeted, and immunotherapies employed in CRC. Finally, we provide an overview of current strategies, including probiotics, engineered bacteria, and fecal microbiota transplantation, that exploit the gut microbiome to improve therapeutic efficacy and reduce toxicity.},
}

@article {pmid42587158,
year = {2026},
author = {Sinha, T and Brushett, S and Fernández-Pato, A and Garmaeva, S and Andreu-Sánchez, S and Spreckels, JE and Mallon, CA and Kuzub, N and Gois, MB and Wu, J and Kruk, M and Jankipersadsing, SA and Dekens, JAM and Gacesa, R and Vila, AV and Bang, C and Perenboom, C and Franke, A and Tytgat, HLP and Mottaz, SC and Peters, L and de Jonge, A and Verkade, HJ and Swertz, MA and Wijmenga, C and Kuipers, F and Scherjon, S and Sikkema, J and Sprikkelman, AB and de Kroon, MLA and Prins, JR and Gordijn, SJ and Koppelman, GH and Reijneveld, SA and , and Fu, J and Yassour, M and Kurilshikov, A and Zhernakova, A},
title = {Maternal influences on infant gut microbiome and health.},
journal = {Nature},
volume = {},
number = {},
pages = {},
pmid = {42587158},
issn = {1476-4687},
abstract = {The establishment of the infant gut microbiome is critical for later health[1,2], yet how it is shaped by maternal and early-life factors remains unclear. Here we metagenomically sequenced 4,526 longitudinal faecal samples from 714 mother-infant pairs in the Dutch birth cohort Lifelines NEXT, spanning 12 weeks of pregnancy to 1 year postpartum. We integrated these data with 474 clinical and exposure variables, and with ultra-deep sequencing of breast milk and vaginal microbiomes. We observe that the maternal gut microbiome undergoes only subtle changes during pregnancy and postpartum, influenced by diet, infections and pre-pregnancy smoking. The maternal gut microbiome is a major reservoir for infant gut strains, with only occasional transmission from vaginal and breast milk microbiomes. Mother-infant gut strain sharing is time dependent, and higher maternal gut species abundance increases the likelihood of strain transmission. We find that the maternal gut microbiome is a predictor of infant eczema. Mode of delivery and feeding mode primarily shaped the infant gut microbiome and its functional profiles, with maternal exposures also having a role. Of 585 vaginally delivered infants, 155 were born at home, but home delivery was only moderately associated with infant gut microbiome composition, similar to other birth parameters such as duration of pushing and ruptured membranes. Overall, we highlight the central role of the mother and her microbiome in shaping the infant gut ecosystem and early health outcomes.},
}

@article {pmid42588196,
year = {2026},
author = {Zhang, X and Li, Y and Luo, R and Wang, H and Guo, J and Zhang, X and Kumar, M and Li, Y and Liu, J},
title = {Dietary Periodicity Disrupts the Gut Microbiota-Enterolactone Axis to Exacerbate MASLD in a Translational Guinea Pig Model.},
journal = {Nutrients},
volume = {18},
number = {15},
pages = {},
doi = {10.3390/nu18152573},
pmid = {42588196},
issn = {2072-6643},
support = {2024YFA1107900//National Key R&D Program of China/ ; 32370791//National Natural Science Foundation of China/ ; 2025A04J7111//Guangzhou Institute of Science and Technology/ ; 2023B1212060050, 2023B1212120009//Department of Science and Technology of Guangdong Province/ ; 2025M772848//China Postdoctoral Science Foundation/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/physiology/drug effects ; Guinea Pigs ; Disease Models, Animal ; *Diet, High-Fat/adverse effects ; Liver/metabolism/pathology ; *Lignans/administration & dosage/pharmacology ; *4-Butyrolactone/analogs & derivatives/metabolism ; Male ; *Fatty Liver/etiology/metabolism/microbiology ; Dysbiosis ; Signal Transduction ; },
abstract = {Background/Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD) is closely linked to Western dietary patterns. Yet, preclinical studies rely on continuous high-fat feeding, overlooking the intermittent nature of human eating. Whether dietary periodicity itself influences the gut-liver axis and MASLD pathogenesis remains unknown. We compared continuous and intermittent high-fat, high-cholesterol (HFHC) diets in guinea pigs, a model that mirrors human lipoprotein metabolism, hepatic cholesterol handling, and hindgut fermentation. Methods: Integrated multi-omics analyses (serum metabolomics, fecal 16S rRNA sequencing, and liver transcriptomics) were employed in a guinea pig model, stratified into normal diet (ND), intermittent HFHC diet (IHD), and IHD with flaxseed lignan supplementation, to compare the effects of dietary regimens and the therapeutic efficacy of lignan on hepatic pathology. Results: Both diets induced hallmark hepatic features of MASLD; however, the intermittent regimen provoked significantly more severe hepatic steatosis, inflammation, oxidative stress, and fibrosis. Hepatic transcriptomic analysis identified the PI3K-Akt signaling pathway as the most significantly enriched pathway in the IHD group. Mechanistically, this aggravated liver injury was linked to gut microbiota dysbiosis and a marked depletion of the microbial metabolite enterolactone. Fecal microbiota transplantation confirmed that the dysbiotic microbiota directly transmits the aggravated liver injury phenotype. Supplementation with flaxseed lignan, the dietary precursor of enterolactone, restored enterolactone production, corrected the dysregulated gut microbiota-enterolactone axis, and largely normalized the expression of PI3K-Akt downstream targets, thereby alleviating hepatic pathology. Conclusions: These findings suggest that alterations in the gut microbiota-enterolactone axis may contribute to diet-periodicity-driven liver injury and highlight its potential involvement in disease progression. Modulating this axis through dietary interventions, such as flaxseed lignan supplementation, may represent a promising nutritional strategy for mitigating MASLD associated with cyclical dietary exposure.},
}

Animals
*Gastrointestinal Microbiome/physiology/drug effects
Guinea Pigs
Disease Models, Animal
*Diet, High-Fat/adverse effects
Liver/metabolism/pathology
*Lignans/administration & dosage/pharmacology
*4-Butyrolactone/analogs & derivatives/metabolism
Male
*Fatty Liver/etiology/metabolism/microbiology
Dysbiosis
Signal Transduction

@article {pmid42588665,
year = {2026},
author = {Subhadra, B and Green, R and Kempaiah, P and Bobban, N and Robinson, LA and Mohapatra, S},
title = {Live Biotherapeutic Zowell Reprograms Microbiota-Lipid Crosstalk to Enhance Cisplatin Efficacy in Lung Cancer.},
journal = {Cancers},
volume = {18},
number = {15},
pages = {},
doi = {10.3390/cancers18152447},
pmid = {42588665},
issn = {2072-6694},
support = {IK6BX004212//United States Department of Veterans Affairs/ ; },
abstract = {BACKGROUND: Lung cancer (LC) remains a leading cause of cancer-related mortality, often compounded by suboptimal chemotherapy efficacy and systemic toxicity. Emerging evidence implicates the gut microbiota in modulating tumor progression, immune function, and treatment outcomes.

METHODS: We evaluated Zowell, a novel live bacterial therapeutic (LBT) developed via LiveBiom[®] co-fermentation, as an adjunct to cisplatin in a murine LC model harboring humanized microbiota. Mice were assigned to treatment groups: Zowell alone, cisplatin alone, their combination, and fecal microbiota transplantation (FMT) as a benchmark.

RESULTS: Zowell monotherapy significantly reduced tumor burden, and its combination with cisplatin produced synergistic anti-tumor effects. 16S rRNA sequencing revealed enrichment of beneficial taxa (Bifidobacterium, Lactobacillus, and Allobaculum) and suppression of contextual genera (Clostridium and Akkermansia). Treatment rebalanced gut ecology, evidenced by a lowered Firmicutes/Bacteroidetes ratio and increased alpha diversity. Zowell outperformed FMT in reducing tumor volume and inflammatory indices. Lipidomic profiling of tumor tissues identified elevated levels of immunomodulatory lipid mediators, including resolvins and prostanoids, suggesting remodeling of the tumor microenvironment toward inflammation resolution and immune activation.

CONCLUSIONS: These findings support Zowell as a precision microbiome therapeutic that potentiates chemotherapy through gut microbial reprogramming and tumor lipid signaling modulation, offering translational promise for enhancing immunotherapeutic response and mitigating chemotherapy-induced toxicity.},
}

@article {pmid42589280,
year = {2026},
author = {Procopciuc, LM and Hangan, AC and Lucaciu, RL},
title = {The Gut-Brain Axis in Metabolic Syndrome: Emerging Mechanisms and Perspectives in Personalized Medicine.},
journal = {International journal of molecular sciences},
volume = {27},
number = {15},
pages = {},
doi = {10.3390/ijms27156622},
pmid = {42589280},
issn = {1422-0067},
mesh = {Humans ; *Metabolic Syndrome/metabolism/microbiology/therapy/etiology ; *Precision Medicine/methods ; Animals ; *Gastrointestinal Microbiome ; *Brain/metabolism ; *Brain-Gut Axis ; Dysbiosis/metabolism ; Prebiotics ; },
abstract = {Metabolic syndrome (MetS) is a multifactorial disorder characterized by central obesity, insulin resistance, dyslipidemia, hypertension, and impaired glucose metabolism, significantly increasing the risk of type 2 diabetes and cardiovascular disease. Recent evidence highlights the important role of the gut-brain axis in the pathogenesis of MetS through complex interactions between the gut microbiota, immune system, endocrine signaling, and host genetics. This narrative review provides an integrative overview of the mechanisms linking dysbiosis to metabolic dysfunction, with particular emphasis on gut microbiota alterations, intestinal permeability, chronic low-grade inflammation, and microbial metabolites such as short-chain fatty acids and lipopolysaccharides. The review also discusses the neural, endocrine, and immune pathways involved in gut-brain communication, including the role of gut-derived neurotransmitters in metabolic regulation. In addition, the contribution of host genetic susceptibility and epigenetic regulation is explored, highlighting how gene-microbiome interactions influence individual metabolic responses and disease risk. Recent advances in multi-omics technologies and precision medicine suggest that personalized approaches targeting both microbial and genetic factors may improve prevention and treatment strategies for MetS. Furthermore, microbiota-targeted interventions, including dietary modifications, probiotics, prebiotics, and fecal microbiota transplantation, are discussed as emerging therapeutic perspectives. Overall, this review emphasizes the importance of considering MetS as a systemic disorder driven by interconnected biological networks involving microbiota, metabolism, immunity, and genetics.},
}

Humans
*Metabolic Syndrome/metabolism/microbiology/therapy/etiology
*Precision Medicine/methods
Animals
*Gastrointestinal Microbiome
*Brain/metabolism
*Brain-Gut Axis
Dysbiosis/metabolism
Prebiotics

@article {pmid42589351,
year = {2026},
author = {Shen, H and Huang, S and Wang, Z and Zhou, S and Huang, L and Zhang, H and Han, Y and Jiang, J and Guo, H},
title = {Glycyrrhizic Acid Alleviates Atherosclerosis in ApoE[-/-] Mice via Microbial Indole-3-Lactic Acid-Mediated AhR-p65 Interaction in the Endothelium.},
journal = {International journal of molecular sciences},
volume = {27},
number = {15},
pages = {},
doi = {10.3390/ijms27156694},
pmid = {42589351},
issn = {1422-0067},
support = {No. 3332025150//Fundamental Research Funds for the Central Universities/ ; No. 2025-I2M-KJ-016//CAMS Innovation Fund for Medical Sciences/ ; },
mesh = {Animals ; *Atherosclerosis/drug therapy/metabolism/microbiology/etiology/pathology ; Mice ; *Glycyrrhizic Acid/pharmacology/therapeutic use ; *Receptors, Aryl Hydrocarbon/metabolism ; *Indoles/metabolism ; Male ; *Transcription Factor RelA/metabolism ; *Apolipoproteins E/deficiency/genetics ; Gastrointestinal Microbiome/drug effects ; Diet, High-Fat/adverse effects ; Mice, Inbred C57BL ; Humans ; Fecal Microbiota Transplantation ; Endothelium, Vascular/metabolism/drug effects ; Mice, Knockout ; },
abstract = {Glycyrrhizic acid (GL), a natural triterpenoid glycoside extracted from the "medicine food homology" herb Glycyrrhiza glabra L., exhibits potent anti-atherosclerotic effects; yet its underlying mechanisms remain unclear due to its poor oral bioavailability. The gut microbiota plays a pivotal role in the development of atherosclerosis (AS). In this study, the microbiota-dependent anti-AS effects of GL were evaluated in high-fat diet (HFD)-fed ApoE[-/-] mice using antibiotic depletion and fecal microbiota transplantation (FMT). Integrated metagenomic and metabolomic analyses were performed to identify the key bioactive microbial metabolite. Further in vivo and in vitro experiments, including co-immunoprecipitation and dual-luciferase reporter assays, were utilized to elucidate the underlying molecular mechanisms. It was demonstrated that oral administration of GL alleviated AS in a microbiota-dependent manner by reversing gut dysbiosis, improving intestinal barrier function, and reducing pro-inflammatory lipopolysaccharide (LPS) levels. GL shifted intestinal tryptophan metabolism toward bacterial-derived indole-3-lactic acid (ILA) production, suppressing LPS-induced vascular endothelial adhesion dysfunction by activating the aryl hydrocarbon receptor (AhR). Mechanistically, ILA-activated AhR interacted with the NF-κB subunit p65 in the cytoplasm, effectively preventing the nuclear translocation of p65 and suppressing the promoter activities of adhesion molecules (VCAM1 and ICAM1), resulting in the amelioration of HFD-induced AS. These findings elucidate the microbiota-dependent mechanism of orally administered GL against AS, and highlight the therapeutic potential of targeting the ILA-AhR-p65 axis in the vascular endothelium as a strategy for AS.},
}

Animals
*Atherosclerosis/drug therapy/metabolism/microbiology/etiology/pathology
Mice
*Glycyrrhizic Acid/pharmacology/therapeutic use
*Receptors, Aryl Hydrocarbon/metabolism
*Indoles/metabolism
Male
*Transcription Factor RelA/metabolism
*Apolipoproteins E/deficiency/genetics
Gastrointestinal Microbiome/drug effects
Diet, High-Fat/adverse effects
Mice, Inbred C57BL
Humans
Fecal Microbiota Transplantation
Endothelium, Vascular/metabolism/drug effects
Mice, Knockout

@article {pmid42589363,
year = {2026},
author = {Liu, Q and Huang, D and Huang, K and Wang, Z},
title = {Intestinal Flora and Myocarditis: Potential Mechanisms and Therapeutic Strategies Affecting Disease Progression and Cardiac Function.},
journal = {International journal of molecular sciences},
volume = {27},
number = {15},
pages = {},
doi = {10.3390/ijms27156706},
pmid = {42589363},
issn = {1422-0067},
support = {82170239//National Natural Science Foundation of China/ ; },
mesh = {Humans ; Animals ; *Gastrointestinal Microbiome ; *Myocarditis/therapy/microbiology ; Disease Progression ; Fecal Microbiota Transplantation ; Dysbiosis/microbiology ; Probiotics/therapeutic use ; },
abstract = {Myocarditis is a clinically challenging form of inflammatory heart disease with heterogeneous etiologies, limited diagnostic tools, no targeted therapies, and a substantial risk of progression to heart failure or sudden cardiac death, particularly in young adults. Emerging evidence has increasingly associated myocarditis with gut microbiota dysbiosis. This review explores the gut-myocarditis axis, highlighting key mechanisms and therapeutic strategies. Significant alterations in gut microbial composition are observed in myocarditis patients and animal models. Gut microbiota influences disease development through multiple pathways: compromised intestinal barrier integrity leading to bacterial translocation and systemic inflammation via MAMP/PRR signaling (e.g., TLRs, NLRs); production of metabolites-including pro-inflammatory trimethylamine N-oxide (TMAO), anti-inflammatory short-chain fatty acids (SCFAs), and immunomodulatory bile acids-that regulate host inflammatory responses, immune cell differentiation, oxidative stress, and fibrotic remodeling; and molecular mimicry, where microbial peptides (e.g., from Bacteroides thetaiotaomicron) trigger cross-reactive autoimmune responses against cardiac proteins. Regarding therapeutic strategies, this review discusses fecal microbiota transplantation (FMT), probiotics, prebiotics, dietary modulation, and emerging approaches including engineered bacteria and oral nanomedicines. Although these strategies hold promise, their efficacy and safety remain to be validated in large-scale clinical trials, and further investigation is warranted.},
}

Humans
Animals
*Gastrointestinal Microbiome
*Myocarditis/therapy/microbiology
Disease Progression
Fecal Microbiota Transplantation
Dysbiosis/microbiology
Probiotics/therapeutic use

@article {pmid42580208,
year = {2026},
author = {Chen, Q and Li, S and Fu, S and Mo, C and Huang, S and Wang, Y and Li, L and Gao, T and Kuang, S and Zheng, R and Wen, J and Lv, Z},
title = {Xiaoyao San exerts antidepressant effects via the gut microbiota-brain axis: An integrative fMRI and multiomics study.},
journal = {Journal of pharmaceutical and biomedical analysis},
volume = {282},
number = {},
pages = {117695},
doi = {10.1016/j.jpba.2026.117695},
pmid = {42580208},
issn = {1873-264X},
abstract = {Depression is characterized by a dysregulated brain-gut axis. Xiaoyao San (XYS), a classic Traditional Chinese Medicine formula for soothing Liver and strengthening Spleen, is clinically effective in alleviating depression. However, the systems-level mechanisms by which XYS coordinates gut-brain communication to exert its antidepressant effects remain insufficiently understood. This study aimed to systematically elucidate the antidepressant mechanisms of XYS, with a focus on identifying a key gut-derived metabolic pathway that modulates prefrontal cortex (PFC) function. A mouse model of depression was established using isolated housing combined with chronic unpredictable mild stress (CUMS). Mice were treated with XYS at low, medium, and high doses or paroxetine. We employed a multimodal approach, integrating behavioral tests, resting-state functional magnetic resonance imaging (rs-fMRI), gut microbiota profiling (16S rRNA sequencing), serum metabolomics and PFC transcriptomics. To establish causal evidence, pseudo-germ-free mice received fecal microbiota transplantation (FMT) from donor mice treated with XYS, followed by comprehensive behavioral and biochemical assessments. XYS treatment significantly ameliorated depressive-like behaviors and restored functional connectivity within emotion-regulation brain networks. Multi-omics integration revealed that XYS reshaped the gut microbiota, which was associated with a reduction in systemic levels of kynurenine (KYN), a key tryptophan-derived metabolite. In the PFC, this decrease in KYN was accompanied by the normalization of aryl hydrocarbon receptor (AhR) signaling activity. Furthermore, GABAergic neurotransmission, mediated by γ-aminobutyric acid (GABA), was enhanced, as evidenced by upregulated expression of glutamate decarboxylase 1 (Gad1), gamma-aminobutyric acid type A receptor subunit alpha1 (Gabra1), increased GABA content, and elevated levels of key synaptic plasticity-related molecules, including brain-derived neurotrophic factor (BDNF), postsynaptic density protein-95 (PSD-95), and synaptophysin (SYN). Critically, FMT from XYS-treated donors recapitulated the antidepressant phenotype in recipient mice, directly implicating the gut microbiota in these therapeutic effects. This study demonstrates that XYS alleviates depression by orchestrating a gut-brain signaling cascade that converges on the PFC to enhance inhibitory synaptic transmission. These findings provide novel and causal mechanistic insights into the brain-gut modulatory action of XYS, offering a comprehensive framework for its therapeutic potential in treating depression.},
}

@article {pmid42580395,
year = {2026},
author = {Barzon, B and Shkodra, A and D'Incalci, M and Sapienza, J and Paribello, P and Nasini, S and Dall'Acqua, S and Bertazzo, A and Pitsikas, N and De Gregorio, D and Valtorta, F and Manchia, M and Squassina, A and Fadda, P and Cavallaro, R and Pisanu, C and Bosia, M and Comai, S},
title = {Melatonin system integrity shapes gut-brain interaction in schizophrenia-derived microbiota transplant phenotype in mice.},
journal = {Life sciences},
volume = {},
number = {},
pages = {124633},
doi = {10.1016/j.lfs.2026.124633},
pmid = {42580395},
issn = {1879-0631},
abstract = {AIMS: This study investigates whether the melatonin (MLT) system modulates the behavioral, neurophysiological and neurochemical effects of fecal microbiota transplantation (FMT) from individuals with schizophrenia (SCZ), highlighting the role of the tryptophan (Trp) to MLT and kynurenine (Kyn) pathways.

MATERIALS AND METHODS: FMT was performed using fecal samples from individuals with SCZ, characterized by distinct clinical, cognitive and metabolic profiles (severe vs mild SCZ), into antibiotic-treated MLT-deficient (C57BL/6) and MLT-proficient (C3H/HeJ) mice. Post-FMT evaluations included locomotor activity assessment (open field test), working memory testing (T-maze), in-vivo electrophysiological recordings from ventral tegmental area (VTA) dopamine (DA) neurons, and quantification of peripheral cytokines and central and peripheral Trp metabolites.

KEY FINDINGS: In MLT-deficient mice, FMT from severe SCZ induced hyperlocomotion and altered peripheral inflammatory markers (decreased IL-1β, increased keratinocyte-derived cytokine) compared to FMT from mild SCZ. Conversely, in MLT-proficient mice, severe SCZ FMT induced persistent spatial working memory deficits and a significant reduction in overall VTA DA neuronal firing, specifically driven by the high-firing subpopulation. Furthermore, MLT-proficient mice receiving severe SCZ FMT selectively exhibited increased brain Trp levels alongside a decreased Kyn/Trp ratio.

SIGNIFICANCE: Our findings identify the MLT system as a key biological switch that gates the impact of SCZ-associated microbiota on brain and behavior, dissociating behavioral from cognitive, neurophysiological and neurochemical outcomes. This work links circadian biology to microbiota-driven effects and points to the Trp-Kyn-MLT axis as a critical interface. This work provides a conceptual framework for targeting circadian-microbiome interactions, as a novel strategy to modulate disease-relevant phenotypes in SCZ.},
}

@article {pmid42581182,
year = {2026},
author = {Alotaibi, BS},
title = {Gut microbiota modulation of systemic immunity and cancer immunotherapy: mechanisms, evidence, and therapeutic implications.},
journal = {Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society},
volume = {34},
number = {4},
pages = {},
pmid = {42581182},
issn = {1319-0164},
abstract = {The gut microbiota plays a critical role in regulating systemic immune responses and has emerged as a key determinant of therapeutic efficacy and toxicity in cancer immunotherapy. Accumulating evidence indicates that specific microbial taxa and microbiota-derived metabolites modulate antitumor immunity by shaping immune cell maturation, cytokine signaling, and the tumor microenvironment. In particular, gut microbial metabolites such as short-chain fatty acids, bile acids, and inosine influence immune checkpoint inhibitor responses by regulating T-cell activation, dendritic cell function, and immune homeostasis beyond the intestinal compartment. Preclinical and clinical studies have demonstrated that alterations in gut microbiota composition are associated with variability in immunotherapy outcomes, including treatment resistance and immune-related adverse events. Importantly, microbiota-targeted interventions such as dietary modulation, probiotics, prebiotics, antibiotics, and fecal microbiota transplantation have shown promise in enhancing immunotherapy efficacy and reducing toxicity. This review synthesizes current mechanistic insights and clinical evidence linking the gut microbiota to systemic immunity and cancer immunotherapy outcomes, highlighting microbiome modulation as a potential therapeutic adjuvant to optimize immunotherapy response and support precision oncology.},
}

@article {pmid42581935,
year = {2026},
author = {Lee, YJ and Lee, JH and Cha, B and Shin, J and Kwon, KS and Shin, YW and Lee, KH and Lim, JH},
title = {Case Report: Fecal microbiota transplantation resensitizes advanced non-small cell lung cancer to platinum-based chemotherapy.},
journal = {Frontiers in oncology},
volume = {16},
number = {},
pages = {1876788},
pmid = {42581935},
issn = {2234-943X},
abstract = {Platinum-based chemotherapy remains a key treatment for advanced non-small cell lung cancer (NSCLC) in patients without actionable mutations or response to immunotherapy. Emerging evidence highlights the gut-lung axis as an important factor influencing lung cancer biology and treatment outcomes. Fecal microbiota transplantation (FMT) may restore gut microbial balance and improve anticancer therapy response. However, evidence in patients receiving conventional chemotherapy is limited. We report a case of FMT used to treat refractory Clostridioides difficile infection (CDI) in a patient with advanced NSCLC and evaluate its effects on gut microbial reconstitution and clinical response to chemotherapy. A 64-year-old woman with heavily pretreated NSCLC developed recurrent CDI during eighth-line chemotherapy (etoposide and carboplatin). After failure of standard antibiotic therapy, she underwent colonoscopic FMT. Gut microbiota shifts were analyzed using 16S rRNA long-read sequencing (V1-V10), with taxonomic assignment based on the NCBI 16S database. Following FMT, diarrheal symptoms resolved, and the patient completed the subsequent chemotherapy cycle. Follow-up chest computed tomography showed radiologic improvement, with a reduction in the linear extent of consolidation from 91.4 to 76.7 mm. Microbiological analysis revealed a shift toward gut homeostasis, including increased abundance of Bacillota (formerly Firmicutes), enrichment of Bifidobacterium breve, and depletion of Klebsiella pneumoniae. This case suggests that FMT effectively treats refractory CDI in patients with advanced cancer and may support the efficacy of conventional cytotoxic chemotherapy by modulating the immunometabolic milieu through the gut-lung axis.},
}

@article {pmid42582282,
year = {2026},
author = {Zeng, Y and Wang, F and Li, S and Liu, Q and Liu, L and Song, B},
title = {Gut microbiota dysbiosis in autism spectrum disorder: 10 years of progress on compositional alterations, metabolic/immune mechanisms, and therapeutic strategies.},
journal = {Frontiers in neuroscience},
volume = {20},
number = {},
pages = {1873864},
pmid = {42582282},
issn = {1662-4548},
abstract = {Autism spectrum disorder (ASD) is a common neurodevelopmental condition frequently accompanied by gastrointestinal symptoms, pointing to a potential role of the gut microbiota-brain axis. To explore this connection, the present review synthesizes findings from studies published between 2016 and 2026, including observational studies, meta-analyses, animal experiments, and clinical trials, with the aim of characterizing gut microbiota alterations in ASD, elucidating underlying mechanisms, and evaluating emerging therapeutic strategies. Across diverse populations, the most consistent microbial signatures in ASD include reduced abundances of Bifidobacterium and Akkermansia muciniphila, together with increased abundances of Clostridium, Bacteroides, and Escherichia-Shigella; however, geographic, age-, and sex-specific variations exist. In addition to bacterial changes, the gut virome and mycobiome are also perturbed, as evidenced by enrichment of Candida albicans and Clostridium phages. Mechanistically, these alterations are linked to reduced short-chain fatty acids (especially butyrate), disrupted tryptophan-serotonin metabolism, and elevated neuroinflammatory cytokines (e.g., TNF-α, IL-6). Causal evidence from animal models using fecal microbiota transplantation further demonstrates that ASD microbiota can directly induce autistic-like behaviors. Building on this causal link, early-phase clinical trials indicate that fecal microbiota transplantation, probiotics, prebiotics, and dietary interventions (e.g., ketogenic diet) can improve both gastrointestinal and behavioral symptoms, although larger double-blind, placebo-controlled trials are needed to confirm efficacy. Furthermore, multi-omics integration and host epigenetic signatures show promise for developing non-invasive diagnostic biomarkers. In conclusion, gut dysbiosis plays a causal role in ASD pathophysiology, and microbiome-based interventions represent a rational and potentially transformative therapeutic avenue.},
}

@article {pmid42582596,
year = {2026},
author = {Zeber-Lubecka, N and Czarnowski, P and Ziemska-Legięcka, J and Wierzbicka-Rucińska, A and Jańczyk, W and Michałkiewicz, J and Obrycki, Ł and Litwin, M and Mikula, M and Socha, P and Ostrowski, J},
title = {Gut Microbiota-Metabolite Alterations Associated with Early Metabolic Dysfunction and Hepatic Steatosis in Adolescents.},
journal = {Computational and structural biotechnology journal},
volume = {35},
number = {1},
pages = {0136},
pmid = {42582596},
issn = {2001-0370},
abstract = {Background: Overweight, obesity, and metabolic dysfunction-associated fatty liver disease (MASLD) are increasingly prevalent in adolescents and are linked to alterations in the gut-liver axis. Gut microbiota may contribute to early metabolic disturbances preceding overt disease. Objective: To compare gut microbiota composition and fecal metabolite profiles, including short-chain fatty acids (SCFAs) and amino acids (AAs), between adolescents with overweight/obesity and normal-weight peers, and to evaluate differences associated with hepatic steatosis assessed by FibroScan-controlled attenuation parameter (CAP). Of 111 participants aged 13 to 17 years, 83 and 28 represented the study group with overweight or obesity and normal-weight control group, respectively. Hepatic steatosis consistent with MASLD was defined as CAP ≥250 dB/m. Gut microbiota was assessed by 16S ribosomal RNA (rRNA) sequencing and fecal metabolites by gas chromatography-mass spectrometry (GC-MS). Results: Adolescents with overweight/obesity showed impaired metabolic profiles compared with controls, while overall microbial α and β diversity did not differ between groups. Differences were observed in the relative abundance of several bacterial genera, including depletion of Lactobacillus. Fecal concentrations of most AAs were significantly elevated in the overweight/obesity group, whereas SCFA levels were unchanged. CAP-based stratification revealed that hepatic steatosis was associated with differences in richness-related α-diversity indices without β-diversity separation. Adolescents with fatty liver exhibited a distinct microbial signature involving low-abundance taxa and higher fecal acetate and butyrate levels. Conclusions: Adolescents with overweight/obesity and fatty liver display subtle but biologically relevant alterations in gut microbiota composition and fecal metabolite profiles despite preserved global microbial diversity. Early metabolic impairment appears to be associated with changes in specific bacterial taxa and AA metabolism rather than generalized dysbiosis.},
}

@article {pmid42583799,
year = {2026},
author = {Lee, I and Suk, KT and Park, JY and Yong, D and Kim, DJ and Kim, BS and Lee, SS},
title = {Fecal microbiota transplantation accelerates clearance of carbapenemase-producing Enterobacterales intestinal carriage: influence of recipient gut microbiome ecology.},
journal = {The Journal of infectious diseases},
volume = {},
number = {},
pages = {},
doi = {10.1093/infdis/jiag414},
pmid = {42583799},
issn = {1537-6613},
abstract = {BACKGROUND: Persistent intestinal carbapenemase-producing Enterobacterales (CPE) carriage challenges infection prevention and antimicrobial stewardship. We evaluated fecal microbiota transplantation (FMT) for decolonization and response-associated recipient microbiome features.

METHODS: This prospective cohort study assessed intestinal CPE clearance in 131 adult carriers (68 receiving FMT; 63 under observation). Responders achieved clearance, defined as three consecutive negative rectal surveillance cultures for CPE, obtained at 3-day intervals within 1 month after FMT. Following least absolute shrinkage and selection operator (LASSO)-based covariate selection, Cox proportional hazards models estimated associations between FMT and time to successful decolonization within prespecified 0-30-day and 0-90-day windows. A longitudinal metagenomic subcohort of 21 FMT recipients (102 fecal samples) underwent shotgun sequencing to characterize taxonomic composition, microbial network organization, functional pathways, antimicrobial resistance genes (ARGs), and donor engraftment.

RESULTS: After LASSO-based covariate selection, FMT was associated with faster CPE clearance than observation at 1 month (hazard ratio, 4.02; 95% confidence interval, 1.84-8.79), with effects sustained at 3 months. Responders showed relatively preserved baseline microbial network organization and enrichment of taxa annotated with arginine-related pathway features, suggesting metabolic relevance to microbial niche competition. After FMT, responders had greater engraftment of donor-associated taxa and donor-like ecological reassembly, with reduced Klebsiella pneumoniae dominance and ARG abundance.

CONCLUSIONS: FMT may accelerate intestinal decolonization in CPE carriers; response variability was associated with recipient gut-microbiome ecology, suggesting microbiome-guided patient selection could optimize microbiota-based strategies.},
}

@article {pmid42586582,
year = {2026},
author = {Rubak, T and Dahl Baunwall, SM and Paaske, SE and Ørum, M and Kongensgaard, R and Kjaerskov, T and Gregersen, M and Hvas, CL},
title = {Development of a checklist to support management of older patients with Clostridioides difficile infection.},
journal = {BMJ open quality},
volume = {15},
number = {3},
pages = {},
doi = {10.1136/bmjoq-2026-004174},
pmid = {42586582},
issn = {2399-6641},
mesh = {Humans ; *Checklist/methods/standards/statistics & numerical data ; *Clostridium Infections/therapy ; Female ; Aged ; Male ; Geriatric Assessment/methods ; Clostridioides difficile/pathogenicity/drug effects ; Aged, 80 and over ; Anti-Bacterial Agents/therapeutic use ; },
abstract = {BACKGROUND: Older patients with Clostridioides difficile infection (CDI) are often frail and multimorbid, with reported 90-day mortality rates of 28%-36%. Despite this, treatment often fails to align with infection severity, and care coordination remains complex. This study describes the development and iterative refinement of a clinical checklist to support structured treatment and care planning in this high-risk group.

METHODS: We conducted a two-phase model development study to identify key management factors. Checklist development followed an iterative quality improvement framework using Plan-Do-Study-Act cycles and driver diagrams. In phase I, older patients with CDI were followed to identify key treatment and care priorities, informing the initial checklist version. In phase II, the checklist was used in a pragmatic, randomised trial investigating Comprehensive Geriatric Assessment (CGA) in older patients with CDI. The checklist was iteratively revised based on clinical use and feedback.

RESULTS: In phase I, treatment courses of 10 older patients with CDI were reviewed, identifying three key priorities for the initial checklist: (1) CDI treatment planning with frailty assessment, (2) medication review and (3) attention to rehydration and nutrition. In phase II, the CDI checklist was applied in 108 patients allocated to CGA. Standardised treatment planning was ensured, including assessment of faecal microbiota transplantation (FMT) eligibility. Among those treated with non-CDI related antibiotics or proton-pump inhibitors, 52% (26/50) and 70% (39/56), respectively, had treatment discontinued. Nutritional and rehydration support was provided in 64 (59%) and 61 (56%) patients. The CDI checklist was subsequently expanded based on clinical use to include new elements, such as post-FMT laxative treatment and cross-specialty coordination.

CONCLUSION: A clinical checklist can support structured and holistic care planning in older adults with CDI. Core components include CDI treatment planning, assessment of FMT eligibility, frailty evaluation, medication review and supportive therapies such as nutrition and rehydration.},
}

Humans
*Checklist/methods/standards/statistics & numerical data
*Clostridium Infections/therapy
Female
Aged
Male
Geriatric Assessment/methods
Clostridioides difficile/pathogenicity/drug effects
Aged, 80 and over
Anti-Bacterial Agents/therapeutic use

@article {pmid42586672,
year = {2026},
author = {Yin, F and Jiang, Z and Hou, C and Gao, J and Li, W and Sun, W and Tian, Y and Xie, D and Wang, M and Wang, B and Ma, W and Dou, X and Dong, C and Sun, D},
title = {An inulin from Asparagus cochinchinensis relieves slow transit constipation associated with Akkermansia muciniphila enrichment, kynurenic acid restoration, and NLRP3 attenuation.},
journal = {Carbohydrate polymers},
volume = {389},
number = {},
pages = {125644},
doi = {10.1016/j.carbpol.2026.125644},
pmid = {42586672},
issn = {1879-1344},
mesh = {Animals ; *Inulin/pharmacology/chemistry/therapeutic use ; *NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; *Constipation/drug therapy/chemically induced/metabolism ; *Kynurenic Acid/metabolism ; Gastrointestinal Transit/drug effects ; Prebiotics ; Loperamide ; Colon/drug effects/metabolism ; Akkermansia ; },
abstract = {Slow transit constipation (STC) involves impaired colonic motility, and effective therapies remain limited. Inulin-type fructans (ITFs) are prebiotic polysaccharides linked to intestinal function, but mixtures with broad chain-length distributions hinder structure-function interpretation. In this study, we adopted a degree of polymerization (DP)-anchored strategy to compare two structurally related ITFs from Asparagus cochinchinensis: ACO (DP = 6) and ACNP (DP = 15). In a loperamide (LOP)-induced STC model, ACNP, but not ACO, improved fecal output and water content, shortened the time to first black stool, and enhanced intestinal transit. ACNP alleviated colonic injury, restored mucus-associated protection, improved epithelial barrier integrity, and preserved enteric neurons and nerve-fiber networks. Multi-omics analyses showed that ACNP treatment was associated with enrichment of Akkermansia muciniphila (AKK), restoration of kynurenic acid (KYNA), reduced proinflammatory mediators, and attenuated NLRP3 inflammasome activation. Antibiotic depletion largely abolished these benefits, whereas fecal microbiota transplantation (FMT) restored them. Moreover, live AKK supplementation and exogenous KYNA reproduced key protective effects and were associated with reduced NLRP3 inflammasome activation. Overall, this DP-anchored comparison identified ACNP as the more effective fructan fraction and supports a microbiota-dependent protective response involving AKK enrichment, KYNA restoration, NLRP3 inflammasome attenuation, barrier protection, and enteric nervous system (ENS) preservation.},
}

Animals
*Inulin/pharmacology/chemistry/therapeutic use
*NLR Family, Pyrin Domain-Containing 3 Protein/metabolism
*Constipation/drug therapy/chemically induced/metabolism
*Kynurenic Acid/metabolism
Gastrointestinal Transit/drug effects
Prebiotics
Loperamide
Colon/drug effects/metabolism
Akkermansia

@article {pmid42574556,
year = {2026},
author = {Eissazade, N and Mosavari, H and Eghdami, S and Rohani, M and Fereshtehnejad, SM and Khoeini, T},
title = {Fecal microbiota transplantation in Parkinson's disease: a systematic review.},
journal = {Neurodegenerative disease management},
volume = {},
number = {},
pages = {1-14},
doi = {10.1080/17582024.2026.2715585},
pmid = {42574556},
issn = {1758-2032},
abstract = {INTRODUCTION: Current Parkinson's disease (PD) treatments offer limited, temporary relief. Fecal microbiota transplantation (FMT) is a potential therapy, but its safety and efficacy remain unclear.

METHODS: PubMed, Scopus, Cochrane Library, and Web of Science were searched on 20 July 2026. Eligible studies included adults with PD receiving FMT reporting motor and non-motor outcomes. Study quality was assessed using Joanna Briggs Institute checklists and Cochrane RoB 2. Due to heterogeneity, results were synthesized narratively.

RESULTS: Fourteen studies (nine trials, three case series, two case reports; 369 participants) were included. FMT protocols varied in stool preparation, delivery route, regimen, and follow-up (3-12 months). Four of six trials reported modest, short-term motor improvements. Non-motor benefits, mainly gastrointestinal function, sleep, and mood, were inconsistent. Microbiota analyses showed partial or temporary restoration toward healthy profiles. FMT was generally safe, with mainly mild, transient adverse events. Risk of bias varied: two high, four some concerns, one low.

CONCLUSIONS: FMT appears safe and may provide short-term improvements in select motor and gastrointestinal outcomes in PD. Evidence is limited by small samples, heterogeneity, and methodological weaknesses. Well-designed, adequately powered RCTs with standardized protocols are needed to determine its therapeutic and disease-modifying potential.

REGISTRATION: PROSPERO (CRD42024508462).},
}

@article {pmid42575469,
year = {2026},
author = {Pan, J and Yang, J and Tang, L and Zhou, X and Yang, X and Li, Y and Wang, L and Chen, G},
title = {Dihydroquercetin regulated PPARγ/AVPR1A/PLCB1/PLA2 pathway to alleviate the colitis of DSS mice.},
journal = {Chemico-biological interactions},
volume = {},
number = {},
pages = {112274},
doi = {10.1016/j.cbi.2026.112274},
pmid = {42575469},
issn = {1872-7786},
abstract = {Inflammatory bowel disease (IBD) is a global disease with limited therapy. It is reported that dihydroquercetin (DHQ) exerts anti-oxidative, anti-inflammatory and cell-protective properties as a natural occurring flavonoid compound, but its effects on IBD remain unclear. In this study, the mice were administered DHQ or fecal transplantation (FMT) followed by DSS administration, after which colitis symptoms, inflammation levels and intestinal barrier function were evaluated. Transcriptome and metabolome analysis of colon were conducted to explore the pathogenesis of colitis. Lastly, we analyzed the potential molecular mechanisms of DHQ in treating colitis by integrating network pharmacology, molecular docking technology and molecular biology experiments. DHQ or FMT protected mice from DSS-induced colitis, suppressed the inflammation and restored the weakened epithelial barrier. Transcriptome and metabolome analysis indicated that decreasing phospholipid level generated by phospholipase D signaling pathway (AVPR1A/PLCB1/PLA2) activation in colon mediated the occurrence of DSS-induced colitis. DHQ or FMT reversed the colitis of mice by regulating PPARγ/AVPR1A/PLCB1/PLA2 pathway. This research firstly discovers that increased phospholipid breakdown caused by PPARγ/AVPR1A/PLCB1/PLA2 leads to the disruption of the intestinal barrier and the occurrence of DSS-induced colitis. This research also provides new perspectives for understanding the pathogenesis of colitis and the protective effects of DHQ.},
}

@article {pmid42576658,
year = {2026},
author = {Wali, AF and Talath, S and Rangraze, IR and El-Tanani, M and Khan, S},
title = {Microbiome-Driven Mechanisms in Breast Cancer: Emerging Evidence From Gut Microbial Signatures to Therapeutic Response.},
journal = {BioMed research international},
volume = {2026},
number = {1},
pages = {e8376859},
pmid = {42576658},
issn = {2314-6141},
mesh = {Humans ; *Breast Neoplasms/microbiology/therapy ; Female ; *Gastrointestinal Microbiome/physiology ; Dysbiosis/microbiology ; Animals ; Probiotics/therapeutic use ; },
abstract = {Breast cancer remains the most frequently diagnosed malignancy among women worldwide, and increasing evidence indicates that the gut microbiome plays a significant role in tumor initiation, progression, and therapeutic response. Microbial dysbiosis and altered metabolite production have been associated with systemic inflammation, estrogen metabolism, immune regulation, and metabolic reprogramming, all of which contribute to breast cancer biology. This review summarizes current preclinical and clinical evidence describing the gut-breast cancer axis and its mechanistic and translational relevance. The review focuses on four major pathways through which gut microbiota may influence breast cancer development and treatment outcomes: immune modulation, estrobolome-mediated estrogen recycling, chronic inflammatory signaling, and microbial metabolite-driven epigenetic and metabolic regulation. Evidence from experimental models and human studies demonstrates that alterations in microbial diversity and enrichment of proinflammatory taxa are associated with tumor progression, subtype-specific biology, and variability in therapeutic response. Emerging findings further indicate that microbiome composition can influence the efficacy and toxicity of chemotherapy, endocrine therapy, radiotherapy, and immunotherapy, highlighting the potential of microbiome-informed precision oncology strategies. In addition, this review discusses current advances in microbiome-targeted interventions including probiotics, dietary modulation, postbiotics, and fecal microbiota transplantation. Despite promising translational potential, significant challenges remain regarding mechanistic validation, standardization of microbiome profiling, reproducibility across cohorts, and clinical implementation. Future research integrating longitudinal multiomics approaches, functional validation studies, and personalized microbiome-based therapeutic strategies may facilitate the development of clinically actionable microbiome interventions for breast cancer management.},
}

Humans
*Breast Neoplasms/microbiology/therapy
Female
*Gastrointestinal Microbiome/physiology
Dysbiosis/microbiology
Animals
Probiotics/therapeutic use

@article {pmid42577302,
year = {2026},
author = {Tian, S and Song, Y and Liu, L and Chen, S and Wu, S and Tuo, Y},
title = {Gut microbiota-derived butyrate and the SIRT1/FoxO1 axis: epigenetic-metabolic regulation of ovarian function in premature ovarian insufficiency-a comprehensive review.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1856217},
pmid = {42577302},
issn = {1664-302X},
abstract = {Premature ovarian insufficiency (POI) is a chronic condition affecting approximately 1.1-3.7% of women worldwide. Beyond its primary impact on fertility, POI poses significant long-term health risks, including cardiovascular disease, osteoporosis, and neurocognitive decline. Current clinical interventions, largely limited to hormone replacement therapy, are primarily palliative and do not address the underlying depletion of ovarian reserve. Recent research has identified a potential link between gut microbiota and POI pathogenesis, suggesting that gut-ovary axis dysbiosis may play a pivotal role. Systemic depletion of butyrate-producing microbiota has been shown to induce oxidative stress and granulosa cell apoptosis. In this review, we propose the gut-butyrate-SIRT1-FoxO1 axis as a central theoretical framework. This model advances beyond the conventional "leaky gut-LPS inflammation" model to demonstrate that gut-derived butyrate functions as a trans-organ "metabolic messenger." Through epigenetic-metabolic coupling, butyrate orchestrates SIRT1-FoxO1 activation. This pathway may mitigate reactive oxygen species (ROS)-induced calcium overload, restore mitochondrial quality control, and preserve granulosa cell homeostasis. Recent preclinical studies have demonstrated that butyrate supplementation can rescue ovarian function in POI models by enhancing SIRT1-mediated FoxO1 deacetylation, This mechanism may suppress pro-apoptotic signaling and promote follicular survival. Furthermore, fecal microbiota transplantation (FMT) from healthy donors has been shown to mitigate ovarian senescence in mice with dysbiotic intestinal microbiota, further substantiating the therapeutic potential of this axis. This review delineates the pleiotropic effects of butyrate across multiple organ systems and provides a robust biological foundation for future microbiota-based interventions. Although substantial experimental validation remains necessary, a deeper understanding of this signaling axis has the potential to transform POI clinical management. Future approaches may shift from palliative, symptomatic treatment to precise disease-modifying therapy.},
}

@article {pmid42570615,
year = {2026},
author = {Lyu, B and Xu, F and Wang, Z and Liu, X and Nie, J and Li, Y and Wu, H and Shang, H and Gou, W and Li, Y and Hou, W},
title = {Taxifolin ameliorates radiation-induced colitis via the gut microbiota-BAs-FXR/NLRP3 axis.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {160},
number = {},
pages = {158675},
doi = {10.1016/j.phymed.2026.158675},
pmid = {42570615},
issn = {1618-095X},
abstract = {BACKGROUND: Radiation-induced colitis (RC) poses a substantial clinical challenge with limited therapeutic options. Taxifolin (TAX), a natural flavonoid, exhibits potential anti-inflammatory properties; however, its clinical application is hindered by poor oral bioavailability and an unclear mechanism of action in the context of radiation injury.

PURPOSE: This study aims to investigate the therapeutic potential and underlying mechanisms of the flavonoid monomer TAX in the context of RC, with a particular focus on the gut microbiota-BAs-FXR/NLRP3 axis.

METHODS: We employed a 13 Gy total abdominal irradiation (TAI) mouse model and HIEC-6 cells. Multi-omics approaches, including 16S rRNA sequencing and untargeted metabolomics, were used to map microbiota and metabolic profiles. Crucially, to establish causality, fecal microbiota transplantation (FMT) was performed to assess the microbiota's mediating role, and the specific FXR antagonist DY268 was utilized to verify the dependency on FXR signaling. Molecular interactions were confirmed via molecular docking, drug affinity responsive target stability (DARTS), and co-immunoprecipitation (Co-IP) assays.

RESULTS: TAX significantly mitigated RC, characterized by preserved intestinal barrier integrity and reduced inflammatory cytokine production. It reshaped microbial homeostasis, specifically enriching bile acid (BA)-metabolizing genera (such as Lachnoclostridium) and promoting the accumulation of specific FXR-activating BAs, including glycocholic acid (GCA), taurochenodeoxycholic acid (TCDCA), and ursodeoxycholic acid (UDCA). FMT from TAX-treated donors successfully recapitulated the radioprotective phenotype in recipient mice, confirming the causal role of the gut microbiota. Mechanistically, both TAX and the enriched BAs directly bound to the farnesoid X receptor (FXR), inducing conformational changes that enhanced its physical interaction with NLRP3, thereby inhibiting inflammasome assembly and downstream signaling. Importantly, pharmacological blockade of FXR by DY268 abolished the protective effects of TAX, confirming that FXR activation is indispensable for its therapeutic action.

CONCLUSIONS: TAX mitigates RC not merely as an antioxidant, but as a microecological modulator. Importantly, TAX acts as a natural modulator of the "gut microbiota-BAs-FXR/NLRP3" signaling axis for RC therapy. TAX-induced microbiota changes promote the production of specific bile acids that amplify intestinal FXR signaling to suppress inflammation. This study provides a robust mechanistic basis for using TAX as an orally active radioprotectant targeting the gut-liver axis.},
}

@article {pmid42571141,
year = {2026},
author = {Piao, L and Huo, J and Dong, Y and Cao, S and Li, X and Xu, D and Li, X and Liu, L},
title = {Cod Skin Collagen Peptides Alleviate Ulcerative Colitis by Regulating Gut Microbiota to Inhibit NLRP3 Inflammasome Activation.},
journal = {Food science & nutrition},
volume = {14},
number = {8},
pages = {e72162},
pmid = {42571141},
issn = {2048-7177},
abstract = {Enteral nutrition is an important intervention for ulcerative colitis, and collagen can improve immune responses and repair the intestinal barrier. Low-molecular-weight peptides from cod skin have demonstrated anti-inflammatory and mucosal protective effects; however, the mechanism by which they alleviate colitis through gut microbiota modulation remains unclear. This study examined the mechanism by which cod skin collagen oligopeptide powder (CP) affects the gut flora to treat ulcerative colitis (UC). This study evaluated CP in mice with dextran sodium sulfate (DSS)-induced UC and used 16S rRNA sequencing to analyze its effect on the gut flora. Fecal microbiota transplantation (FMT) demonstrated the role of CP in modulating gut microbiota in the treatment of UC. Hematoxylin and eosin staining, immunohistochemistry, histology, and enzyme-linked immunosorbent assay (ELISA) assessed CP's effects on colon structure and inflammation. 16S rRNA sequencing showed that CP therapy significantly altered the diversity and organization of the intestinal microbiota in UC mice. FMT demonstrated that CP alleviates UC by modifying the gut microbiota, providing insights into the underlying mechanisms. CP treatment significantly improved body weight, colon length, and histopathological scores in DSS-induced colitis mice, reduced the levels of NLRP3, Caspase-1, ASC, IL-1β, and IL-18, promoted colonic healing, and alleviated tissue damage. CP inhibited fibrosis by upregulating ZO-1 and Occludin while downregulating α-SMA, Vimentin, Snail, and Slug. In conclusion, CP may treat colitis in mice by suppressing NLRP3 inflammasome activation via regulation of the gut microbiota.},
}

@article {pmid42573711,
year = {2026},
author = {Haneesh, M and Amalraj, S and Anusha, G and Karthick, V and Poongavanam, SS and Thamarai, R},
title = {Microbiome-Driven Therapeutic Strategies for Type 2 Diabetes: A Systematic Review of Microbiota Modulation, Glycaemic Outcomes, and Transplantation.},
journal = {Applied biochemistry and biotechnology},
volume = {},
number = {},
pages = {},
pmid = {42573711},
issn = {1559-0291},
abstract = {Type 2 diabetes mellitus (T2DM) arises from the body's ineffective use or production of insulin. Recent research highlights the significant role of the gut microbiome in metabolism and immunity, indicating that microbial dysbiosis may be associated with T2DM development. This systematic review will explore the link between gut dysbiosis and Type 2 Diabetes Mellitus (T2DM), assess the impact of microbially-targeted therapies such as probiotics, prebiotics, dietary changes, and fecal microbiota transplantation (FMT) on glycaemic and metabolic outcomes in adults with T2DM, and determine if clinical trials validate the application of these therapies for T2DM treatment. An extensive literature search was conducted using PubMed up to January 2024, adhering to PRISMA 2020 guidelines, to identify eligible studies. The studies included were randomized controlled trials or observational studies reporting measurable outcomes related to metabolic health in adults aged 18 and older. A total of 25 studies show that individuals with Type 2 Diabetes Mellitus (T2DM) have lower gut microbial diversity, featuring fewer butyrate-producing bacteria and more inflammation-related bacteria. Probiotic supplementation and dietary fiber intake significantly improve hemoglobin A1c (HbA1c) levels and insulin sensitivity in T2DM patients. Gut microbiota dysbiosis is linked to Type 2 Diabetes Mellitus (T2DM), suggesting that the gut microbiome could be a therapeutic focus. However, while interventions like dietary changes, probiotics, and fecal microbiota transplantation show potential, current evidence does not support their routine clinical application. Recommendations for microbiome interventions should rely on strong evidence from effective longitudinal clinical trials verifying both efficacy and safety.},
}

@article {pmid42569584,
year = {2026},
author = {Huo, W and Wang, M and Han, Y and Weng, K and Xia, X},
title = {Polyethylene microplastics exposure reduces flesh quality and disturbs muscle fiber characteristics in freshwater fish (Paramisgurnus dabryanus): associations with gut microbiota alterations.},
journal = {Current research in food science},
volume = {13},
number = {},
pages = {101516},
pmid = {42569584},
issn = {2665-9271},
abstract = {Microplastics (MPs) pose a significant risk to fish health, yet their effects on meat quality in fish remain poorly understood. To investigate the effects of MPs on meat quality, large-scale loach (Paramisgurnus dabryanus) were exposed to polyethylene MPs (PE-MPs) at 0, 2.5, 5.0, and 10 mg/L for 30 days. The results showed that PE-MPs exposure significantly reduced condition factor (CF), weight gain rate (WGR), specific growth rate (SGR), hepatosomatic index (HSI), viscerosomatic index (VSI). Flesh quality measurements showed that PE-MP exposure impaired flesh quality, as evidenced by decreased intramuscular fat, essential amino acids content, and polyunsaturated fatty acids levels. Fluorescence spectroscopy combined with particle identification indicated the presence of PE-MPs in muscle, with particle counts increasing over exposure time and concentration. Hematoxylin and eosin (H&E) staining and Real-time quantitative PCR (RT-qPCR) revealed that PE-MPs exposure increased muscle fiber cross-sectional area (CSA), diameter, and spacing, while decreasing type I fiber density. 16S rRNA sequencing analysis showed that PE-MPs ingestion was associated with gut microbiota alterations, which were strongly correlated with muscle fiber characteristics by Spearman analysis. Fecal microbiota transplantation (FMT) trial revealed that recipients receiving microbiota from PE-MP-exposed donors partially exhibited similar alterations in skeletal muscle fiber characteristics, growth performance, and flesh quality. Collectively, our findings suggest that PE-MPs exposure may induce gut microbiota alterations, and that these shifts in the gut microbiota were associated with reduced flesh quality and altered muscle fiber characteristics in large-scale loach. These findings provide new insights into the detrimental effects of PE-MPs on flesh quality.},
}

@article {pmid42564344,
year = {2026},
author = {Ruan, Z and Sheng, F and Lin, M and Wu, S and Hu, C and Shao, Z and Hu, H and Xu, L},
title = {Gut microbiota in asthma: mechanisms, clinical evidence, and therapeutic opportunities.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1842331},
pmid = {42564344},
issn = {2235-2988},
mesh = {Humans ; *Asthma/therapy/microbiology/immunology ; Animals ; *Gastrointestinal Microbiome ; Dysbiosis ; Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; Disease Models, Animal ; Lung/immunology ; Prebiotics/administration & dosage ; },
abstract = {Asthma is a heterogeneous chronic airway inflammatory disease associated with high global prevalence and substantial clinical burden. Conventional therapies remain limited in controlling refractory phenotypes and preventing disease progression. The gut-lung axis has emerged as a fundamental regulatory network connecting intestinal homeostasis with pulmonary immune function, and mounting evidence has established a close mechanistic link between gut dysbiosis and the onset, persistence, and exacerbation of asthma. This review comprehensively integrates evidence from epidemiological investigations, animal models, clinical observational studies, and randomized controlled trials published between 2011 and 2025 to elucidate the crosstalk mechanisms of the gut-lung axis in asthma, characterize compositional and functional alterations of the gut microbiome, evaluate microbiota-targeted interventions such as probiotics, prebiotics, synbiotics, postbiotics, and fecal microbiota transplantation, and discuss current translational challenges. We highlight that the gut microbiota orchestrates airway inflammatory responses through fine-tuning immune cell differentiation, mediating microbial metabolite signaling, and maintaining intestinal barrier function, with discernible microbial signatures evident across allergic versus non-allergic and pediatric versus adult asthma phenotypes. Despite promising preclinical and preliminary clinical findings, causal evidence remains insufficient, and intervention heterogeneity limits clinical application. This review underscores the potential of microbiome-based precision strategies and identifies key directions for future mechanistic research and clinical translation.},
}

Humans
*Asthma/therapy/microbiology/immunology
Animals
*Gastrointestinal Microbiome
Dysbiosis
Fecal Microbiota Transplantation
Probiotics/therapeutic use
Disease Models, Animal
Lung/immunology
Prebiotics/administration & dosage

@article {pmid42566286,
year = {2026},
author = {Dhiman, NK and Ahmad, SR},
title = {From Dysbiosis to systemic health: Microbiome modulation as a unified therapeutic framework.},
journal = {Acta microbiologica et immunologica Hungarica},
volume = {},
number = {},
pages = {},
doi = {10.1556/030.2026.03015},
pmid = {42566286},
issn = {1588-2640},
abstract = {The gut microbiome is a dynamic microbial ecosystem regulating gastrointestinal, metabolic, immune, and neurobehavioral physiology. Dysbiosis has been linked to irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), and systemic disorders including metabolic syndrome, autoimmune conditions, and neurodegenerative diseases. This narrative review synthesizes mechanistic, clinical, and translational evidence to delineate molecular pathways of microbiome-targeted interventions, evaluates clinical outcomes in IBS and IBD, and proposes a unified framework linking gastrointestinal modulation to systemic health. A structured literature search across PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar (2012-2024) identified approximately 68 eligible sources, appraised using Cochrane Risk of Bias 2.0 and AMSTAR-2. Five principal molecular pathways were identified: competitive pathogen exclusion, epithelial barrier reinforcement, immune modulation, short-chain fatty acid (SCFA) production, and neurotransmitter signaling. Clinically, dietary strategies, biological agents (probiotics, prebiotics, synbiotics, postbiotics, and fecal microbiota transplantation [FMT]), advanced modalities (rifaximin, psychobiotics, bacteriophage therapy), and lifestyle interventions collectively engage these pathways. The same mechanisms underpin emerging applications in metabolic, autoimmune, neurological, and cardiovascular disease. We propose a three-tier model progressing from molecular mechanisms through gastrointestinal outcomes to systemic benefits, with precision medicine and standardized trial designs as prerequisites for therapeutic translation.},
}

@article {pmid42568471,
year = {2026},
author = {Witkowski, M and Przybyciński, J and Wojciuk, B and Czaja, W and Gołembiewska, N and Gołembiewska, E},
title = {The role of gut microbiome disruption in the development of metabolic dysfunction-associated kidney disease.},
journal = {Acta biochimica Polonica},
volume = {73},
number = {},
pages = {16436},
pmid = {42568471},
issn = {1734-154X},
mesh = {Humans ; *Gastrointestinal Microbiome ; Animals ; *Renal Insufficiency, Chronic/microbiology/metabolism ; *Dysbiosis/microbiology/metabolism/complications ; *Metabolic Diseases/microbiology/complications/metabolism ; Diabetes Mellitus, Type 2/microbiology/metabolism ; },
abstract = {Metabolic dysfunction-associated kidney disease (MDAKD) is increasingly recognised as a major clinical consequence of the global rise in obesity, type 2 diabetes, hypertension, and cardiovascular disease. Accumulating evidence suggests that the gut microbiota may contribute to the development and progression of metabolic and renal disorders through complex mechanisms involving microbial metabolites, immune activation, and disruption of the intestinal barrier. This review provides an overview of current knowledge regarding the role of the gut microbiota and gut-derived metabolites in the pathogenesis of chronic kidney disease (CKD) associated with metabolic disorders. Special attention is given to short-chain fatty acids, bile acids, N-trimethylamine oxide, branched-chain amino acids, indoxyl sulfate, p-cresol sulfate, and lipopolysaccharides. Accumulating experimental and clinical evidence suggests that dysbiosis may contribute to chronic low-grade inflammation, insulin resistance, endothelial dysfunction, lipotoxicity, and profibrotic signaling pathways associated with kidney injury and cardiovascular complications. The review also identifies significant limitations in current microbiome research, such as the predominance of animal studies, methodological challenges in metabolite quantification, and difficulties in establishing causality in humans. Emerging therapeutic strategies targeting the gut microbiota, including dietary interventions, prebiotics, probiotics, sodium-glucose cotransporter 2 inhibitors, glucagon-like peptide-1 receptor agonists, and faecal microbiota transplantation, may offer novel approaches to slowing CKD progression and improving metabolic health. However, further mechanistic and clinical studies are required to determine the efficacy of microbiota-targeted therapies in MDAKD.},
}

Humans
*Gastrointestinal Microbiome
Animals
*Renal Insufficiency, Chronic/microbiology/metabolism
*Dysbiosis/microbiology/metabolism/complications
*Metabolic Diseases/microbiology/complications/metabolism
Diabetes Mellitus, Type 2/microbiology/metabolism

@article {pmid42569219,
year = {2026},
author = {Belhasan, D and Kuchma, N and Fischer, M and Allegretti, JR and Kelly, CR and Khoruts, A and Vaughn, BP},
title = {Colonoscopic or Capsule Fecal Microbiota Transplantation for Recurrent Clostridioides difficile Infection: A Prospective Cohort.},
journal = {Gastro hep advances},
volume = {5},
number = {9},
pages = {101051},
doi = {10.1016/j.gastha.2026.101051},
pmid = {42569219},
issn = {2772-5723},
abstract = {BACKGROUND AND AIMS: Fecal microbiota transplant (FMT) is effective for preventing recurrent Clostridioides difficile infection (rCDI). Prior studies suggest that capsule and colonoscopic FMT administration are similarly effective, although the studies may be limited by small sample size or selection bias. The aim of this study was to compare the CDI recurrent rates following capsule or colonoscopic FMT.

METHODS: Prospective cohort of patients with rCDI treated with capsule or colonoscopic FMT between 7/1/19 and 11/29/23. This study's primary outcome was 1-month CDI recurrence rates. Predictors of recurrence were assessed using multivariate logistic regression.

RESULTS: Overall, 652 individuals received FMT (421 capsule, 223 colonoscopy). Those receiving capsule FMT were older (median 70 vs 59 years, P < .001). At 1 month, CDI recurrence was higher with capsule compared to colonoscopic FMT (18% vs 7.4%, P = .001). On multivariate analysis, capsule FMT was associated with increased rCDI risk (adjusted odds ratio [OR]: 2.37, 95% confidence interval [CI]: 1.16-5.24, P = .023). Stratified analyses by age showed capsule FMT increased recurrence risk only in patients ≥65 years (OR: 2.7, 95% CI: 1.2-6.4), but not in those <65 years (OR: 2.7, 95% CI: 1.2-6.4). Beyond 1-month, non-CDI antibiotic exposure became the predominant predictor of recurrence.

CONCLUSION: FMT by capsule may be associated with higher CDI recurrence compared to FMT by colonoscopy. This effect appears be greater in individuals older than 65 years, thus highlighting the importance of individualized treatment decisions that balance FMT efficacy with procedural risks. Development of microbiota-based therapeutics for CDI should account for the impact of administration route on efficacy.},
}

@article {pmid42561662,
year = {2026},
author = {Tan, J and Huang, S and Yin, G and Wang, L and Wang, J and Yuan, P and Liu, J and Yao, K},
title = {Astragalus polysaccharides prevent kidney stone formation in an ethylene glycol-induced rat model via modulation of gut microbiota and short-chain fatty acid production.},
journal = {International immunopharmacology},
volume = {187},
number = {},
pages = {117209},
doi = {10.1016/j.intimp.2026.117209},
pmid = {42561662},
issn = {1878-1705},
abstract = {Kidney stones are a common urological disorder associated with significant pain and renal complications. Astragalus polysaccharides (APS) are a bioactive component of Traditional Chinese Medicine that has shown therapeutic potential in renal disorders, potentially through the modulation of the gut microbiota and its metabolites. Based on its properties, it was hypothesized that APS could prevent kidney stone formation by modulating gut microbiota and altering short-chain fatty acid (SCFA) production. In this study, an ethylene glycol-induced rat model was used to investigate APS's effects on kidney stone formation, renal injury, gut microbiome composition, and targeted SCFAs metabolomics. APS treatment significantly reduced calcium oxalate crystal deposition and urinary oxalate levels, alleviated renal tissue damage, and regulated key bacterial taxa involved in oxalate metabolism and SCFA production, particularly restoring serum butyric acid levels. Sodium butyrate supplements further enhanced the protective function of APS in kidney stones. Fecal microbiota transplantation (FMT) results revealed that antibiotic-depleted recipients of microbiota from healthy mice donors or APS-treated mice donors exhibited improved renal function compared with recipients of stone microbiota. These findings support that APS prevents kidney stone formation by modulating the gut-kidney axis through microbiota and metabolite changes, with FMT demonstrating the functional contribution of gut microbial communities to disease outcomes. Therefore, APS represents a promising natural therapeutic approach for kidney stone prevention and highlights the relevance of microbiota-based strategies in managing kidney stones.},
}

@article {pmid42562498,
year = {2026},
author = {Gao, H and Xiao, Y and Wang, T and Liu, R and Li, Q},
title = {Encapsulated tannic acid protects against ETEC-induced intestinal damage via modulating gut microbiota and barrier function.},
journal = {Food research international (Ottawa, Ont.)},
volume = {241},
number = {},
pages = {119724},
doi = {10.1016/j.foodres.2026.119724},
pmid = {42562498},
issn = {1873-7145},
mesh = {Animals ; *Enterotoxigenic Escherichia coli/drug effects ; *Tannins/pharmacology/administration & dosage ; Intestinal Barrier Function/drug effects ; *Gastrointestinal Microbiome/drug effects ; *Escherichia coli Infections/microbiology/prevention & control ; Mice ; Intestinal Mucosa/drug effects ; Male ; *Intestines/drug effects/microbiology ; Oxidative Stress/drug effects ; Polyphenols ; },
abstract = {Enterotoxigenic Escherichia coli (ETEC) can cause diarrheal disease in both humans and young livestock, posing substantial challenges to intestinal health. This study investigated the protective effects and mechanisms of encapsulated tannic acid (ETA) against ETEC-induced intestinal injury. ETA was successfully prepared, and in vitro digestion experiments showed that the release rate of tannic acid was 10.27% in simulated gastric fluid, with a cumulative release rate of 78.97% in simulated intestinal fluid after 360 min, indicating its excellent controlled-release property. In vivo, 500 mg/kg ETA was selected as the optimal dose and alleviated ETEC-induced growth inhibition, reduced the spleen weight ratio, and mitigated intestinal inflammation. Histologically, ETA improved intestinal morphology by increasing villus height and decreasing crypt depth, and its efficacy was better than that of TA. ETA also attenuated inflammation by downregulating TNF-α, IL-1β, IL-8 and the TLR4/MYD88/TAK1 pathway, relieved oxidative stress by increasing SOD activity and decreasing MDA content, and restored intestinal barrier function. Additionally, In vitro, 0.6% ETA digestion supernatant alleviated ETEC-induced damage in IPEC-J2 cells. ETA also reshaped ETEC-induced cecal microbiota dysbiosis by reducing α-diversity, increasing the abundance of beneficial bacteria and decreasing pathogenic bacteria, and restored short-chain fatty acid levels. Mechanistically, antibiotic-induced gut microbiota depletion abolished the protective effects of ETA, while fecal microbiota transplantation from ETA-treated donors replicated these protective effects. These findings demonstrate that ETA attenuates ETEC-induced intestinal injury through gut microbiota modulation, providing a promising strategy for the prevention and treatment of bacterial enteritis.},
}

Animals
*Enterotoxigenic Escherichia coli/drug effects
*Tannins/pharmacology/administration & dosage
Intestinal Barrier Function/drug effects
*Gastrointestinal Microbiome/drug effects
*Escherichia coli Infections/microbiology/prevention & control
Mice
Intestinal Mucosa/drug effects
Male
*Intestines/drug effects/microbiology
Oxidative Stress/drug effects
Polyphenols

@article {pmid42563598,
year = {2026},
author = {Hu, Z and Xu, J and Jiang, F and Liu, Y},
title = {Global research landscape on the brain-gut axis in early life: a bibliometric and visualized study.},
journal = {Nutricion hospitalaria},
volume = {},
number = {},
pages = {},
doi = {10.20960/nh.06142},
pmid = {42563598},
issn = {1699-5198},
abstract = {BACKGROUND: the brain-gut axis was recognized as a bidirectional communication system linking the central and enteric nervous systems through neural, hormonal, immune, and metabolic pathways. It played a pivotal role in early-life neurodevelopment, immune programming, and gastrointestinal function. Although the field had grown rapidly, a comprehensive bibliometric evaluation of global research trends, hotspots, and collaborations was lacking.

METHODS: we conducted a bibliometric and visualized analysis of publications on the brain-gut axis in early life from 2004 to 2024, using the Web of Science Core Collection (WoSCC) database. CiteSpace was used to generate co-authorship, institutional collaboration, keyword co-occurrence, and co-citation networks, as well as burst detection, timeline views, and dual-map overlays.

RESULTS: a total of 1,429 publications were analyzed. Research output increased steadily from 2015 and peaked in 2023, reflecting growing global interest. The United States and China were the most productive countries, with strong collaborative ties observed among institutions in North America, Europe, and East Asia. University College Cork, University of California System, and Harvard University were the leading institutions, while J. F. Cryan, T. G. Dinan, and G. Clarke were the most influential authors. Early studies focused on anatomical and developmental aspects, while recent hotspots included autism spectrum disorder, intestinal permeability, fecal microbiota transplantation, and psychological stress. Mechanistic keywords highlighted short-chain fatty acids, tryptophan metabolism, vagus nerve signaling, and microglia-immune interactions.

CONCLUSIONS: this study provided a comprehensive bibliometric overview of early-life brain-gut axis research over the past two decades. It revealed dynamic thematic evolution, expanding interdisciplinary collaboration, and the emergence of translational opportunities. These findings offer a valuable reference for future research directions in pediatric neurogastroenterology and microbiota-based interventions.},
}

@article {pmid42564168,
year = {2026},
author = {Zhu, G and Man, J},
title = {Gut microbiota-derived metabolites in cardiovascular disease: mechanisms, disease-specific roles, and translational opportunities.},
journal = {Frontiers in cardiovascular medicine},
volume = {13},
number = {},
pages = {1884283},
pmid = {42564168},
issn = {2297-055X},
abstract = {Cardiovascular disease remains the leading cause of global morbidity and mortality and arises from complex interactions among metabolic dysregulation, inflammation, thrombosis, and vascular dysfunction. In recent years, the gut microbiota has emerged as an important regulator of cardiovascular pathophysiology, largely through the production of bioactive metabolites that act on distant organs. This review summarizes the major classes of gut microbiota-derived metabolites involved in cardiovascular disease, with particular emphasis on trimethylamine N-oxide, short-chain fatty acids, phenylacetylglutamine, bile acids, and tryptophan-derived metabolites. We discuss how these metabolites influence endothelial dysfunction, immune activation, lipid handling, platelet reactivity, cardiac remodeling, gut barrier integrity, and blood pressure regulation through interconnected signaling pathways. We further examine their disease-specific relevance in atherosclerosis, heart failure, hypertension, and coronary artery disease/acute coronary syndrome. In addition, we evaluate current translational strategies targeting microbial metabolism, including dietary modulation, probiotics and prebiotics, fecal microbiota transplantation, and selective inhibition of microbial enzymes. Rather than viewing individual metabolites as uniformly harmful or protective, we propose that cardiovascular risk is better understood as the net consequence of interacting microbial metabolic pathways within specific host contexts. This metabolite-centered framework may help refine biomarker development, risk stratification, and pathway-guided interventions in cardiovascular medicine.},
}

@article {pmid42564235,
year = {2026},
author = {Azabou, E and Frouin, PY and Bellaïche, M and Duff, I and Bao, G and Pillot, A and Mehlal, S and Bergounioux, J and Staats, PS and Rangon, CM},
title = {Vagus nerve-driven microbiota homeostasis: a promising integrative add-on therapy for neurodevelopmental disorders.},
journal = {Frontiers in neuroscience},
volume = {20},
number = {},
pages = {1855953},
pmid = {42564235},
issn = {1662-4548},
abstract = {Over the past two decades, the conceptualization of neurodevelopmental disorders (NDDs) has undergone a profound transformation, shifting from a primarily brain-centric framework toward a systems-level perspective that integrates peripheral physiological processes. Among these, the gut microbiota has emerged as a critical determinant of neurodevelopmental trajectories. Through its involvement in immune modulation, metabolic signaling, and neural communication, the microbiota-gut-brain axis (MGBA) exerts a pervasive influence on brain maturation and function. A growing body of evidence indicates that early-life disruptions of microbiota composition-commonly referred to as dysbiosis-are associated with an increased risk of NDDs, including autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder (ADHD), and epilepsy. These disruptions are frequently driven by environmental exposures such as antibiotic use, cesarean delivery, dietary patterns, and psychosocial stress. Despite the expanding recognition of these associations, current therapeutic strategies aimed at restoring microbiota balance, including probiotics and fecal microbiota transplantation, have yielded inconsistent and often transient results. In this context, Vagus Nerve Stimulation (VNS), particularly in its non-invasive forms (nVNS), has emerged as a promising approach capable of modulating environmental exposures through the host-centered regulatory mechanisms of the MGBA. By influencing autonomic tone, activating the cholinergic anti-inflammatory pathway, and modulating neurotransmitter systems, nVNS may restore microbiota homeostasis while simultaneously improving neurodevelopmental outcomes. This article provides a comprehensive and integrative review of the mechanistic, preclinical, and clinical evidence supporting the role of nVNS as a microbiota-modulating intervention. We further discuss its potential as a safe, cost-effective and promising therapeutic strategy for neurodevelopmental disorders, with a particular emphasis on pediatric populations.},
}

@article {pmid42555752,
year = {2026},
author = {Rachid, R and Martinez-Blanco, M and Kuziel, GA and Stephen-Victor, E and Groussin, M and Orakov, A and Russell, G and Nguyen, LTT and Poyet, M and Mukhatayev, Z and Yee, CSK and Albuhairi, S and Kteish, R and Rahman, EA and Farraj, FA and Wang, Z and Dahlberg, S and Ryan, M and Fitzgerald, M and Elverson, W and Lee, JJ and Schneider, L and MacGinnitie, A and Crestani, E and Queheillalt, D and Burke-Roberts, E and Watson, J and Elliott, RJ and Wong, WF and Osman, M and Voyksner, R and Hohmann, E and Huttenhower, C and Alm, E and Rakoff-Nahoum, S and Chatila, TA},
title = {Fecal microbiome transplant in food allergy in humans and mice identifies a role for bile acid metabolites in oral tolerance.},
journal = {Science translational medicine},
volume = {18},
number = {861},
pages = {eaee3263},
doi = {10.1126/scitranslmed.aee3263},
pmid = {42555752},
issn = {1946-6242},
mesh = {Animals ; Humans ; *Bile Acids and Salts/metabolism ; *Food Hypersensitivity/immunology/therapy/microbiology ; *Fecal Microbiota Transplantation ; Mice ; Adult ; T-Lymphocytes, Regulatory/immunology ; Administration, Oral ; Female ; *Immune Tolerance ; Male ; },
abstract = {The gut microbiome has been implicated in the pathogenesis of food allergy (FA), prompting microbiome-focused interventions. We evaluated, in a phase 1 open-label trial (NCT02960074), the safety and efficacy of oral encapsulated fecal microbiome transplantation (FMT) in 15 adults with peanut allergies. An increase in the peanut reactivity threshold was noted in 3 of 10 participants not pretreated with antibiotics and 3 of 5 participants pretreated with antibiotics, without safety issues. In responders, FMT increased tolerogenic RORγt[+] regulatory T cells (Treg cells) and decreased T helper 2 cells (TH2 cells). Mice transplanted with the microbiomes of post-FMT responders were protected from FA in association with increased RORγt[+] Treg cell percentages and increased colonization with members of the gut Bacteroides. In both humans and mice, protection by FMT was associated with increased bile acid metabolites. Deletion of a bile salt hydrolase in a candidate protective Bacteroides abrogated FA suppression in mice. These results suggest that FMT is a safe and potentially promising therapeutic modality for treating FA.},
}

Animals
Humans
*Bile Acids and Salts/metabolism
*Food Hypersensitivity/immunology/therapy/microbiology
*Fecal Microbiota Transplantation
Mice
Adult
T-Lymphocytes, Regulatory/immunology
Administration, Oral
Female
*Immune Tolerance
Male

@article {pmid42555996,
year = {2026},
author = {Kovacs, S and Szigeti, K and Laczi, K and Hofmeister, B and Makra, N and Dunai, ZA and Ostorhazi, E and Budai, A and Juhasz, M and Banky, B and Szijarto, A and Fulop, A},
title = {Preoperative prebiotic supplementation alleviates colitis and improves anastomotic healing associated with modulation of the gut microbiota in rats.},
journal = {Surgery},
volume = {198},
number = {},
pages = {110443},
doi = {10.1016/j.surg.2026.110443},
pmid = {42555996},
issn = {1532-7361},
abstract = {BACKGROUND: Anastomotic leak is among the most feared complications in colorectal surgery. Patients with inflammatory bowel disease are particularly susceptible to impaired anastomotic healing, partially because of bacterial dysbiosis. Aiming to improve anastomotic healing, we examined the role of microbiota-targeted prehabilitation with a complex prebiotic supplement containing arabinogalactan, humic substances, and micronutrients in a rat model of experimental colitis.

METHOD: Rats were subjected to standard or prebiotic-supplemented diets for 4 weeks before receiving water or dextran sulfate sodium to induce colitis. Then, fecal samples were collected for microbial analysis with 16S ribosomal ribonucleic acid gene sequencing before colon resection surgery. Symptoms, laboratory parameters, and histopathologic changes were measured to determine colitis severity. To evaluate anastomotic healing, immunohistochemistry for caspase-1, claudin-1, matrix metalloproteinase-9, and a colorimetric hydroxyproline assay were performed after macroscopic assessment and bursting pressure tests.

RESULTS: Prebiotic pretreatment protected against colitis-related microbial shifts by increasing the abundance of Lachnospiraceae NK4A136, decreasing Romboutsia, and preventing severe colonic damage caused by dextran sulfate sodium, reflected in improvements in all measured parameters. Prehabilitation with a complex prebiotic supplement enhanced epithelial barrier integrity and strengthened the anastomosis through favorable collagen homeostasis, which correlated with microbial diversity and led to accelerated surgical recovery.

CONCLUSION: Our findings indicate that a complex prebiotic supplement containing arabinogalactan, humic substances, and micronutrients protects against colitis-induced disturbed anastomotic healing, supporting its potential role in microbiota-targeted prehabilitation.},
}

@article {pmid42558256,
year = {2026},
author = {Chen, Z and Wu, W and Chen, Y and Li, F and Xie, X and Lin, Y and Zhang, X and Ye, Q},
title = {Targeting the gut microbiota: emerging strategies to enhance healing of diabetic foot ulcers.},
journal = {Frontiers in endocrinology},
volume = {17},
number = {},
pages = {1865273},
pmid = {42558256},
issn = {1664-2392},
mesh = {Humans ; *Diabetic Foot/microbiology/therapy ; *Wound Healing/physiology ; *Gastrointestinal Microbiome/physiology ; Animals ; *Diabetes Mellitus, Type 2/complications/microbiology ; Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; Prebiotics/administration & dosage ; },
abstract = {Diabetic foot ulcer (DFU) affects up to 34% of diabetic patients, with a 1-year recurrence rate of approximately 40%. This review primarily focuses on type 2 diabetes mellitus (T2DM), the most common form of diabetes associated with DFUs. Emerging evidence shows that gut microbiota critically influences DFUs healing through immune modulation (e.g., Treg/Th17 balance), regulation of inflammatory responses via short-chain fatty acids (SCFAs) that inhibit NF-κB, the gut-immune-skin axis, and systemic effects of microbial metabolites. Microbiota-targeted interventions-probiotics, prebiotics, fecal microbiota transplantation, and dietary strategies-can restore microbial balance and reduce inflammation, thereby promoting DFUs healing. These findings provide a mechanistic foundation for microbiome-based therapies and guide future clinical research.},
}

Humans
*Diabetic Foot/microbiology/therapy
*Wound Healing/physiology
*Gastrointestinal Microbiome/physiology
Animals
*Diabetes Mellitus, Type 2/complications/microbiology
Fecal Microbiota Transplantation
Probiotics/therapeutic use
Prebiotics/administration & dosage

@article {pmid42558510,
year = {2026},
author = {Xiong, Z and Liu, X and Deng, X and Zhang, C and Yang, K and Zhao, Z and Ding, T and Liu, S and Zhou, Z},
title = {Recombinant Bacillus subtilis spores expressing cholera toxin B and ovalbumin prevent ovalbumin-specific food allergy in mice by upregulating regulatory T cells and modulating gut microbiome flora.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1872151},
pmid = {42558510},
issn = {1664-3224},
mesh = {Animals ; *Bacillus subtilis/genetics/immunology ; *Ovalbumin/immunology/genetics ; *Food Hypersensitivity/immunology/prevention & control/microbiology ; *T-Lymphocytes, Regulatory/immunology/metabolism ; *Cholera Toxin/genetics/immunology ; Mice ; Female ; Mice, Inbred BALB C ; *Gastrointestinal Microbiome/immunology ; *Spores, Bacterial/genetics/immunology ; Immunoglobulin E/blood ; Disease Models, Animal ; Cytokines/metabolism ; Allergens/immunology ; Immune Tolerance ; },
abstract = {BACKGROUND: Although oral immunotherapy has shown clinical efficacy in treating food allergies, its broader implementation is constrained by the occurrence of adverse effects. Consequently, inducing allergen-specific immune tolerance during early life can be a preventive strategy to reduce the development of food allergy.

OBJECTIVE: Here, we developed a novel fusion protein cholera toxin B (CTB)-ovalbumin (OVA) expressed on Bacillus subtilis (B.s-CotC-CTB-OVA) spore surface and investigated whether B.s-CotC-CTB-OVA spores prevent OVA-induced food allergy in a mouse model and explored the potential underlying mechanisms.

METHOD: Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and Western blot were used to confirm that CTB-OVA was expressed on B. subtilis spores. Female BALB/c mice were orally administered with B.s-CotC-CTB-OVA spores and B. subtilis spore control (B.s-CotC and B.s-CotC-CTB) for 4 weeks. Then, sensitization and challenge with OVA were performed on mice. Fecal OVA-secretory IgA (sIgA) and serum OVA-IgE, IgG1, and IgG2a levels were measured by enzyme-linked immunosorbent assay (ELISA). The gut microbiome was analyzed by 16S rDNA sequencing. After challenge, diarrhea score, anaphylactic reactions score, splenocyte interleukin (IL)-10, IL-4, and interferon-γ (IFN-γ), and Treg levels were measured. mRNA of IL-10, IL-4, IFN-γ, and Foxp3 were measured. Fecal microbiota transplant (FMT) was used to explore the mechanisms of microbiome in B. subtilis on food allergy.

RESULTS: Recombinant CTB-OVA was successfully expressed on the surface of B. subtilis. Oral administration of B.s-CotC-CTB-OVA can increase fecal OVA-sIgA, alleviate food allergy symptoms, and decrease serum OVA-IgE in mice with significance (p < 0.05). Moreover, oral administration of B.s-CotC-CTB-OVA can significantly reduce serum OVA-IgG1, OVA-IgG2, IL-4, spleen mast cells, and eosinophil levels and significantly increase serum IL-10 and Treg levels (p < 0.05). Additionally, microbiome analysis shows that oral administration of B.s-CotC-CTB-OVA can significantly increase the relative abundance of Muribaculaceae and significantly decrease the relative abundance of Alistipes. FMT partially reproduced the reduction in serum OVA-specific IgE, but did not significantly improve allergic symptom or diarrhea scores, suggesting that gut microbiota alterations may partially contribute to the immunological effects of B.s-CotC-CTB-OVA.

CONCLUSION: These findings suggest that B.s-CotC-CTB-OVA spores may serve as a preventive oral antigen-delivery strategy to promote antigen-specific immune regulation and partially modulate microbiota-associated immune responses in OVA-induced food allergy.},
}

Animals
*Bacillus subtilis/genetics/immunology
*Ovalbumin/immunology/genetics
*Food Hypersensitivity/immunology/prevention & control/microbiology
*T-Lymphocytes, Regulatory/immunology/metabolism
*Cholera Toxin/genetics/immunology
Mice
Female
Mice, Inbred BALB C
*Gastrointestinal Microbiome/immunology
*Spores, Bacterial/genetics/immunology
Immunoglobulin E/blood
Disease Models, Animal
Cytokines/metabolism
Allergens/immunology
Immune Tolerance

@article {pmid42559770,
year = {2026},
author = {Iftikhar, R and Khan, M and Mahnoor, M and Awais, KAD and Risalat, A and Gilani, M and Shamshad, GU and Malik, SS and Skoetz, N and Monsef, I and Hashmi, S},
title = {Faecal microbiota transplantation for treating acute lower gastrointestinal graft-versus-host disease after allogeneic haematopoietic stem cell transplantation.},
journal = {The Cochrane database of systematic reviews},
volume = {8},
number = {},
pages = {CD016225},
doi = {10.1002/14651858.CD016225},
pmid = {42559770},
issn = {1469-493X},
mesh = {Humans ; *Hematopoietic Stem Cell Transplantation/adverse effects ; *Graft vs Host Disease/therapy ; *Fecal Microbiota Transplantation/adverse effects ; Acute Disease ; Randomized Controlled Trials as Topic ; Transplantation, Homologous ; },
abstract = {This is a protocol for a Cochrane Review (intervention). The objectives are as follows: To evaluate the benefits and harms of faecal microbiota transplantation for treating steroid-refractory, acute lower gastrointestinal graft-versus-host disease in recipients of allogeneic haematopoietic stem cell transplantation, compared with standard care, observation, placebo, or other comparator interventions.},
}

Humans
*Hematopoietic Stem Cell Transplantation/adverse effects
*Graft vs Host Disease/therapy
*Fecal Microbiota Transplantation/adverse effects
Acute Disease
Randomized Controlled Trials as Topic
Transplantation, Homologous

@article {pmid42551230,
year = {2026},
author = {Zhuang, T and Wang, X and Zheng, W and Lu, W and Hao, L and Wang, X and Huang, C and Wang, R and Hu, Y and Wang, Z and Chen, K and Li, T and Yang, Q and Yang, L and Ding, L},
title = {Enrichment of Akkermansia muciniphila by red ginseng promotes GDF15 secretion and suppresses obesity in mice.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {160},
number = {},
pages = {158600},
doi = {10.1016/j.phymed.2026.158600},
pmid = {42551230},
issn = {1618-095X},
abstract = {BACKGROUND: Obesity is a growing global health burden with rising incidence. Red ginseng (RGS), a traditional processed ginseng product, shows potential for improving metabolic parameters, though its anti-obesity mechanism remains incompletely understood.

PURPOSE: This study investigated the therapeutic effects of short-term RGS administration on obesity and sought to elucidate the underlying mechanism.

METHODS: A high-fat diet (HFD)-induced obese mouse model was used to assess short-term RGS effects. Antibiotic treatment and fecal microbiota transplantation were performed to evaluate gut microbiota involvement. 16S rRNA sequencing and metagenomic analysis identified key bacterial species, and mass spectrometry-based proteomics identified A. muciniphila-derived proteins. The growth differentiation factor 15 (GDF15)-GFRAL axis was interrogated using Gfral[‒/‒] mice.

RESULTS: Short-term RGS treatment suppressed appetite, reduced body weight, and elevated circulating GDF15 in diet-induced obese (DIO) mice. RGS enriched A. muciniphila, and its depletion abrogated RGS-mediated weight loss and appetite suppression. The A. muciniphila-derived protein Amuc_1631 was identified as a key effector promoting GDF15 secretion. Mechanistically, RGS upregulated colonic Gdf15 transcription via the PERK-eIF2α-ATF4-CHOP axis and activated the brainstem GDF15-GFRAL pathway. The RGS 50% ethanol eluate (RGS/50) fraction was identified as the potential active component responsible for A. muciniphila enrichment and GDF15 elevation.

CONCLUSIONS: This study identifies a gut microbiota-dependent mechanism underlying the anti-obesity effects of RGS, centered on A. muciniphila enrichment and its derived protein Amuc_1631, which promotes GDF15 secretion to suppress food intake via the GDF15-GFRAL axis.},
}

@article {pmid42551232,
year = {2026},
author = {Liu, S and Lu, T and Wang, X and Li, J and Dong, H and Liu, W},
title = {Stachyose alleviates alcohol liver injury in mice associated with modulation of TGF-β signaling pathway and gut microbiota.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {160},
number = {},
pages = {158656},
doi = {10.1016/j.phymed.2026.158656},
pmid = {42551232},
issn = {1618-095X},
abstract = {BACKGROUND: Alcoholic liver disease (ALD) is a widespread chronic disease that seriously affects physical and mental health. Stachyose (STA), a dietary supplement, has been demonstrated to be a potential active oligosaccharide for alleviating ALD, while its mechanism has not been fully revealed.

PURPOSE: This study aims to explore the effects of STA on ALD and its underlying mechanism.

METHODS: The efficacy of STA on ALD was evaluated using an ALD mouse model. The changes in the lipid profile were investigated through lipidomics. The potential mechanism was explored using transcriptomics, and the expression of key pathways was validated by Western blotting. The impact of STA on gut microbiota and SCFAs was analyzed. Finally, the fecal microbiota transplantation method was used to verify the importance of gut microbiota in the treatment of ALD with STA.

RESULTS: Our findings illustrated that STA alleviated liver injury, as evidenced by decreased levels of ALT and AST. Liver lipidomics analysis showed that STA down-regulated the levels of TG, PC, PI, PS, and DG. STA also restored the dynamic balance of the inflammatory response and oxidative stress. Mechanistically, STA treatment was predominantly associated with inhibiting the activation of the TGF-β signaling pathway in the liver. Furthermore, STA restored the intestinal homeostasis by increasing the abundance of Faecalibaculum and Muribaculum as well as decreasing the abundance of Butyricimonas, Clostridium, and Parabacteroides. Interestingly, administration of an STA-derived microbiome could also alleviate ALD.

CONCLUSION: These findings identify STA as a key bioactive ingredient capable of improving ALD, and emphasize the gut microbiota-dependent mechanism underlying its therapeutic effects.},
}

@article {pmid42553370,
year = {2026},
author = {Zhang, T and Wang, Q and Qiu, W and Zhang, D and Shang, Y},
title = {Gut microbiota dysbiosis in sepsis and sepsis-associated organ injury: mechanisms, gut-organ axes, and therapeutic strategies.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1886655},
pmid = {42553370},
issn = {1664-302X},
abstract = {Sepsis is a life-threatening syndrome caused by a dysregulated host response to infection and remains a major cause of morbidity, mortality, and organ dysfunction worldwide. Gut microbial dysbiosis in sepsis may result from both disease pathophysiology and ICU interventions, including broad-spectrum antibiotics, vasopressors, enteral or parenteral nutrition, mechanical ventilation, renal replacement therapy, immune status, and baseline comorbidities. Increasing evidence suggests that gut microbial dysbiosis is closely associated with sepsis progression and sepsis-associated organ injury, and may act as both a consequence of critical illness and a potential contributor to disease progression in selected experimental and clinical contexts. Host-microbe interactions, microbial metabolites, and immune-metabolic signaling help explain how gut dysbiosis contributes to sepsis pathophysiology. At the same time, probiotics, fecal microbiota transplantation, and selected microbial metabolites have shown possible benefits, mainly in experimental or selected clinical settings. This review integrates gut dysbiosis, microbial product translocation, microbial metabolites, and host-microbe interactions into a gut-organ axis framework, and evaluates how these mechanisms may contribute to sepsis progression, organ injury, and microbiota-targeted therapeutic strategies.},
}

@article {pmid42553381,
year = {2026},
author = {Zhou, J and Tao, H and Zou, F and Guo, H and Ding, R and Lei, Q and Zhou, X and Mei, S},
title = {Global research trends and emerging frontiers of intratumoral microbiota in cancer immunotherapy: a bibliometric and visualization analysis.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1865305},
pmid = {42553381},
issn = {1664-3224},
mesh = {Humans ; Bibliometrics ; *Immunotherapy/methods/trends ; *Neoplasms/therapy/immunology/microbiology ; *Tumor Microenvironment/immunology ; *Microbiota/immunology ; Animals ; },
abstract = {BACKGROUND: Intratumoral microbiota, an important component of the tumor microenvironment (TME), have attracted increasing attention in cancer immunotherapy. Emerging evidence links intratumoral microbiota to tumor immune microenvironment (TIME) remodeling, immune cell infiltration, and heterogeneous responses to immune checkpoint inhibitors (ICIs). However, the overall research landscape, knowledge base, and hotspot evolution in this field remain insufficiently characterized. This study aimed to systematically map this field through bibliometric and visualization analyses.

METHODS: Publications up to November 8, 2025, were retrieved from the Web of Science Core Collection, Scopus, and PubMed. After screening, deduplication, and data standardization, bibliometric analyses were performed using R, VOSviewer, CiteSpace, and Scimago Graphica to examine publication trends, collaboration networks, knowledge bases, and keyword evolution.

RESULTS: A total of 245 publications were included, comprising 141 original articles and 104 reviews. Since the first publication appeared in 2017, the field has grown exponentially, with a compound annual growth rate (CAGR) of 63.1% from 2017 to 2024. China ranked first in publication output, followed by the United States, while the United States occupied a more central position in total citations and international collaboration. Frontiers in Immunology was the most productive journal, whereas Science, Cell, and Nature constituted the major co-cited knowledge base, with 1,172, 729, and 670 co-citations, respectively. Keyword analysis showed that "intratumoral microbiota" was the most frequent term (90 occurrences), with excellent clustering quality (modularity Q = 0.6963; silhouette S = 0.9351). Research hotspots have gradually shifted from early explorations of gut microbiota, CD8[+] T cells, and immune mechanisms toward immunotherapy resistance, microbial biomarkers, and microbiota-targeted interventions, including engineered bacteria, extracellular vesicles, and fecal microbiota transplantation.

CONCLUSION: Research on intratumoral microbiota in cancer immunotherapy has rapidly developed into a distinct interdisciplinary field. Current hotspots are moving from mechanistic exploration toward response prediction and translational intervention. Future studies should prioritize standardized detection, spatial and multi-omics validation, and multicenter prospective evaluation to support the clinical translation of microbiota-based biomarkers and therapeutic strategies.},
}

Humans
Bibliometrics
*Immunotherapy/methods/trends
*Neoplasms/therapy/immunology/microbiology
*Tumor Microenvironment/immunology
*Microbiota/immunology
Animals

@article {pmid42553399,
year = {2026},
author = {Shi, C and Li, L and Ge, W and Gao, Y and Li, Y and Li, W and Liu, J},
title = {The role of the gut microbiota-uric acid metabolism axis in high-altitude hyperuricemia: dysregulation mechanisms, pathway associations and therapeutic perspectives.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1882007},
pmid = {42553399},
issn = {1664-302X},
abstract = {High-altitude areas (≥2500 m) are characterized by low oxygen concentrations, which leads more people affected by high uronic acid in the blood. This review systematically investigates the "gut microbiota-uric acid metabolism axis" as a potential target for inhibiting Hyperuricemia (HUA). This review introduces the four functions of the axis: direct reduction of uric acid, intestinal excretion, regulation of uricase expression, and the intestinal-renal axis signal; then investigates how hypoxia alters all of these paths. In addition, this review illustrates how this axis is related to the classical metabolic pathway of purine synthesis, renal excretion, lactate metabolism, inflammatory-oxidative stress and genetic susceptibility. Adaptation difference: Native highlanders and migrants show different degrees of adjustment to life in the mountains, and migrants are relatively more prone to axis dysfunction. Finally, this review introduces targeted intervention strategies, such as probiotics, prebiotics, fecal microbiota transplantation, and their combination with uric acid-lowering or anti-inflammatory drugs, and put forward a population-stratified precision intervention framework. Overall, this paper provides a theoretical foundation and novel direction for understanding and preventing plateau HUA.},
}

@article {pmid42555388,
year = {2026},
author = {Sun, W and Xiao, M and Ali, SL and Jin, C and Khan, A and Shakirullah, and Ni, R and An, Y and Zhang, M and Tian, Y and Kaushik, S and Zhang, Y and Gong, W},
title = {Harnessing the gut microbiome to combat tuberculosis: a technological and clinical review.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1847443},
doi = {10.3389/fcimb.2026.1847443},
pmid = {42555388},
issn = {2235-2988},
mesh = {Humans ; *Tuberculosis/therapy/diagnosis/microbiology/prevention & control ; *Gastrointestinal Microbiome ; Artificial Intelligence ; Probiotics/therapeutic use ; Fecal Microbiota Transplantation ; Biomarkers ; Multiomics ; },
abstract = {Tuberculosis (TB), especially multidrug-resistant and extensively drug-resistant strains, remains a severe global health threat. Advances in high-throughput sequencing, omics technologies and artificial intelligence have revealed the critical involvement of the gut microbiome (GM) in TB pathogenesis, diagnosis and treatment via the gut-lung axis. The GM modulates host immunity and metabolism; TB patients typically show reduced microbial diversity and enriched pro-inflammatory taxa closely linked to disease severity and treatment responses. Omics research has identified promising biomarkers and pathways for early diagnosis and personalized management, while artificial intelligence improves diagnostic accuracy and treatment outcome prediction. GM-targeted interventions, including probiotics, dietary adjustment and fecal microbiota transplantation, can enhance therapeutic efficacy and relieve adverse drug reactions. Current limitations include insufficient validation of the gut-lung axis' causal mechanisms, lagged clinical translation of biomarkers, biases and errors in diagnosis and prediction, data privacy and security concerns, gaps in intervention research, and poor accessibility of related technologies in resource-scarce medical regions. Future studies need rigorous causal analyses, real-time monitoring tools and large-scale multicenter trials to validate microbiome-based strategies. This review highlights the translational potential of GM interventions to optimize personalized TB prevention, diagnosis and treatment and improve clinical outcomes.},
}

Humans
*Tuberculosis/therapy/diagnosis/microbiology/prevention & control
*Gastrointestinal Microbiome
Artificial Intelligence
Probiotics/therapeutic use
Fecal Microbiota Transplantation
Biomarkers
Multiomics

@article {pmid42555417,
year = {2026},
author = {Kamaljeet, and Vijukumar, A and Shahi, A and Kumar, A and Bhatia, R},
title = {AUTO-brewery syndrome and the human microbiome: Insights into endogenous ethanol production and human diseases.},
journal = {Food science and biotechnology},
volume = {35},
number = {9},
pages = {2415-2436},
doi = {10.1007/s10068-026-02103-1},
pmid = {42555417},
issn = {2092-6456},
abstract = {Auto-Brewery Syndrome (ABS) is a metabolic condition where microbiota dysbiosis undergoes ethanolic fermentation within the gastrointestinal tract. Because the microbial ethanolic fermentation of dietary carbohydrates occurs entirely within the host's gastrointestinal tract, resulting ethanol is referred as "endogenous" while the gut dysbiosis in ABS can rise from multiple fungal or bacterial species. The pathophysiology of ABS is frequently linked to shifts in gut microbiota composition often arising from antibiotics use, high carbohydrate diets, or an underlying immunological or metabolic condition. In this review, the mechanisms behind microbial endogenous ethanol production, the connection between gut, liver, brain, and microbial ethanol-producing routes are examined. Treatments for ABS have been evaluated including antifungals, low-carbohydrate diets, probiotics, and faecal-microbiota transplantation. Lastly, the social, legal, and mental impacts of ABS have been discussed. It would be wise for future studies to develop customized microbiome approaches for detection and treatment guided by omics and AI technologies.},
}

@article {pmid42546090,
year = {2026},
author = {Li, J and Zhou, L and Yang, J and Li, Y and Jiao, Z},
title = {Gut Lysophosphatidylcholine Aggravates Donation After Circulatory Death Liver Injury via Lysosomal Dysregulation During Normothermic Regional Perfusion.},
journal = {Transplantation},
volume = {},
number = {},
pages = {},
doi = {10.1097/TP.0000000000005861},
pmid = {42546090},
issn = {1534-6080},
support = {25ZDFA002//Major Science and Technology Program of Gansu Province/ ; No.2020M683610//the Postdoctoral Fund/ ; },
abstract = {BACKGROUND: Normothermic regional perfusion (NRP) is increasingly used in donation after circulatory death liver transplantation, yet the impact of the accompanying intestinal ischemia/reperfusion injury and gut microbiota dysbiosis on liver grafts remains unclear.

METHODS: A rat model of donation after circulatory death followed by NRP was established. Intestinal microbiota composition was characterized by 16S rRNA gene sequencing, and the contribution of microbiota alterations to liver injury during NRP was assessed using antibiotic-treated rats and fecal microbiota transplantation. Untargeted metabolomics of intestinal contents was subsequently performed to identify candidate metabolites potentially involved in microbiota-associated liver injury. Lysophosphatidylcholine (LPC) was further investigated in vivo and in vitro by transcriptomic analysis and studies of lysosomal function and autophagic flux.

RESULTS: NRP induced intestinal microbiota dysbiosis. Antibiotic treatment attenuated liver injury, whereas fecal microbiota transplantation from NRP donors aggravated liver injury. Untargeted metabolomics identified LPC as a markedly increased metabolite during NRP, with elevated levels in intestinal contents, portal venous plasma, and liver tissue. Transcriptomic analysis and complementary in vivo and in vitro experiments showed that increased LPC exposure exacerbated hepatocellular injury and was associated with lysosomal dysfunction and impaired autophagic flux.

CONCLUSIONS: NRP induced gut microbiota dysbiosis and alterations in the intestinal metabolome. LPC was increased during NRP and aggravated liver injury, accompanied by lysosomal dysfunction and impaired autophagic flux, suggesting that modulation of the intestinal microenvironment and LPC-targeted intervention may offer potential strategies to mitigate liver injury during NRP.},
}

@article {pmid42547174,
year = {2026},
author = {Donskey, CJ},
title = {Update on Clostridioides difficile Infection in Older Adults.},
journal = {Clinics in geriatric medicine},
volume = {42},
number = {3},
pages = {491-507},
doi = {10.1016/j.cger.2025.09.002},
pmid = {42547174},
issn = {1879-8853},
mesh = {Humans ; *Clostridium Infections/diagnosis/epidemiology/therapy ; *Clostridioides difficile/isolation & purification ; Aged ; *Anti-Bacterial Agents/therapeutic use ; Fecal Microbiota Transplantation/methods ; *Cross Infection/epidemiology/diagnosis/therapy ; Long-Term Care ; Quality of Life ; },
abstract = {Clostridioides difficile is a common cause of community-associated and health care-associated infections. Older adults are disproportionately affected, and long-term care facilities (LTCFs) have borne a substantial proportion of the burden of C difficile infection (CDI). Recurrences of CDI are common in older adults and have substantial adverse effects on quality of life. Appropriate diagnostic testing and management is essential for older adults in the community and in LTCFs. This review focuses on current concepts related to the epidemiology, diagnosis, and management of CDI in older adults.},
}

Humans
*Clostridium Infections/diagnosis/epidemiology/therapy
*Clostridioides difficile/isolation & purification
Aged
*Anti-Bacterial Agents/therapeutic use
Fecal Microbiota Transplantation/methods
*Cross Infection/epidemiology/diagnosis/therapy
Long-Term Care
Quality of Life

@article {pmid42548192,
year = {2026},
author = {Feng, J and Wang, Z and Xu, Y and Peng, J and Xu, C and Xie, Q and Li, Y and Chen, W and Chen, J and Wang, X and Gao, WQ and Li, L and Meng, X},
title = {Intestinal epithelial SETD2 maintains gut microbial homeostasis to attenuate colitis.},
journal = {Clinical and translational medicine},
volume = {16},
number = {8},
pages = {e70754},
doi = {10.1002/ctm2.70754},
pmid = {42548192},
issn = {2001-1326},
support = {2022YFA1302704//National Key R&D Program of China/ ; 2023YFC1404101//National Key R&D Program of China/ ; YG2024ZD11//Interdisciplinary Program of Shanghai Jiao Tong University/ ; 32570684//National Natural Science Foundation of China/ ; 82372604//National Natural Science Foundation of China/ ; U23A20441//National Natural Science Foundation of China/ ; W2431055//National Natural Science Foundation of China/ ; },
mesh = {Animals ; Mice ; *Colitis ; *Histone-Lysine N-Methyltransferase/metabolism/genetics ; *Homeostasis ; *Gastrointestinal Microbiome/physiology/drug effects/genetics ; Mice, Knockout ; *Intestinal Mucosa/metabolism ; Male ; },
abstract = {BACKGROUND: Disruption of host-microbiota homeostasis is a fundamental hallmark of inflammatory bowel disease (IBD) pathogenesis. Host epigenetic modifications and corresponding alterations in gene expression levels can impact the composition of gut microbes. SET domain containing 2 (SETD2) is a critical epigenetic regulator with established tumor-suppressive roles, but its function in intestinal microbial ecology and colitis progression remains unexplored. We aimed to investigate the specific role of SETD2 in maintaining gut microbial homeostasis and modulating colitis progression.

METHODS: RNA sequencing (RNA-seq), assay for transposase-accessible chromatin with high-throughput sequencing (ATAC-seq) and cleavage under targets and tagmentation sequencing (CUT&Tag-seq) were conducted on colonic epithelial cells from intestinal epithelial cell-specific SETD2 knockout (Setd2[vil-ko]) mice to identify key mediators contributing to colitis development. Faecal samples underwent 16S rRNA sequencing and non-targeted metabolomics analysis to characterise microbial dysbiosis and metabolic perturbations. Molecular experiments and faecal microbiome transplantation experiment were conducted to explore and validate the role of SETD2 in colitis development.

RESULTS: SETD2 deficiency induced overproduction of Reg3 lectins and disrupted gut microbiota composition. Beneficial commensal bacteria were depleted and dysregulated metabolites were accumulated in Setd2[vil-ko] mice. Supplementation with healthy-like gut microbiota significantly ameliorated the exacerbated colitis induced by SETD2 deficiency.

CONCLUSIONS: Our findings uncover a previously unrecognised role for SETD2 in maintaining microbial homeostasis, offering new mechanistic insights into how epigenetic regulation preserves intestinal homeostasis and suggesting novel therapeutic avenues for IBD.},
}

Animals
Mice
*Colitis
*Histone-Lysine N-Methyltransferase/metabolism/genetics
*Homeostasis
*Gastrointestinal Microbiome/physiology/drug effects/genetics
Mice, Knockout
*Intestinal Mucosa/metabolism
Male

@article {pmid42548549,
year = {2026},
author = {Chen, Y and Duan, W and Du, M and Guo, M and Sun, Y},
title = {Gut microbiota and constipation: from causal evidence to therapeutic strategies-a state-of-the-art narrative review.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1817279},
pmid = {42548549},
issn = {1664-302X},
abstract = {Constipation is a common functional disorder of the gastrointestinal tract with a global prevalence of approximately 10-20%, which seriously affects patients' quality of life and imposes a heavy socioeconomic burden. In recent years, the role of the gut microbiota in the pathogenesis of constipation has received increasing attention, particularly in the context of the brain-gut axis theory. In this narrative review, we critically examine the research literature on constipation and intestinal microecology published over the past decade, focusing on four aspects: (1) the characteristics of the gut microbiota in patients with constipation, including changes in microbial diversity, alterations in the abundance of specific taxa, and differences across constipation subtypes; (2) Mendelian randomization studies that provide genetic-level evidence consistent with the hypothesis that certain microbiota alterations may precede constipation rather than merely result from it; (3) mechanisms of microbiota-host interactions mediated by the brain-gut axis, with an emphasis on neural, metabolic and immune pathways; and (4) microbiota-based intervention strategies (probiotics, prebiotics, synbiotics, postbiotics and fecal microbiota transplantation) and their clinical evidence. Our findings suggest that specific microbiota alterations may contribute to constipation pathophysiology and the promise of personalized, microbiome-based therapies. Although microbiota-based interventions show potential therapeutic value in selected patients, current evidence is limited by substantial heterogeneity in study design, small sample sizes, inconsistent microbiome signatures, and limited long-term safety data. High-quality evidence from large, well-designed RCTs is lacking for most interventions, and findings from low-certainty studies (e.g., conference abstracts, animal experiments, small uncontrolled trials) should be interpreted as preliminary and hypothesis-generating rather than conclusive. Therefore, microbiota-targeted therapies should currently be considered exploratory or adjunctive rather than established standard treatments for constipation. Future progress will require standardized methodologies, mechanistic validation studies, and phenotype-stratified clinical trials to support translation toward precision microbiome-based medicine.},
}

@article {pmid42548844,
year = {2026},
author = {Lu, E and Zhang, M and Zhao, Y and Meng, H and Xu, Z},
title = {Fecal microbiota transplantation in ulcerative colitis: mucosal immune mechanisms and precision microbiota therapy.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1888117},
pmid = {42548844},
issn = {1664-3224},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods/adverse effects ; *Colitis, Ulcerative/therapy/immunology/microbiology ; *Immunity, Mucosal ; Animals ; *Gastrointestinal Microbiome/immunology ; *Intestinal Mucosa/immunology/microbiology/metabolism ; Precision Medicine ; Intestinal Barrier Function ; Treatment Outcome ; },
abstract = {Fecal microbiota transplantation (FMT) has emerged as an investigational microbiota-targeted strategy for ulcerative colitis (UC), aiming to restore dysbiotic gut ecosystems and microbiota-host homeostasis. Mechanistic studies suggest that FMT may reshape microbial community structure, enrich short-chain fatty acid-producing bacteria, remodel bile acid and tryptophan-aryl hydrocarbon signaling, enhance epithelial barrier integrity, and regulate mucosal immunity, including Th17/Treg balance, IgA-associated responses, macrophage reprogramming, IL-10/IL-22 signaling, and neutrophil extracellular trap formation. Randomized controlled trials indicate that FMT can induce clinical and endoscopic remission in selected patients with UC, particularly when administered through the lower gastrointestinal route and using multi-donor or optimized regimens. Current guidelines do not recommend conventional FMT as routine therapy for UC outside clinical trials, reflecting the heterogeneity and low certainty of available evidence. However, its efficacy appears limited in moderate-to-severe or biologic-refractory disease, underscoring the importance of host inflammatory burden and recipient ecological receptivity. Personalized strategies, including donor-recipient functional matching, dietary modulation, combination therapy, and next-generation microbiota therapeutics, may improve response and safety but require prospective validation. This review integrates microbiota-metabolite-barrier-immune mechanisms with clinical evidence to define where FMT may be useful, where its benefit appears limited, and how future studies can move the field toward precision microbiota therapy in UC.},
}

Humans
*Fecal Microbiota Transplantation/methods/adverse effects
*Colitis, Ulcerative/therapy/immunology/microbiology
*Immunity, Mucosal
Animals
*Gastrointestinal Microbiome/immunology
*Intestinal Mucosa/immunology/microbiology/metabolism
Precision Medicine
Intestinal Barrier Function
Treatment Outcome

@article {pmid42549413,
year = {2026},
author = {Feng, S and Si, X and Lu, C and Gao, Z and Wang, J and Yang, Q and Lu, S and Su, T and Yang, J and He, X and Wu, L},
title = {Washed microbiota transplantation improves clinical symptoms, gut microbiota, and metabolic profiles in autism spectrum disorder in a twin cohort.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1885281},
pmid = {42549413},
issn = {1664-302X},
abstract = {OBJECTIVE: Autism spectrum disorder (ASD) is a heterogeneous neurodevelopmental condition characterized by impaired social communication, repetitive behaviors, and restricted interests. Dysregulation of the microbiota-gut-brain axis is closely associated with the pathogenesis of ASD. Washed microbiota transplantation (WMT) has emerged as a promising intervention for ASD, but existing cohort studies lack genetically identical controls, making it difficult to distinguish intervention-related changes from genetic and environmental confounding factors. This twin-paired controlled study adopted a study design that minimizes the influence of genetics and shared environment, to explore the associations of WMT with clinical symptoms, gut microbiota, and metabolic profiles in children with ASD.

METHODS: Three pairs of age- and environment-matched twins (one ASD-affected, one typically developing sibling) were enrolled. WMT was administered to the ASD participant in each pair. Fecal samples were collected at baseline and post-intervention. Gut microbiota and metabolic profiles were analyzed using metagenomic sequencing and targeted metabolomics, respectively. Clinical outcomes were evaluated using the Childhood Autism Rating Scale (CARS), Autism Behavior Checklist (ABC), Sleep Disturbance Scale for Children (SDSC), and Bristol Stool Form Scale (BSFS). Relevant observations were carried out to explore potential changing trends.

RESULTS: After WMT, CARS, ABC, SDSC, and BSFS exhibited small numerical directional shifts toward healthier values, but none reached statistical significance. Gut microbial structure and function presented a shifting trend toward the profile of their typically developing twin siblings. Abnormal lipid and energy metabolism indicators showed partial ameliorative trends, and the number of differential metabolites between ASD patients and healthy siblings was markedly reduced. Tyrosine and phenylalanine metabolic pathways, together with Segatella, Negativibacillus, and Sangeribacter, may be associated with incomplete phenotypic changes in this cohort.

LIMITATIONS: Although the twin-pair design has high internal validity and can provide strong causal inference evidence for the effect of microbiota transplantation in treating ASD, this study has limitations such as a small sample size, a single-center non-randomized observational design. All findings in this pilot study are merely descriptive trends, and the relevant mechanism analysis only provides correlational clues. A single session of microbiota transplantation failed to fully adjust aromatic amino acid metabolism in ASD children. No definitive causal relationship can be concluded based on the findings of this small-sample pilot study.

CONCLUSION: Under tightly controlled genetic and environmental conditions, gut microbial dysbiosis presents correlational characteristics with ASD-related phenotypes. WMT was associated with consistent remodeling of gut microbial ecology and partial resolution of metabolic dysregulation in ASD children, with multi-omic signatures converging toward healthy twins. Clinical rating scales only displayed non-significant minor numerical shifts, which cannot be interpreted as evidence of clinical symptom improvement. These initial findings provide exploratory mechanistic clues and phenotypic data supporting WMT as a targeted microbiome intervention approach for ASD, and await further validation through large-scale randomized controlled trials.

CLINICAL TRIAL REGISTRATION: Identifier ChiCTR2400091105.},
}

@article {pmid42549688,
year = {2026},
author = {Jia, Q and Wang, H and Yin, W and Zhang, C and Xu, X and Liang, S and Pan, W and Tang, B and Xiao, W and Liu, S and Lü, M},
title = {Sex differences in fecal microbiota transplantation for mitigating radiation-induced thrombocytopenia in mice: efficacy amplified by inulin.},
journal = {Platelets},
volume = {},
number = {},
pages = {2701022},
doi = {10.1080/09537104.2026.2701022},
pmid = {42549688},
issn = {1369-1635},
abstract = {BACKGROUND: Fecal microbiota transplantation (FMT) shows potential in promoting hematopoiesis, with efficacy influenced by donor sex. However, its role in radiation-induced thrombocytopenia (RIT) and its sex-specific effects remain unclear. While inulin may enhance FMT efficacy, this has not been explored in the context of RIT.

METHODS: We established an irradiation-induced thrombocytopenia (RIT) model in male and female mice via 4 Gy X-rays exposure. FMT was administered orally as a fecal suspension. Platelet recovery was monitored via hematology analyzer, megakaryopoiesis was assessed by flow cytometry and H&E staining; gut microbiota changes were evaluated by 16S rRNA sequencing.

RESULTS: Sex-matched FMT accelerated platelet recovery and promoted megakaryocyte production in the bone marrow and spleen only in female mice, accompanied by an increase in Akkermansia abundance. Furthermore, transplanting feces from female donors also accelerated platelet recovery in irradiated male mice, whereas feces from male donors does not. INU selectively enriched probiotic colonization, thereby fostering a favorable microbial structure that enhanced FMT efficacy.

CONCLUSIONS: The sexually dimorphic gut microbiota contributes to sex-specific FMT efficacy in alleviating radiation-induced thrombocytopenia, which can be further amplified by inulin. This study offers sex-specific microbial therapy for radiation-induced thrombocytopenia and a prebiotic-based strategy to boost FMT efficacy.},
}

@article {pmid42550158,
year = {2026},
author = {Fan, X and Zhou, C and Zhang, P and Ming, Y},
title = {Effects of Different Living Environments on Intestinal Flora in Patients With Schistosoma Japonicum-Induced Liver Fibrosis.},
journal = {MicrobiologyOpen},
volume = {15},
number = {4},
pages = {e70366},
doi = {10.1002/mbo3.70366},
pmid = {42550158},
issn = {2045-8827},
support = {81771722//National Natural Science Foundation of China/ ; 2021SK2032//Key Research and Development Plan of Hunan Province/ ; },
mesh = {Humans ; *Schistosomiasis japonica/complications/microbiology ; *Liver Cirrhosis/parasitology/microbiology/etiology ; Animals ; *Schistosoma japonicum ; RNA, Ribosomal, 16S/genetics ; *Gastrointestinal Microbiome ; China ; Feces/microbiology ; Female ; *Bacteria/classification/genetics/isolation & purification ; Male ; Sequence Analysis, DNA ; Adult ; DNA, Bacterial/genetics/chemistry ; DNA, Ribosomal/genetics/chemistry ; Middle Aged ; },
abstract = {Schistosomiasis japonica is a parasitic disease leading to liver cirrhosis. China's "fishermen going ashore" policy divides patients with schistosomiasis liver fibrosis into two groups: those near the infected waters and those inland far from the infected water. This study aims to compare the differences in intestinal flora between two groups from the perspective of intestinal flora, and provide a basis for future prevention and control priorities. This study collected feces and basic information of patients with Schistosoma japonicum cirrhosis living near infected water and living on land. The characteristics of intestinal flora of the two types of patients were compared by 16sRNA sequencing technology. The infected water contact group and the terrestrial living group showed significant differences in intestinal flora characteristics: the former showed dominance of Firmicutes, high α-diversity, enrichment of butyrate-producing bacteria (such as Blautia), and enhanced environmental adaptability; the latter showed an imbalanced state with increased Proteobacteria and reduced α-diversity, accompanied by abnormal lipid metabolism and barrier function damage.},
}

Humans
*Schistosomiasis japonica/complications/microbiology
*Liver Cirrhosis/parasitology/microbiology/etiology
Animals
*Schistosoma japonicum
RNA, Ribosomal, 16S/genetics
*Gastrointestinal Microbiome
China
Feces/microbiology
Female
*Bacteria/classification/genetics/isolation & purification
Male
Sequence Analysis, DNA
Adult
DNA, Bacterial/genetics/chemistry
DNA, Ribosomal/genetics/chemistry
Middle Aged

@article {pmid42550338,
year = {2026},
author = {Kardan, R and Hemmati, J and Nazari, M and Chegini, Z and Ansariniya, H},
title = {Recent insights in pathogenesis of endometriosis with focus on gut microbiota.},
journal = {Molecular biology reports},
volume = {53},
number = {1},
pages = {},
pmid = {42550338},
issn = {1573-4978},
mesh = {Humans ; *Endometriosis/microbiology/metabolism/immunology ; Female ; *Gastrointestinal Microbiome/physiology ; Animals ; Dysbiosis/microbiology ; Fecal Microbiota Transplantation ; Estrogens/metabolism ; },
abstract = {EMs is a chronic, estrogen-dependent systemic inflammatory disorder defined by the ectopic implantation of endometrial glands and stroma and is frequently associated with dysmenorrhea, chronic pelvic pain, infertility, and substantial impairment in quality of life. Despite its high prevalence and socioeconomic burden, the etiopathogenesis of EMs remains incompletely elucidated and appears to involve intricate interactions among endocrine dysregulation, immune dysfunction, epigenetic reprogramming, ferroptosis, miRNA-mediated gene regulation, environmental exposures, and lifestyle-related factors. Accumulating evidence has increasingly implicated GM dysbiosis in EMs development and progression. Alterations in microbial diversity and composition have been associated with changes in host immune homeostasis, estrogen metabolism, intestinal barrier integrity, inflammatory signaling cascades, microbial-derived metabolites, and gut-brain axis communication, which may foster a pro-inflammatory pelvic microenvironment that in turn may facilitate lesion implantation, angiogenesis, neuroinflammation, and pain sensitization. Elevated lipopolysaccharide levels, reduced short-chain fatty acid production, Th17/Treg imbalance, macrophage polarization, and epigenetic modulation have also been associated with GM perturbations in EMs. This review synthesizes current advances in understanding the multifactorial mechanisms underlying EMs pathogenesis, with a particular emphasis on microbiota-host interactions. We also discuss emerging microbiota-targeted therapeutic strategies, including probiotics, dietary modulation, and fecal microbiota transplantation, highlighting their translational potential as adjunctive approaches for disease management and personalized medicine in EMs.},
}

Humans
*Endometriosis/microbiology/metabolism/immunology
Female
*Gastrointestinal Microbiome/physiology
Animals
Dysbiosis/microbiology
Fecal Microbiota Transplantation
Estrogens/metabolism

@article {pmid42550453,
year = {2026},
author = {Li, S and Zhang, Y and Li, Y and Lei, Y and Wu, H and Liu, P and Xi, W and Zhuo, X and Huang, P and Yang, T and Bai, T and Li, J and Cheng, L and Wang, Y and Li, T and Wu, Y},
title = {The maternal gut microbiota influences myocardial maturation and diastolic function of offspring in mice.},
journal = {Science China. Life sciences},
volume = {},
number = {},
pages = {},
pmid = {42550453},
issn = {1869-1889},
abstract = {Although the maternal microbiome is recognized as a critical regulator of offspring physiology, its role in heart development and the pathogenesis of heart failure remains largely unclear. Using a germ-free (GF) mouse model, we demonstrated that maternal microbiota depletion leads to spontaneous heart failure with preserved ejection fraction (HFpEF) in adult female offspring, recapitulating the phenotypes of human diastolic dysfunction. Integrated transcriptomic and proteomic profiling of fetal hearts revealed impaired structural cardiomyocyte maturation in GF offspring, characterized by suppressed sarcomere assembly. Metabolomic analysis revealed that acetate was concurrently downregulated in maternal serum and fetal cardiomyocytes. Importantly, prenatal acetate supplementation and fecal microbiota transplantation rescued fetal cardiomyocyte maturation defects and prevented the onset of HFpEF in adult female offspring. Mechanistically, maternal microbe-derived acetate regulates fetal cardiomyocyte maturation by enhancing the levels of H3K9ac and H3K27ac in the MYL2 promoter region, thereby promoting the transcriptional enhancement of MYL2. This developmental reprogramming provides lifelong protection against diastolic dysfunction. In addition, the concentration of acetate in pregnant women's serum was positively correlated with myocardial thickness in the left ventricle of the fetus. Our findings establish maternal microbial metabolites as determinants of cardiac maturation and suggest prenatal acetate supplementation as a novel preventive intervention for developmental diastolic dysfunction.},
}

@article {pmid41733389,
year = {2026},
author = {DeMeules, MM and Proll, SC and Hua, X and Srinivasan, S and Loeffelholz, T and Liu, C and Wu, MC and Fiedler, TL and Hoffman, NG and Bourassa, LA and Pergam, SA and Fredricks, DN},
title = {Gut Microbiota and Intestinal Monodomination as a Predictor for Bacteremia in Allogeneic Hematopoietic Cell Transplant Recipients.},
journal = {The Journal of infectious diseases},
volume = {234},
number = {1},
pages = {e81-e89},
doi = {10.1093/infdis/jiag005},
pmid = {41733389},
issn = {1537-6613},
support = {R01 AI134808/AI/NIAID NIH HHS/United States ; //National Institute of Allergy and Infectious Diseases/ ; R01 AI134808/NH/NIH HHS/United States ; P30CA015704//Fred Hutch Cancer Center/ ; R01 AI134808/NH/NIH HHS/United States ; },
mesh = {Humans ; *Hematopoietic Stem Cell Transplantation/adverse effects ; *Bacteremia/microbiology/etiology/diagnosis ; Female ; Male ; RNA, Ribosomal, 16S/genetics ; *Gastrointestinal Microbiome ; Feces/microbiology ; Middle Aged ; Transplantation, Homologous/adverse effects ; Adult ; Young Adult ; Aged ; Adolescent ; },
abstract = {BACKGROUND: Bacteremia is a frequent complication in patients undergoing allogeneic hematopoietic cell transplantation (HCT). Alterations to the gut microbiota after HCT have been associated with adverse outcomes including bacteremia and reduced overall survival. Previous studies suggest that loss of gut bacterial diversity and domination by a single species may predict bloodstream infections, but the degree of domination leading to the optimal positive predictive value (PPV) has not been defined.

METHODS: Stool samples were collected weekly from allogeneic HCT recipients and were analyzed by 16S rRNA gene PCR with sequencing to determine gut microbiota composition and document domination events. Bacteremia events were captured by review of medical records. The PPV for bacteremia of any detection of that species in stool and for domination events at 10%, 30%, and 50% abundance were calculated.

RESULTS: Of 277 HCT recipients, 95 experienced bacteremia, with 130 bacteremia events. Intestinal domination was associated with but not highly predictive for bacteremia, reflected by low PPV. Presence of coagulase-negative Staphylococcus in the gut at >30% relative abundance was associated with increased risk of coagulase-negative Staphylococcus bloodstream infections with PPV of 38%.

CONCLUSIONS: Hematopoietic cell transplantation is associated with significant disruption to the gut microbiota, particularly in patients who subsequently develop bacteremia. Intestinal domination may not be as useful as previously thought given its low PPV for most species implicated in bloodstream infections. The association between gut colonization with Staphylococcus and bacteremia events suggests that the gut may be an under-recognized portal of entry for these organisms in patients after HCT.},
}

Humans
*Hematopoietic Stem Cell Transplantation/adverse effects
*Bacteremia/microbiology/etiology/diagnosis
Female
Male
RNA, Ribosomal, 16S/genetics
*Gastrointestinal Microbiome
Feces/microbiology
Middle Aged
Transplantation, Homologous/adverse effects
Adult
Young Adult
Aged
Adolescent

@article {pmid42543158,
year = {2026},
author = {Jiao, Y and Li, L and Ji, X and Cheng, H},
title = {The Role of Gut Microbiota Interventions in the Management of Frailty Syndrome: A Scoping Review and Bibliometric Analysis.},
journal = {Geriatrics & gerontology international},
volume = {26},
number = {8},
pages = {e70734},
doi = {10.1111/ggi.70734},
pmid = {42543158},
issn = {1447-0594},
support = {82301786//National Natural Science Foundation of China (Youth Science Fund Project)/ ; },
mesh = {Humans ; *Frailty/therapy ; *Gastrointestinal Microbiome ; *Fecal Microbiota Transplantation ; Bibliometrics ; Probiotics/therapeutic use ; Prebiotics ; Frail Elderly ; Aged ; },
abstract = {AIM: The primary aim of this scoping review is to synthesize fragmented evidence on gut microbiota-targeted interventions for frailty. As a complementary objective, we conducted a bibliometric analysis to map the evolving knowledge landscape of this interdisciplinary field, thereby informing the development of future personalized therapeutic strategies and research priorities.

METHODS: We searched nine databases (PubMed, Embase, Web of Science, Scopus, Cochrane Library, CNKI, Wanfang, SinoMed, and VIP) from inception to July 2025 for the scoping review. A dedicated search of the Web of Science Core Collection (up to September 2025) was conducted for the bibliometric analysis to ensure data consistency. Two reviewers independently screened and extracted data. Bibliometric analyses (collaboration networks, keyword co-occurrence, and research trends) and visualizations were performed using CiteSpace (v6.3.R1).

RESULTS: The scoping review screened 3216 records and included 10 studies. Interventions-probiotics, prebiotics, synbiotics, and fecal microbiota transplantation-lasted 4 weeks to 6 months. Frailty was mainly assessed using Fried's phenotype, with outcomes covering frailty severity, physical function, gut microbiota composition, and inflammatory/metabolic markers. Bibliometric analysis identified 358 publications, revealing a sharp rise after 2016. China produced the most studies, and the University of Parma was the top institution. Key themes included gut microbiota, frailty, aging, inflammation, and sarcopenia.

CONCLUSIONS: Given the rapidly growing interest, gut microbiota-targeted interventions represent a promising strategy to slow frailty progression. Future efforts should therefore focus on establishing standardized, multidisciplinary assessment frameworks and elucidating the underlying mechanisms to advance precision nutrition for healthy aging.},
}

Humans
*Frailty/therapy
*Gastrointestinal Microbiome
*Fecal Microbiota Transplantation
Bibliometrics
Probiotics/therapeutic use
Prebiotics
Frail Elderly
Aged

@article {pmid42543274,
year = {2026},
author = {DU, YZ and Wang, Z and Ma, DC and Liu, T and Ma, LL and Zhou, YM and Li, XL and Dou, FY and Lyu, RL and Chai, MN and Zhang, YG and Li, YF},
title = {[Research progress on active ingredients of Astragali Radix and Acori Tatarinowii Rhizoma and mechanism of their herb pair against Alzheimer's disease].},
journal = {Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica},
volume = {51},
number = {11},
pages = {3152-3159},
doi = {10.19540/j.cnki.cjcmm.20260209.501},
pmid = {42543274},
issn = {1001-5302},
mesh = {*Alzheimer Disease/drug therapy/metabolism/genetics ; *Drugs, Chinese Herbal/chemistry/administration & dosage ; Humans ; Animals ; *Acorus/chemistry ; *Astragalus Plant/chemistry ; Rhizome/chemistry ; },
abstract = {Alzheimer's disease(AD) is a highly prevalent neurodegenerative disorder with complex pathogenesis. Currently available mainstream drugs offer limited efficacy and often cause significant side effects. The herb pair of Astragali Radix and Acori Tatarinowii Rhizoma, known for its Qi-tonifying and orifice-opening properties in TCM, has demonstrated advantages in multi-target and holistic regulation in anti-AD research. This review systematically summarizes the synergistic mechanisms of active ingredients such as astragaloside Ⅳ, calycosin, and β-asarone against AD through multiple pathways, including peroxisome proliferator-activated receptor γ(PPARγ)/brain-derived neurotrophic factor(BDNF) pathway, phosphatidylinositol 3-kinase(PI3K)/protein kinase B(Akt) pathway, and gut-brain axis. It also points out that current studies remain largely confined to in vitro and animal experiments, with insufficient evidence for clinical translation. Building on this, the review further proposes innovative research directions, such as constructing astragaloside Ⅳ-β-asarone co-delivery nanosystems, optimizing the compatibility ratio of the herb pair, and combining with fecal microbiota transplantation to validate causal mechanisms via microbiota-gut-brain axis. These proposals aim to provide a systematic theoretical framework and experimental pathway for the in-depth development and clinical translation of the herb pair of Astragali Radix and Acori Tatarinowii Rhizoma.},
}

*Alzheimer Disease/drug therapy/metabolism/genetics
*Drugs, Chinese Herbal/chemistry/administration & dosage
Humans
Animals
*Acorus/chemistry
*Astragalus Plant/chemistry
Rhizome/chemistry

@article {pmid42545016,
year = {2026},
author = {Seo, Y and Kim, J and Yeom, M and Park, S-Y and Lee, S and Ahn, S and Hahm, D-H and Kim, K and Kwon, S-K and Park, H-J},
title = {Gut microbiota contributes to the therapeutic effect of acupuncture in atopic dermatitis.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0391225},
doi = {10.1128/spectrum.03912-25},
pmid = {42545016},
issn = {2165-0497},
abstract = {UNLABELLED: The gut microbiome is increasingly recognized as a central regulator of immune homeostasis, metabolic balance, and therapeutic outcomes. Atopic dermatitis (AD), a chronic inflammatory skin disease, is closely linked to gut microbial dysbiosis. Traditionally regarded as a neurostimulatory therapy, acupuncture (Acu) has demonstrated increasing efficacy in alleviating AD symptoms and improving gastrointestinal function. These observations suggest that the therapeutic effects of Acu in AD may be mediated, in part, by modulation of the gut microbiome. In this study, AD patients were stratified into responder (R) and non-responder (NR) groups based on clinical improvement. Gut microbiome profiling revealed that R patients exhibited greater microbial diversity and compositional stability, indicative of a more balanced gut ecosystem. Specific taxa, including Alistipes ihumii and Odoribacter splanchnicus, were enriched in R individuals and may serve as microbial predictors of treatment responsiveness. Importantly, fecal microbiota transplantation (FMT) from R donors restored Acu efficacy in a mouse model of AD, whereas FMT from NR donors did not. These findings support the gut-skin axis and highlight the integral role of the gut microbiome in mediating the therapeutic effects of Acu for AD, suggesting potential for microbiome-based personalized treatment.

IMPORTANCE: Increasing evidence supports the gut microbiome's role in modulating treatment responses in atopic dermatitis (AD), but direct evidence linking acupuncture efficacy with microbiome composition has been lacking. Previous studies did not assess causal relationships via fecal microbiota transplantation (FMT) or functional metagenomics. This study identifies specific gut microbes associated with acupuncture response in AD and confirms their causal role using FMT. It also links functional metabolic pathways to therapeutic efficacy, offering a mechanism-based insight. Our findings support microbiome-informed personalized acupuncture approaches for AD and suggest gut microbiota as a therapeutic modulator in neuroimmune regulation.

CLINICAL TRIALS: This study was registered in the Korean Clinical Trial Registry (CRIS, registration number: KCT0005422).},
}

@article {pmid42542073,
year = {2026},
author = {Oriquat, G and Rizaev, J and Abdulqader, AF and Kadhim, AA and Jamuna, KV and Singhal, D and Bainsal, N and Mansurova, N},
title = {Gut microbiota and brain health: Disease-specific pathways and emerging therapeutic strategies.},
journal = {Multiple sclerosis and related disorders},
volume = {113},
number = {},
pages = {107407},
doi = {10.1016/j.msard.2026.107407},
pmid = {42542073},
issn = {2211-0356},
abstract = {The microbiota-gut-brain axis (MGBA) has emerged as a dynamic, bidirectional communication system linking the gastrointestinal tract and the central nervous system (CNS) through neural, immune, endocrine, and metabolic mechanisms. Increasing evidence indicates that alterations in gut microbial communities are associated with a wide range of neurological disorders; however, the strength of this association varies across diseases, and many mechanistic observations still rely predominantly on experimental models rather than human studies. This review provides an overview of current evidence regarding the role of the gut microbiota in maintaining CNS homeostasis, with particular emphasis on intestinal barrier function, immune modulation, vagal and enteric communication, and the generation of biologically active microbial metabolites, including short-chain fatty acids, bile acids, and neurotransmitter-related compounds. Studies in both clinical and experimental settings have reported disease-specific microbial signatures in conditions such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, autism spectrum disorders, and amyotrophic lateral sclerosis. In parallel, microbiota-directed interventions-including probiotics, prebiotics, dietary approaches, fecal microbiota transplantation, and strategies targeting microbial metabolites-have produced encouraging findings in preclinical studies and early-stage clinical investigations. Nevertheless, considerable heterogeneity in study populations, experimental methodologies, and therapeutic protocols continues to limit the translation of these findings into routine clinical practice. Collectively, current evidence supports the MGBA as a valuable framework for understanding neurological diseases while underscoring the need for rigorously designed longitudinal studies and well-controlled clinical trials to define its therapeutic relevance better.},
}

@article {pmid42542278,
year = {2026},
author = {Shukla, A and Rughwani, D and Aditya, AK and Ray, AK},
title = {The Impact of Climatic Extreme Temperatures on Gut Microbiome-mediated Cardio-Metabolic Health.},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {},
number = {},
pages = {128877},
doi = {10.1016/j.envpol.2026.128877},
pmid = {42542278},
issn = {1873-6424},
abstract = {Climate change increases extreme temperature events, like heat and cold waves. Temperature stress can cause gut dysbiosis, potentially affecting cardiometabolic health. In temperature stress conditions, beneficial microbes like Lactobacillus and Bifidobacterium, and favourable metabolites like short-chain fatty acids are observed to be downregulated, while features like Proteobacteria and Prevotella were found to be upregulated. These alterations may lead to upregulation of lipopolysaccharides, trimethylamine N-oxide, and dysregulation in bile acid metabolism, highlighting this as a potential biomarker for disease risk. Furthermore, we discussed mechanistic pathways potentially impacted, including endothelial dysfunction, gut barrier integrity, and energy homeostasis, that link microbial perturbations to metabolic dysfunction and increased risk of cardiometabolic diseases. Moreover, this review proposes potential therapeutic strategies like faecal microbiota transplantation, probiotic supplementation, nanomedicine, and dietary modulation that target the gut microbiome to alleviate the cardiometabolic risks exacerbated by temperature stress. This is the first review to comprehensively synthesize recent scientific findings on the impact of temperature stress in gut microbiome across multiple animal models, and its potential implications on cardiometabolic health.},
}

@article {pmid42538093,
year = {2026},
author = {Berry, P and Allegretti, JR and Khanna, S},
title = {Food and Drug Administration-Approved Fecal Microbiota-Based Therapies for Recurrent Clostridioides difficile Infection.},
journal = {Gastroenterology clinics of North America},
volume = {55},
number = {3},
pages = {503-516},
doi = {10.1016/j.gtc.2026.05.010},
pmid = {42538093},
issn = {1558-1942},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; *Clostridium Infections/therapy ; Recurrence ; United States ; Clostridioides difficile ; Anti-Bacterial Agents/therapeutic use ; United States Food and Drug Administration ; Secondary Prevention/methods ; },
abstract = {Recurrent Clostridioides difficile infection remains common despite optimized antibiotic therapy. Two Food and Drug Administration-approved donor-derived fecal microbiota-based products, fecal microbiota, live-jslm (Rebyota / RBL) and fecal microbiota spores, live-brpk (Vowst / VOS) reduce recurrence when administered after completion of standard antibiotics. This review summarizes the clinical development programs supporting these products, including pivotal randomized trials, open-label extensions, durability data, safety outcomes, and emerging real-world evidence. We also discuss patient selection, timing after antibiotics, diagnostic considerations, and practical implementation. These therapies represent standardized, evidence-based approaches to restoring colonization resistance and preventing recurrent infection in appropriately selected adults.},
}

Humans
*Fecal Microbiota Transplantation/methods
*Clostridium Infections/therapy
Recurrence
United States
Clostridioides difficile
Anti-Bacterial Agents/therapeutic use
United States Food and Drug Administration
Secondary Prevention/methods

@article {pmid42538384,
year = {2026},
author = {Chang, M and Wang, Y and Ha, J and Neale, ZR and Ajami, NJ and Diggs, LP and Nalin, AP and Ma, Y and Dong, S and Hoballah, YM and Day, A and Jeong, SD and Wu, A and Schrank, BR and Edwards, JL and Wang, T and Wang, X and Chang, YT and Tang, C and Lim, AJ and Torres, MN and Deng, W and Peitsch, T and Dufilho, MJ and Goswami, S and Jiang, D and Koong, AC and Sharma, P and Wargo, JA and Jiang, W and Kim, BYS},
title = {A transferable gut microbiota-bile acid pathway programs nanomedicine pharmacokinetics and therapeutic response.},
journal = {Nature materials},
volume = {},
number = {},
pages = {},
pmid = {42538384},
issn = {1476-4660},
abstract = {The clinical efficacy of nanomedicines is often limited by hepatic sequestration, yet the endogenous programs determining this clearance state remain incompletely understood. Here we identify the gut microbiota as a regulator of nanomedicine biodistribution through bile-acid-associated programming of Kupffer cell phagocytic state. Using germ-free mice, microbial perturbation, faecal microbiota transplantation and multiomic profiling, we show that metronidazole remodels the gut microbial ecology and reprograms Kupffer cells into a reduced-uptake state, thereby suppressing hepatic clearance and enhancing the tumour accumulation of nanomedicines across multiple formulations and tumour models. Single-cell RNA sequencing reveals a shift in Kupffer cell populations from phagocytic to quiescent states, whereas metabolomic profiling identifies microbiota-dependent reductions in bile acid availability. Gut-bacteria-derived bile acids induce Kupffer cell phagocytosis, and faecal transfer transmits the low-clearance phenotype, defining a transferable gut microbiota-bile acid-Kupffer cell pathway affecting nanomedicine clearance.},
}

@article {pmid42538676,
year = {2026},
author = {Aksoy, ÖY and Baskın, E and Siddiqui, MA and Akdeniz, A and Özçay, F and Şafak, A and Karakaya, E and Yıldırım, S and Haberal, M},
title = {Microbiological Evaluation of Diarrhea in Pediatric Kidney Transplant Recipients: A Retrospective Analysis.},
journal = {Experimental and clinical transplantation : official journal of the Middle East Society for Organ Transplantation},
volume = {24},
number = {Suppl 2},
pages = {172-176},
doi = {10.6002/ect.MESOT2025.O60},
pmid = {42538676},
issn = {2146-8427},
mesh = {Humans ; Retrospective Studies ; *Kidney Transplantation/adverse effects ; *Diarrhea/microbiology/diagnosis/virology/drug therapy/immunology ; Female ; Child ; Male ; Child, Preschool ; Adolescent ; *Feces/microbiology/virology ; Treatment Outcome ; Risk Factors ; Turkey ; Infant ; Age Factors ; *Bacterial Infections/microbiology/diagnosis ; *Bacteria/isolation & purification ; },
abstract = {OBJECTIVES: Diarrhea often occurs in pediatric kidney transplant recipients and can result from infectious or noninfectious causes. Identifying underlying issues can allow for proper management and prevent complications such as dehydration, graft dysfunction, and prolonged hospital stay.

MATERIALS AND METHODS: We retrospectively evaluated stool samples of 204 pediatric kidney transplant recipients seen at the Başkent University Hospital with complaint of diarrhea. Direct microscoping evaluation, bacterial cultures, and viral antigen testing for rotavirus and adenovirus were performed. Presence of cytomegalovirus and Clostridium difficile were evaluated in selected patients. In 18 patients, a comprehensive viral panel was performed based on clinical suspicion.

RESULTS: One patient each showed Shigella species and enteropathogenic Escherichia coli. Candida species was isolated in 1 sample. Rotavirus was detected in 4 patients, adenovirus in 2 patients, and Clostridium difficile toxin in 0 patients. Among the 18 patients who underwent detailed panel testing, norovirus was detected in 2 patients and sapovirus in 1 patient. Forty -seven stool culture samples showed reduced or absent normal intestinal flora, suggesting possible intestinal dysbiosis. Entamoeba was detected in 7 patients. Cytomegalovirus was positive in 24 of 204 patients (11 %). On direct microscopic examination, 19 patients showed minimal findings, and 24 patients had moderate findings. Fourteen patients had high numbers of leukocytes and erythrocytes in their stool. Because amebic colitis and Clostridium difficile infection could not be excluded, patients with moderate to severe findings were treated with metronidazole.

CONCLUSIONS: Among pediatric kidney transplant patients with diarrhea, the rate of intestinal pathogens was slow but reduced normal flora in stool cultures was common, indicating microbiota -related etiologies. The high rate of cytomegalovirus infection among patients suggested that cytomegalovirus infection should be considered as a potential etiological factor in pediatric transplant patients presenting with diarrhea. Noninfectious causes should also be considered in differential diagnosis of diarrhea in solid -organ transplant recipients.},
}

Humans
Retrospective Studies
*Kidney Transplantation/adverse effects
*Diarrhea/microbiology/diagnosis/virology/drug therapy/immunology
Female
Child
Male
Child, Preschool
Adolescent
*Feces/microbiology/virology
Treatment Outcome
Risk Factors
Turkey
Infant
Age Factors
*Bacterial Infections/microbiology/diagnosis
*Bacteria/isolation & purification

@article {pmid42539524,
year = {2026},
author = {Fletcher, AA and Koberssy, Z and Daher, J and Moussallem, N and McComsey, GA},
title = {Feeding the gut-immune axis: dietary, prebiotic, and probiotic strategies to target persistent inflammation in ART-treated HIV: a narrative review.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1877822},
doi = {10.3389/fimmu.2026.1877822},
pmid = {42539524},
issn = {1664-3224},
mesh = {Humans ; *HIV Infections/immunology/drug therapy ; *Probiotics/therapeutic use/administration & dosage ; *Prebiotics/administration & dosage ; *Inflammation/immunology/therapy ; *Gastrointestinal Microbiome/immunology ; Dysbiosis ; Intestinal Barrier Function ; },
abstract = {People living with HIV (PWH) experience ongoing systemic inflammation driven by gut dysbiosis, epithelial barrier disruption, and microbial translocation, despite antiretroviral therapy (ART). This review examines evidence from randomized controlled trials, mechanistic studies, systematic reviews, and meta-analyses evaluating nutritional and microbiome-based interventions to reduce inflammation in PWH. Reduced production of short-chain fatty acids (SCFAs) by the gut microbiota has been observed to precede morbidity and mortality in PWH, with SCFAs, mainly butyrate, exerting immunomodulatory effects through promoting regulatory T-cell differentiation via histone deacetylase inhibition and G protein-coupled receptor 43 (GPR43) and GPR109A signaling, suppressing nuclear factor kappa B (NF-κB)-mediated pro-inflammatory cytokine production, and enhancing epithelial tight junction integrity. Probiotics, prebiotics, synbiotics, and fecal microbiota transplantation have demonstrated reductions in inflammatory biomarkers including soluble CD14 (sCD14), lipopolysaccharide-binding protein (LBP), and high-sensitivity C-reactive protein (hsCRP). The Mediterranean diet, omega-3 fatty acids, and polyphenol-rich foods represent an underexplored area as modulators of gut microbiota composition and SCFA production. Existing gaps in the literature include a lack of trials with clinically meaningful endpoints, optimal probiotic strains and doses, and lack of randomized trials evaluating anti-inflammatory dietary patterns in PWH. We propose a research agenda prioritizing Mediterranean diet intervention trials, precision microbiome interventions, and combination approaches integrating dietary modification with microbiome-targeted therapies. Lastly, we provide practical nutritional recommendations for clinicians managing PWH.},
}

Humans
*HIV Infections/immunology/drug therapy
*Probiotics/therapeutic use/administration & dosage
*Prebiotics/administration & dosage
*Inflammation/immunology/therapy
*Gastrointestinal Microbiome/immunology
Dysbiosis
Intestinal Barrier Function

@article {pmid42539626,
year = {2026},
author = {Han, J and Zhao, W and Deng, R and Wang, Y and Gong, W and Wang, Z and Sun, G and Liu, H and Geng, M and Zhang, Y},
title = {Sodium oligomannate reduces cerebral infarction and improves neurological function through microbiota remodeling in MCAO/R rats.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1880590},
doi = {10.3389/fphar.2026.1880590},
pmid = {42539626},
issn = {1663-9812},
abstract = {BACKGROUND: Ischemic stroke is the second leading cause of death worldwide, characterized by high mortality and a narrow therapeutic window for thrombolysis. Gut microbiota dysbiosis and gliosis following ischemic stroke are key drivers of post-stroke neurological impairment. Sodium oligomannate (GV-971) is a low-molecular-weight acidic oligosaccharide that targets the gut-brain axis. It alleviates gliosis and improves cognitive dysfunction by remodeling gut microbiota in Alzheimer's disease. However, it is still unknown whether GV-971 has pharmacological activity against ischemic stroke.

METHODS: Here, we explore the efficacy of GV-971 on infarct volume, gliosis, blood-brain barrier integrity, gut microbiota composition, and post-stroke cognitive impairment (PSCI) using a middle cerebral artery occlusion/reperfusion (MCAO/R) model in male Sprague-Dawley rats.

RESULTS: Administer medication before surgery for 4 consecutive days and once after surgery, after stroke 24-hour triphenyltetrazolium chloride (TTC) staining revealed that 0.3 mg/kg GV-971 significantly reduced infarct volume in ischemic brain tissue from 37.81±2.391% to 13.30±4.801% and neurological impairment score of GV-971 treatment significantly decreased from 11.50±0.54 to 7.29±1.47. After stroke 24-hour immunofluorescence analysis of glial activation confirmed that GV-971 significantly reduced central inflammatory responses. Western blot combined with Evans blue staining collectively demonstrated that after stroke 24-hour, GV-971 exerts a significant protective effect on the blood-brain barrier. In the gut, GV-971 reversed microbial dysbiosis, as revealed by shotgun metagenomics, enhanced intestinal barrier integrity, and suppressed colonic inflammation. Antibiotic depletion abolished GV-971's neuroprotective effect, while fecal microbiota transplantation from GV-971-treated donors restored protection, supporting a microbiota-dependent contribution. Furthermore, GV-971-treated rats subjected to MCAO/R exhibited significant improvements in motor and cognitive function. For example, on day 35, Y-maze test results indicated that GV-971 administered either before MCAO/R (pre-treatment) or during the perioperative period (co-treatment) increased spontaneous alternation rate from 60.95±4.91% to 85.60±6.32% and 85.64±5.027%. On day 32, novel object recognition assay results indicated that GV-971 treatment increased new-object exploration from 0.2039±0.03752 to 0.3991±0.1122 (pre-treatment) and 0.5066±0.06982 (co-treatment). On day 42, Barnes maze test results indicated that GV-971 treatment reduced the time required to locate the target hole from 76.45±17.41s to 31.03±20.75 s and 33.37±19.30 s for pre- and co-treatment, respectively.

CONCLUSION: Taken together, GV-971 demonstrated neuroprotective potential in experimental ischemic stroke.},
}

@article {pmid42539659,
year = {2026},
author = {He, Q and Zhang, P and Chen, Z and Wen, C and Wang, M},
title = {Frontier research and clinical application prospects of microbiome biomarkers in autoimmune diseases.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1752840},
doi = {10.3389/fimmu.2026.1752840},
pmid = {42539659},
issn = {1664-3224},
mesh = {Humans ; *Autoimmune Diseases/microbiology/therapy/diagnosis/immunology/etiology ; Biomarkers ; *Microbiota/immunology ; Dysbiosis/immunology ; Animals ; Multiomics ; Precision Medicine ; },
abstract = {The microbiome is increasingly recognized as a master regulator of immune homeostasis and a key environmental factor associated with the pathogenesis of autoimmune diseases (ADs). This review comprehensively synthesizes current knowledge on how microbial communities and their metabolites may contribute to ADs' development through microbial-immune interactions, dysbiosis, and the involvement of viral and fungal components within an integrated inter-kingdom ecosystem. We propose an operational definition of microbiome biomarkers as measurable microbiome-associated features reflecting disease susceptibility, activity, prognosis, or therapeutic response and categorize them into three classes: taxonomic, functional/metabolic, and host-microbiome interaction-derived biomarkers. We critically evaluate the evidence for specific microbial signatures as biomarkers for early diagnosis, disease monitoring, and prediction of therapeutic responses, incorporating evidence grading that distinguishes validated biomarkers from those that remain exploratory and discussing shared versus disease-specific signatures across ADs. The translational potential of microbiome-targeted interventions, including probiotics, prebiotics, and fecal microbiota transplantation, is examined within a personalized medicine framework, with barriers to clinical implementation explicitly addressed. Key confounding factors such as diet, geographic origin, and medication use are highlighted as critical variables shaping microbiome signatures independently of disease. Looking forward, the convergence of multi-omics technologies and artificial intelligence for biomarker discovery, multi-omics integration, and clinical validation promises to unravel the complex microbiome-immune crosstalk, enabling more accurate diagnosis, prognostic stratification, and ultimately, individualized microbiota-informed therapy.},
}

Humans
*Autoimmune Diseases/microbiology/therapy/diagnosis/immunology/etiology
Biomarkers
*Microbiota/immunology
Dysbiosis/immunology
Animals
Multiomics
Precision Medicine

@article {pmid42540216,
year = {2026},
author = {Ahmadi, P and Mahmoudi, M and Mozaffari-Jovin, S and Kheder, RK and Faraj, TA and Mollazadeh, S and Hajavi, J and Kolahdooz, H and Esmaeili, SA},
title = {The Impact of Oral-Gut Microbiota Structure and Its Manipulation on RA Development and Management.},
journal = {Food science & nutrition},
volume = {14},
number = {8},
pages = {e72090},
doi = {10.1002/fsn3.72090},
pmid = {42540216},
issn = {2048-7177},
abstract = {Rheumatoid arthritis (RA) is a prevalent autoimmune disease shaped by genetic susceptibility and environmental triggers, particularly the microbiota. Numerous studies have documented substantial structural differences in the oral-gut microbiota between patients with RA and healthy individuals. Emerging evidence suggests that upregulation of specific pathobionts-including Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, and Prevotella copri-coupled with autoantigen mimicry and inflammatory cascades, may contribute to RA initiation at extra-articular sites. Conversely, several immunoregulatory bacterial species, such as Bacteroides fragilis, Prevotella histicola, and Clostridium spp., are depleted in patients with RA. Importantly, nutritional factors (including, minerals, vitamins, fiber, flavonoids and polyphenols) and dietary patterns (e.g., Western diet, high-fat diet, Mediterranean diet, fasting, protein- or carbohydrate-rich diets) profoundly shape oral-gut microbial composition, and dietary interventions can either potentiate or suppress these microbial populations. Accordingly, recent management strategies have focused on manipulating dysbiosis through probiotic supplementation (e.g., immunomodulatory Lactobacillus strains), fecal microbiota transplantation (FMT), antibiotic administration, and targeted nutritional interventions that support probiotic efficacy and restore eubiosis. This review discusses the characteristic microbiota structure in patients with RA and evaluates emerging therapeutic strategies-FMT, antibiotics, probiotics, and nutrition-as integrated approaches for RA management.},
}

@article {pmid42541796,
year = {2026},
author = {Kroneislová, G and Závora, J and Adámková, V},
title = {[Clostridioides difficile infection: Current perspectives on diagnosis and therapy].},
journal = {Klinicka mikrobiologie a infekcni lekarstvi},
volume = {32},
number = {2},
pages = {90-93},
pmid = {42541796},
issn = {1211-264X},
mesh = {Humans ; *Clostridium Infections/diagnosis/therapy/drug therapy ; Anti-Bacterial Agents/therapeutic use ; Clostridioides difficile ; Fecal Microbiota Transplantation ; },
abstract = {Clostridioides difficile is an important opportunistic pathogen mainly linked to healthcare-associated infections, which arise when the intestinal microbiota is disrupted - most often due to antibiotic treatment. In recent years, however, its presence in the community has been reported more frequently. The incidence of C. difficile infection reflects both the quality of antibiotic policies and the rigor of infection control, while mortality remains substantial, especially among the elderly and patients with multiple comorbidities. The pathogenesis of the disease is based on the production of toxins A and B, which damage the intestinal epithelium and lead to the development of manifestations ranging from mild diarrhea to fulminant colitis. Diagnosis requires correlation of the clinical presentation with evidence of a toxigenic strain or its toxins while colonization alone, without clinical symptoms, is not an indication for treatment. The high rate of recurrence remains a significant problem. A rational antibiotic policy and strict hygiene measures play a crucial role in prevention. The treatment of C. difficile infection has undergone a significant shift in recent years. Current recommendations favor fidaxomicin as the first-line treatment for the initial episode due to a lower risk of recurrence; oral vancomycin is an alternative. For recurrent forms, an individualized approach is necessary, including the possibility of using fecal microbiota transplant or monoclonal antibodies. In the Czech Republic, oral vancomycin is still widely used; it is now also available in a standardized capsule form, which improves pharmaceutical safety and facilitates dosing. Keywords: Clostridioides difficile, fidaxomicin, oral vancomycin, antimicrobial stewardship.},
}

Humans
*Clostridium Infections/diagnosis/therapy/drug therapy
Anti-Bacterial Agents/therapeutic use
Clostridioides difficile
Fecal Microbiota Transplantation

@article {pmid42542058,
year = {2026},
author = {Jia, R and Wang, Y and Wang, J and Zhang, M and Zhu, A},
title = {Huangjin Shuangshen Jiawei decoction alleviated coronary heart disease comorbid with depression partly through gut microbiota-mediated regulation of the SRSF1-p53-ASPP1 signaling axis.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {160},
number = {},
pages = {158617},
doi = {10.1016/j.phymed.2026.158617},
pmid = {42542058},
issn = {1618-095X},
abstract = {BACKGROUND: Coronary heart disease comorbid with depression (CHDD) was associated with poor clinical outcomes and was increasingly linked to gut microbiota dysregulation. Huangjin Shuangshen Jiawei decoction (HJSSJW) showed therapeutic potential in CHDD; however, the microbiota-dependent mechanisms underlying its protective effects remained unclear.

PURPOSE: This study was designed to evaluate the effects of HJSSJW on the gut microbiota in murine models of CHDD and to elucidate the potential molecular mechanisms underlying its protective effects.

METHODS: The protective effects of HJSSJW were evaluated in a murine model of CHDD using cardiac ultrasound, histopathological analysis, behavioral assessments, and immunofluorescence staining. To investigate the role of the gut microbiota, microbiota depletion was achieved through antibiotic (ABX) treatment, and fecal microbiota transplantation (FMT) was performed to assess microbiota-mediated effects. In parallel, three bacterial strains enriched in CHDD patients following HJSSJW treatment-Faecalibacterium prausnitzii, Parabacteroides goldsteinii, and Butyricicoccus pullicaecorum-were identified and selected for further validation. Their protective effects were further evaluated through colonization experiments in ABX-treated CHDD mice.

RESULTS: HJSSJW markedly improved cardiac function in CHDD mice, significantly reduced serum myocardial injury markers, decreased cardiomyocyte apoptosis, and alleviated depressive-like behaviors. In ABX-treated CHDD mice, gut microbiota depletion attenuated the therapeutic efficacy of HJSSJW, whereas FMT from HJSSJW-treated donors partially reproduced these protective effects, suggesting that its actions were at least partially mediated by the gut microbiota. Moreover, colonization with Faecalibacterium prausnitzii, Parabacteroides goldsteinii, or Butyricicoccus pullicaecorum similarly improved cardiac function, reduced myocardial injury markers, attenuated cardiomyocyte apoptosis, and ameliorated depressive-like behaviors in CHDD mice, supporting the contributory roles of these bacteria in the protective effects of HJSSJW.

CONCLUSION: HJSSJW exerted coordinated cardioprotective and antidepressant effects in CHDD, which were at least partially mediated by the gut microbiota and were associated with the restoration of the dysregulated SRSF1-p53-ASPP1 signaling axis in cardiac and brain tissues. These findings suggested that HJSSJW might represent a multitarget therapeutic strategy for CHDD and further supported gut microbiota-targeted interventions as a promising therapeutic approach for CHDD.},
}

@article {pmid42542061,
year = {2026},
author = {Xie, Y and Zhang, C and Guo, C and Chen, Y and Xia, M and Yu, W and Wang, D and Dai, X},
title = {Refined Changqin NO.1 regulates gut microbiota and their metabolites to mediate PANoptosis and alleviate traumatic brain injury.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {160},
number = {},
pages = {158520},
doi = {10.1016/j.phymed.2026.158520},
pmid = {42542061},
issn = {1618-095X},
abstract = {BACKGROUND: Refined Changqin NO.1 (R-Cq1) has shown favorable therapeutic effects in traumatic brain injury (TBI), which triggers neuronal PANoptosis and involves dysregulation of gut microbiota and metabolites.

PURPOSE: This study investigates whether R-Cq1 improves TBI through gut-brain axis-mediated neuronal PANoptosis.

STUDY DESIGN: A TBI mouse model and injured neurons were used to assess the effects of R-Cq1 on gut microbiota, short-chain fatty acid (SCFA) profiles, TNF-α signaling, and neuronal PANoptosis.

METHODS: R-Cq1 was administered to TBI mice, and their fecal samples were subjected to 16S rRNA sequencing and targeted metabolomics. Injured neurons were treated with 3-methylbutanoic acid (3-MA), R-Cq1, and TNF-α inhibitor 3,6'-dithiothalidomide, followed by assessment of neuronal PANoptosis. Anaerotruncus colihominis was transplanted into R-Cq1-treated TBI mice, which underwent neurological function assessment.

RESULTS: R-Cq1 improved neurological outcomes in TBI mice and attenuated TBI-induced neuronal death. Immunofluorescence analysis of the gut revealed TBI-induced intestinal barrier disruption, which was mitigated by R-Cq1. Consistently, R-Cq1 reshaped the gut microbiota, reducing the abundance of the genus Anaerotruncus in TBI mice. Anaerotruncus showed a significant positive correlation with modified neurological severity scores. TBI induced alterations in SCFA profiles, with 3-MA significantly increased, which was suppressed by R-Cq1 treatment. 3-MA was positively correlated with modified neurological severity scores and genus Anaerotruncus. In vitro, 3-MA exacerbated PANoptosis, as indicated by increased levels of N-GSDMD, p-MLKL, and cleaved caspase-8, and reversed the inhibitory effect of R-Cq1 on PANoptosis. We also found that 3-MA upregulated TNF-α in scratched neurons. However, when TNF-α was inhibited, the pro-PANoptotic effect of 3-MA was attenuated. In TBI mice treated with R-Cq1, gavage with 3-MA-related Anaerotruncus colihominis abolished the neuroprotective effects of R-Cq1 and increased neuronal death.

CONCLUSION: Collectively, R-Cq1 suppresses Anaerotruncus-associated 3-MA to hinder TNF-α upregulation, thereby alleviating neuronal PANoptosis and TBI. This study elucidates the underlying therapeutic mechanism of R-Cq1 in TBI.},
}

@article {pmid42533067,
year = {2026},
author = {McCallin, S and Classen, AY and Lieberknecht-Jouy, SC and Abdula, F and Dugas, S and Gross, O and Koliwer-Brandl, H and Lassen, S and Scheidegger, J and Dunne, M and Kahles, A and Eigler, J and Farowski, F and Higgins, PG and Milek, S and Chemych, O and Du, J and Loessner, MJ and Kessler, TM and Vehreschild, MJGT and Leitner, L and Biehl, LM},
title = {Combined phage therapy and faecal microbiota transplantation to treat recurrent urinary tract infection: a case series.},
journal = {Nature microbiology},
volume = {11},
number = {8},
pages = {2112-2118},
pmid = {42533067},
issn = {2058-5276},
support = {FK-22-052//Universität Zürich (University of Zurich)/ ; 955974 (VIROINF)//EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 Marie Skłodowska-Curie Actions (H2020 Excellent Science - Marie Skłodowska-Curie Actions)/ ; CRSII5_189957//Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (Swiss National Science Foundation)/ ; CRSII5_189957//Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (Swiss National Science Foundation)/ ; DZIF TI 07.005_Biehl//Deutsches Zentrum für Infektionsforschung (German Center for Infection Research)/ ; },
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; *Urinary Tract Infections/therapy/microbiology ; Female ; *Phage Therapy/methods ; Recurrence ; Escherichia coli/isolation & purification ; Middle Aged ; Aged ; Escherichia coli Infections/therapy/microbiology ; Treatment Outcome ; Feces/microbiology ; Combined Modality Therapy ; },
abstract = {Recurrent urinary tract infections are recalcitrant and difficult-to-treat bacterial infections that primarily affect women. Here we combine phage therapy with faecal microbiota transplantation to decolonize the urinary and intestinal reservoirs of patients with recurrent urinary tract infections. Three women received oral and intravesical phage therapy for 8 days, and two underwent subsequent faecal microbiota transplantation. Treatments were well tolerated, and although Escherichia coli was detected in follow-up samples, patients experienced none or fewer and less severe episodes of urinary tract infection 24 months post-treatment.},
}

Humans
*Fecal Microbiota Transplantation/methods
*Urinary Tract Infections/therapy/microbiology
Female
*Phage Therapy/methods
Recurrence
Escherichia coli/isolation & purification
Middle Aged
Aged
Escherichia coli Infections/therapy/microbiology
Treatment Outcome
Feces/microbiology
Combined Modality Therapy

@article {pmid42533232,
year = {2026},
author = {Siam, AM and Moubarak, ES and Mahmoud, NE and Khelifa, H and Aljalawy, F and Hassan, AA and Ahmed, NAT and Wagdy, M and Heikal, Y and Abbas, OF},
title = {Efficacy and safety of fecal microbiota transplantation in Parkinson's disease: a systematic review and meta-analysis of randomized controlled trials with GRADE assessment.},
journal = {Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology},
volume = {47},
number = {8},
pages = {},
pmid = {42533232},
issn = {1590-3478},
mesh = {Humans ; *Parkinson Disease/therapy ; *Randomized Controlled Trials as Topic ; *Fecal Microbiota Transplantation/methods/adverse effects ; Treatment Outcome ; },
abstract = {BACKGROUND: Parkinson's disease (PD) is a common neurodegenerative disease that is a growing public health challenge. Recent evidence showed that gut microbiota dysbiosis is involved in the pathogenesis of PD, prompting interest in fecal microbiota transplantation (FMT) as a potential disease-modifying intervention. This systematic review and meta-analysis aim to evaluate the efficacy and safety of FMT in patients with PD.

METHODS: We conducted a systematic literature review using PubMed, Scopus, Web of Science, and the Cochrane Library till June 4, 2026, to identify RCTs comparing FMT with placebo or control interventions in PD. After removal of duplicates alongside title and abstract screening, followed by full-text screening, seven randomized controlled trials were included in this systematic review and meta-analysis.

RESULTS: A total of seven randomized controlled trials (RCTs) with 318 subjects were analyzed. FMT was delivered via oral capsules, nasojejunal tubes, or colonoscopy, with follow-up periods ranging from 12 to 52 weeks. The meta-analysis indicated a notable short-term enhancement in daily motor activities, as assessed by MDSUPDRS Part II, after one month (mean difference - 2.19, 95% confidence interval - 4.32 to -0.06; P = 0.044). Nevertheless, no significant estimates were noted for MDS-UPDRS Part III, aggregate MDS-UPDRS scores, motor complications, non-motor symptoms, or overall life quality at any assessed time frame. Some individual studies reported gains in cognitive ability, anxious feelings, quality of life related to constipation, and certain PDQ-39 categories, although these improvements were not uniformly observed. Overall, FMT was well tolerated by participants, with adverse reactions mostly comprising mild, self-resolving gastrointestinal issues and no major safety risks.

CONCLUSIONS: FMT is a safe treatment for individuals with PD and may offer modest short-term advantages in performing daily motor tasks. However, current evidence does not indicate lasting enhancements in overall motor capabilities, non-motor symptoms, or life quality. More extensive and sufficiently powered trials utilizing standardized FMT procedures and longer observation periods are necessary to elucidate the therapeutic benefits of FMT in Parkinson's disease.},
}

Humans
*Parkinson Disease/therapy
*Randomized Controlled Trials as Topic
*Fecal Microbiota Transplantation/methods/adverse effects
Treatment Outcome

@article {pmid42534583,
year = {2026},
author = {Tan, Z and Hu, J and Ye, B and Liu, W},
title = {Gastrointestinal acute graft versus host disease: a translational perspective from pathogenesis to precision prevention and treatment.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1876441},
pmid = {42534583},
issn = {1664-3224},
mesh = {Humans ; *Graft vs Host Disease/prevention & control/therapy/etiology/immunology/diagnosis ; Precision Medicine ; Gastrointestinal Microbiome/immunology ; *Gastrointestinal Diseases/therapy/etiology/prevention & control ; Animals ; *Hematopoietic Stem Cell Transplantation/adverse effects ; Fecal Microbiota Transplantation ; Acute Disease ; Biomarkers ; },
abstract = {Allo-HSCT represents a curative option for various hematological disorders. However, aGVHD remains the leading cause of non-relapse mortality following transplantation. The gastrointestinal tract is the most severely affected and prognostically unfavorable target organ in aGVHD, driven by donor T-cell-mediated epithelial damage, microbiota dysbiosis-driven immune amplification, and a self-perpetuating cycle of barrier disruption. Recent multi-omics studies have identified key pathogenic mechanisms, including microbiota-driven MHC-II expression and immunomodulation by microbial metabolites. Biomarker-driven risk stratification using the MAGIC algorithm has shifted management toward precision medicine, while targeted agents such as ruxolitinib, vedolizumab, and microbiota-directed interventions are reshaping therapeutic strategies. Novel interventional modalities, including FMT, recombinant LCN2, and specific bile acids, have forged innovative avenues that synergize microbiota-directed approaches with immunomodulation for the prevention and treatment of GI-aGVHD. This review systematically delineates the latest advances in the pathogenesis, risk stratification, and therapeutic strategies for GI-aGVHD, and envisions future directions for precision medicine centered on personalized microbiota-immune interventions.},
}

Humans
*Graft vs Host Disease/prevention & control/therapy/etiology/immunology/diagnosis
Precision Medicine
Gastrointestinal Microbiome/immunology
*Gastrointestinal Diseases/therapy/etiology/prevention & control
Animals
*Hematopoietic Stem Cell Transplantation/adverse effects
Fecal Microbiota Transplantation
Acute Disease
Biomarkers

@article {pmid42534787,
year = {2026},
author = {Xiao, J and Xu, T and Fu, Y and Xia, J and Chen, Z and Yin, X and Chen, X},
title = {Microbiota-derived metabolites and cognitive dysfunction in dialysis patients: mechanisms and targeted therapeutic strategies.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1878545},
pmid = {42534787},
issn = {1664-302X},
abstract = {Cognitive impairment (CI) in dialysis patients is a common and serious complication that significantly affects prognosis, with lack of effective treatment strategies. However, its mechanisms are still not fully clear, and effective treatment strategies are still limited. In recent years, more evidence has suggested that gut microbiota dysbiosis and changes in gut-derived metabolites may be involved in the development of CI in dialysis patients through the microbiota-gut-kidney-brain axis. Recent studies have shown that gut microbiota dysbiosis in dialysis patients may promote the progression of CI through several pathways. These include the accumulation of gut-derived uremic toxins, such as indoxyl sulfate (IS), p-cresyl sulfate (PCS), and Trimethylamine N oxide (TMAO), changes in bile acid metabolism; and the reduction of short-chain fatty acids (SCFAs) with neuroprotective effects. These changes may damage the intestinal barrier and the blood-brain barrier (BBB), and promote systemic inflammation, oxidative stress, and neuroinflammation. As a result, cognitive dysfunction in dialysis patients may be further aggravated. Therefore, targeting the gut microbiota has become a promising treatment direction. These strategies include dietary intervention, probiotics and related preparations, fecal microbiota transplantation (FMT), and targeted removal of uremic toxins and their derivatives. This review summarizes the gut microbiota composition associated with CI in dialysis patients, examines the molecular mechanisms of injury mediated by the microbiota-gut-brain-kidney axis, evaluates current microbiota-targeted interventions, and discusses future research directions for improving clinical prevention and treatment.},
}

@article {pmid42535042,
year = {2026},
author = {Ahad, A and Kumar, S and Kolomar, H and Williams, J and Abdallah, AI and Sadeghzadegan, A and Yateem, D and Kharel, P and Chowdhury, D and Alnajar, F and Ali, M},
title = {Fecal Microbiota Transplantation (FMT) in the Management of Ulcerative Colitis: A Comprehensive Systematic Review and Meta-Analysis of Randomized Controlled Trials (RCTs).},
journal = {Cureus},
volume = {18},
number = {6},
pages = {e111804},
pmid = {42535042},
issn = {2168-8184},
abstract = {Ulcerative colitis (UC) is a chronic inflammatory disorder of the colon with increasing global prevalence, particularly in newly industrialized countries. Fecal microbiota transplantation (FMT) has worked as an effective therapeutic strategy aimed at restoring immune homeostasis and gut microbial balance. However, a lack of standardized protocols and comprehensive safety data necessitates further evaluation. This meta-analysis aims to comprehensively analyze the efficacy of FMT in inducing clinical remission in UC, incorporating the latest randomized controlled trials (RCTs). A systematic review and meta-analysis of RCTs investigating FMT in UC were conducted. The primary outcomes were clinical and endoscopic remission, while adverse events (AEs) were assessed as secondary outcomes. Pooled risk ratios (RRs) with 95% confidence intervals (CIs) were calculated, and heterogeneity was analyzed using the I[2] statistic and Cochran's Q test. Overall, FMT demonstrated a significant benefit in inducing clinical remission compared with placebo (RR 1.55; 95% CI 1.22-1.96; p = 0.0003). For endoscopic remission, FMT showed a significant overall effect (RR 1.68; 95% CI 1.15-2.46; p = 0.007). The incidence of AEs was comparable between the FMT and control groups (RR 0.88; 95% CI 0.77-1.00; p = 0.06). This meta-analysis gives strong confirmation for the efficacy of FMT in inducing both clinical and endoscopic remission in UC patients, with a favorable safety profile. Multi-donor FMT and oral capsule administration appear to be particularly promising. Future research should focus on standardizing protocols, elucidating mechanisms of action, and conducting larger, long-term trials to optimize FMT for UC.},
}

@article {pmid42535602,
year = {2026},
author = {Pérez-Gordo, M and Álvarez-Lafuente, R and Bartra, J and Fernández-Nebro, A and Muñoz-Cano, R and Núñez, R and Pérez-Sánchez, N and Rodríguez-Rodríguez, L and Zanón-Moreno, V and Cornejo-García, JA},
title = {Gut Microbiota and Inflammatory Diseases: Emerging Insights and Therapeutic Perspectives. A Report From the Spanish Inflammatory Diseases Network.},
journal = {Journal of investigational allergology & clinical immunology},
volume = {},
number = {},
pages = {0},
doi = {10.18176/jiaci.1196},
pmid = {42535602},
issn = {1018-9068},
abstract = {The gut microbiota constitutes a highly complex ecosystem that plays a pivotal role in maintaining human health and modulating the immune response. Dysbiosis, an imbalance in the composition of gut microbiota, has been linked to the development and progression of multiple immune-mediated inflammatory diseases (IMIDs) and allergic disorders. Advances in sequencing and bioinformatics have enabled a deeper understanding of microbial diversity and function, revealing the crucial role of metabolites such as short-chain fatty acids (SCFAs) and secondary bile acids in sustaining epithelial integrity and immune tolerance. Altered microbiota profiles are associated with increased intestinal permeability, systemic inflammation, and autoimmune conditions including multiple sclerosis, rheumatoid arthritis, and inflammatory eye disease. Early-life establishment of microbiota is also critical, influencing susceptibility to asthma, food allergy, and other atopic conditions, such as drug hypersensitivity. Emerging therapeutic strategies aim to restore microbial balance through interventions such as the administration of probiotics, prebiotics, symbiotics, or postbiotics and fecal microbiota transplantation. Preliminary clinical evidence suggests these interventions may enhance barrier function, modulate inflammation, and improve clinical outcomes, although methodological heterogeneity and limited sample sizes constrain their application. Specific findings highlight that modulation of SCFAs and targeted bacterial taxa may influence disease activity and response to treatment. Future research should focus on identifying disease-specific microbial signatures, optimizing therapeutic formulations, and standardizing protocols for microbiota-based interventions. Integrating multiomics analyses and artificial intelligence will be essential if we are to develop predictive biomarkers and personalized therapies. Modulation of the microbiota is therefore positioned as a promising avenue in the prevention and management of IMIDs and allergic diseases.},
}

@article {pmid42537291,
year = {2026},
author = {Wu, Y and Dong, Z and Wang, D and Dong, J and Jiang, X and Fu, G and Cheng, M},
title = {Oral exposure to non-brain-penetrable microplastics induces neurotoxicity via disrupting the gut microbiota-tryptophan metabolism-microglial autophagy cascade.},
journal = {Journal of hazardous materials},
volume = {515},
number = {},
pages = {143127},
doi = {10.1016/j.jhazmat.2026.143127},
pmid = {42537291},
issn = {1873-3336},
abstract = {The neurotoxic potential of microplastics (MPs) is an emerging environmental health crisis. However, the majority of environmental MPs are unable to penetrate the blood-brain barrier (BBB), leaving their mechanism of neurotoxicity largely unknown. Here, we show that oral exposure to pristine polystyrene MPs (which do not translocate to the brain) induces hippocampal-dependent cognitive deficits, impaired neurogenesis, and synaptic loss in mice, without detectable brain particle accumulation. This neurotoxicity is mediated by gut-brain axis disruption, characterized by gut microbiota dysbiosis, altered tryptophan metabolism, and increased permeability of both the intestinal barrier and the BBB. Crucially, hippocampal microglia exhibited a sustained pro-inflammatory shift (M1↑/M2↓) accompanied by defective autophagy. Fecal microbiota transplantation from healthy donors rescued the cognitive impairments and microglial dysfunction, establishing a causal role for the gut microbiota. Integrated multi-omics and correlation analyses identified the commensal bacterium Alloprevotella and the tryptophan-kynurenine metabolite 3-hydroxyanthranilic acid (3-HAA) as key mediators. In vitro, treatment of microglia with fecal supernatant from MPs-exposed mice recapitulated the M1/M2 imbalance, suppressed autophagy, and impaired brain-derived neurotrophic factor (BDNF) maturation. Remarkably, supplementation with 3-HAA restored autophagy in microglia, which in turn rebalanced their phenotypic polarization and rescued BDNF maturation. Our findings delineate a complete pathway from oral non-BBB-penetrable MPs exposure to cognitive dysfunction, orchestrated through the disruption of gut microbiota-3-HAA-microglial autophagy axis. This work unveils a fundamental indirect mechanism for the neurotoxicity of non-brain-penetrant environmental pollutants and identifies novel microbiota- and metabolite-centric targets for intervention.},
}

@article {pmid42538089,
year = {2026},
author = {Weyant, RB and Gîlcă-Blanariu, GE and Fischer, M and Kao, D},
title = {Treatment of Severe and Fulminant Clostridioides difficile Infections.},
journal = {Gastroenterology clinics of North America},
volume = {55},
number = {3},
pages = {459-472},
doi = {10.1016/j.gtc.2026.05.006},
pmid = {42538089},
issn = {1558-1942},
mesh = {Humans ; *Fecal Microbiota Transplantation ; *Clostridium Infections/therapy/diagnosis ; *Clostridioides difficile ; Anti-Bacterial Agents/therapeutic use ; Colectomy ; Enterocolitis, Pseudomembranous/therapy ; },
abstract = {Severe and fulminant Clostridioides difficile infection (CDI) represent distinct clinical entities that portend poor outcomes and require close monitoring and multidisciplinary management. Early recognition is key, and CDI-directed antimicrobials are the mainstay of therapy. If patients fail to improve despite maximal medical therapy, fecal microbiota transplantation (FMT) or surgical intervention should be considered. If FMT is performed, repeated dosing is often required. Surgical interventions such as colectomy or loop ileostomy are necessary in FMT nonresponders or those who have developed a complication such as perforation.},
}

Humans
*Fecal Microbiota Transplantation
*Clostridium Infections/therapy/diagnosis
*Clostridioides difficile
Anti-Bacterial Agents/therapeutic use
Colectomy
Enterocolitis, Pseudomembranous/therapy

@article {pmid42538091,
year = {2026},
author = {Bachour, SP and Grinspan, A},
title = {Fecal Microbiota Transplantation for Recurrent Clostridioides difficile Infection.},
journal = {Gastroenterology clinics of North America},
volume = {55},
number = {3},
pages = {485-492},
doi = {10.1016/j.gtc.2026.05.008},
pmid = {42538091},
issn = {1558-1942},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods/adverse effects ; *Clostridium Infections/therapy/microbiology ; Recurrence ; Clostridioides difficile ; Treatment Outcome ; },
abstract = {This article synthesizes the evidence supporting fecal microbiota transplantation (FMT) as a paradigm-shifting therapy for recurrent Clostridioides difficile infection (rCDI), highlighting the mechanisms, clinical efficacy across populations, and delivery methods. FMT has been shown to increase gut microbial diversity, restore bile acid metabolism, and induce resistance against colonization, resulting in the treatment of rCDI. Randomized controlled trials and meta-analyses of real-world data demonstrate clinical resolution rates of 85% to 90%, with higher cure rates observed after multiple FMTs. We further examine predictors of FMT failure and outcomes in special populations, underscoring the safety and efficacy of FMT in high-risk patients.},
}

Humans
*Fecal Microbiota Transplantation/methods/adverse effects
*Clostridium Infections/therapy/microbiology
Recurrence
Clostridioides difficile
Treatment Outcome

@article {pmid42538092,
year = {2026},
author = {Adamopoulos, A and Stollman, N},
title = {Non-Fecal Microbiota Transplantation Strategies for Treatment of Recurrent Clostridioides difficile Infection.},
journal = {Gastroenterology clinics of North America},
volume = {55},
number = {3},
pages = {493-501},
doi = {10.1016/j.gtc.2026.05.009},
pmid = {42538092},
issn = {1558-1942},
mesh = {Humans ; *Clostridium Infections/therapy/microbiology ; Anti-Bacterial Agents/therapeutic use ; Recurrence ; Clostridioides difficile ; Fidaxomicin/therapeutic use ; Vancomycin/therapeutic use ; *Gastrointestinal Microbiome ; Fecal Microbiota Transplantation ; Secondary Prevention ; Microbiota ; },
abstract = {Clostridioides difficile infection (CDI) is a leading healthcare-associated illness with significant recurrence rates and clinical burden. Recurrent CDI (rCDI) arises from microbiota disruption, often exacerbated by antibiotic therapy. Current treatment strategies include fidaxomicin and vancomycin taper regimens, with adjunctive options such as rifaximin in select cases. Preventive approaches focus on environmental decontamination and microbiome preservation. Emerging therapies, including live biotherapeutics, non-toxigenic strains, and microbiome-protective agents, show promise in reducing recurrence. Dietary interventions that enhance microbial diversity may also support recovery. Together, these strategies highlight a shift toward microbiome-centered management of rCDI.},
}

Humans
*Clostridium Infections/therapy/microbiology
Anti-Bacterial Agents/therapeutic use
Recurrence
Clostridioides difficile
Fidaxomicin/therapeutic use
Vancomycin/therapeutic use
*Gastrointestinal Microbiome
Fecal Microbiota Transplantation
Secondary Prevention
Microbiota

@article {pmid42526859,
year = {2026},
author = {Lee, JH and Jo, SN and Kim, JS and Jang, JC},
title = {Effects of heat stress on physiological, endocrine, and reproductive functions in swine: a review.},
journal = {Animal bioscience},
volume = {},
number = {},
pages = {},
doi = {10.5713/ab.250866},
pmid = {42526859},
issn = {2765-0189},
abstract = {Climate change driven heat stress (HS) causes major losses in the productive and reproductive performance of swine. Using temperature-humidity index (THI) based quantification of heat load as a framework, this review integrates HS effects across the endocrine and metabolic axis, the gut barrier microbiota, immune axis, and the reproductive axis. Heat stress, in the context of hypothalamic, pituitary, adrenal (HPA) sympathetic-adrenomedullary activation and insulin, catecholamine, and cortisol crosstalk, is accompanied by relative hyperinsulinemia and, via pyruvate dehydrogenase kinase 4 mediated pyruvate dehydrogenase inhibition and the lactate dehydrogenase/hypoxia-inducible factor-1α (HIF-1α) axis, repartitions substrate utilization toward glucose, thereby constraining lipid mobilization. Within the gut immune axis, β-diversity, centered dysbiosis and short chain fatty acids (SCFA) depletion weaken HIF-1α, dependent mucosal barrier defenses; together with increased lipopolysaccharide translocation, this hyperactivates TLR4/ NF-κB signaling, the NLR family pyrin domain containing 3 inflammasome, and Th17/IL-17 pathways. Evidence from fecal microbiota transplantation supports a causal role for dysbiosis in pathogenesis. In the reproductive axis, dysregulated hypothalamic-pituitary-gonadal-HPA crosstalk impairs follicular and luteal function and compromises placental nutrient transport; intrauterine HS can reprogram F1 offspring, with lasting effects on metabolism, immunity, and reproduction. In conclusion, HS is a systems level stressor that perturbs multiple physiological axes; progress will require standardized HS models, multi omics and multigenerational follow up, and integrated environment, nutrition, and management strategies. Beta diversity shifts in the gut microbiota and SCFA depletion emerge as core pathophysiologic mediators, supporting their use as early biomarkers and intervention targets and underscoring the need for focused investigation.},
}

@article {pmid42527128,
year = {2026},
author = {, and , and , },
title = {[Expert consensus on the clinical application and management of pediatric fecal microbiota transplantation (2026)].},
journal = {Zhonghua er ke za zhi = Chinese journal of pediatrics},
volume = {64},
number = {8},
pages = {863-872},
doi = {10.3760/cma.j.cn112140-20260120-00064},
pmid = {42527128},
issn = {0578-1310},
mesh = {Humans ; *Fecal Microbiota Transplantation/standards/methods ; Child ; *Gastrointestinal Microbiome ; China ; Pediatrics ; },
}

Humans
*Fecal Microbiota Transplantation/standards/methods
Child
*Gastrointestinal Microbiome
China
Pediatrics

@article {pmid42528685,
year = {2026},
author = {Yu, X and Liu, Q and Huang, Y and Wang, Q and Wang, Y and Zhao, G},
title = {Microbial dysbiosis and wound healing in diabetic foot ulcers: a mini review with a note on the role of artificial intelligence.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1891884},
pmid = {42528685},
issn = {2235-2988},
mesh = {Humans ; *Diabetic Foot/microbiology/therapy ; *Dysbiosis/microbiology/therapy ; *Wound Healing ; *Artificial Intelligence ; Biofilms/growth & development ; Probiotics/therapeutic use ; Gastrointestinal Microbiome ; Animals ; Skin Microbiome ; },
abstract = {Diabetic foot ulcers (DFUs) are a serious diabetes-related complication characterized by high rates of amputation and mortality. Emerging evidence suggests that DFUs are not simply the result of infection, but also involve microbiome dysbiosis, which impairs healing. Systemically, disturbances to the gut microbiota via the gut-skin axis promote systemic inflammation and metabolic dysfunction. Locally, skin microbial diversity is significantly reduced, allowing opportunistic pathogens such as Staphylococcus aureus and Pseudomonas aeruginosa to form resilient biofilms. These biofilms resist antibiotics and host immunity, while microbial virulence factors exacerbate tissue damage and disrupt the healing cascade. This synergy between host pathology and dysbiosis perpetuates chronic ulceration. Novel therapeutic strategies therefore aim to modulate this aberrant ecology by shifting from broad-spectrum eradication to targeted restoration. Promising approaches include probiotics, phage therapy, traditional Chinese medicine, and faecal microbiota transplantation, which seek to recalibrate the microbiome and promote healing. However, translation into clinical practice requires more robust evidence from large-scale trials. Future perspectives point towards personalized microbial medicine, integrating multi-omics data and artificial intelligence to match interventions with specific microbial ecotypes, which may reduce the global burden of DFUs.},
}

Humans
*Diabetic Foot/microbiology/therapy
*Dysbiosis/microbiology/therapy
*Wound Healing
*Artificial Intelligence
Biofilms/growth & development
Probiotics/therapeutic use
Gastrointestinal Microbiome
Animals
Skin Microbiome