@article {pmid40753182,
year = {2025},
author = {Lan, Q and Liufu, S and Chen, B and Wang, K and Chen, W and Xiao, L and Liu, X and Yi, L and Liu, J and Xu, X and Liu, C and Liu, M and Yin, Y and Ma, H},
title = {Gut-resident Phascolarctobacterium succinatutens decreases fat accumulation via MYC-driven epigenetic regulation of arginine biosynthesis.},
journal = {NPJ biofilms and microbiomes},
volume = {11},
number = {1},
pages = {150},
doi = {10.1038/s41522-025-00792-w},
pmid = {40753182},
issn = {2055-5008},
support = {2023ZD04046//Biological Breeding-National Science and Technology Major Project/ ; U23A20229//National Natural Science Foundation of China/ ; U23A20229//National Natural Science Foundation of China/ ; 202305AF150211//Program of talent of science & technology and platforms of Yunnan Province/ ; 202305AF150211//Program of talent of science & technology and platforms of Yunnan Province/ ; 202202AE090032//Major Science and Technology Special Plan of Yunnan Province/ ; 202202AE090032//Major Science and Technology Special Plan of Yunnan Province/ ; 2021kjc-js072//Breeding of Lancang Black Pigs and its application/ ; 2021kjc-js072//Breeding of Lancang Black Pigs and its application/ ; SNQYKJXT-01//Key technologies for the exploration of excellent genetic resources and their efficient farming and its application in Tibetan pigs/ ; SNQYKJXT-01//Key technologies for the exploration of excellent genetic resources and their efficient farming and its application in Tibetan pigs/ ; },
mesh = {Animals ; *Arginine/biosynthesis/blood ; Swine ; *Epigenesis, Genetic ; Mice ; *Gastrointestinal Microbiome ; Fecal Microbiota Transplantation ; *Proto-Oncogene Proteins c-myc/genetics/metabolism ; *Clostridiales ; },
abstract = {Uncovering the mechanisms of excessive fat accumulation in livestock can not only protect animal health but also maintain the revenue of the intensive feeding industry. In this study, a bacteria-wide association study was conducted in a cohort of 129 commercial Yorkshire pigs. We found that Phascolarctobacterium succinatutens (P. succinatutens) was a key bacterium with greater abundance in low backfat thickness (LBF) pigs and was positively correlated with serum arginine concentrations. Fecal microbiota transplantation (FMT) experiment verified the beneficial roles of P. succinatutens in intestinal and lipid homeostasis. Administration of P. succinatutens in mice curbed weight gain, reduced adipocyte size, attenuated gut inflammation aggravation, and elevated circulating arginine levels. Propionate, a main metabolite produced by P. succinatutens, played a significant role in the above effects. Mechanistically, we indicated that P. succinatutens-generated propionate alleviated colonic inflammation by inhibiting the TLR4 signaling cascade. Importantly, propionate was found to stimulate the de novo synthesis of arginine by inhibiting the chromatin accessibility of MYC near the intron region. Finally, we found that the increase of arginine induced by P. succinatutens reduced fat deposition by suppressing the PI3K/Akt/FOXO3a signaling pathway. Our work provides novel insights into the epigenetic regulation of probiotic-mediated anti-obesity effects and highlights the potential of P. succinatutens in combating excessive obesity in commercial pigs.},
}

Animals
*Arginine/biosynthesis/blood
Swine
*Epigenesis, Genetic
Mice
*Gastrointestinal Microbiome
Fecal Microbiota Transplantation
*Proto-Oncogene Proteins c-myc/genetics/metabolism
*Clostridiales

@article {pmid40752199,
year = {2025},
author = {Zhou, X and You, Y and Ren, L and Akhtar, M and Ji, H and Wang, T and Meng, N and Fan, X and Yang, S and Zhou, Z and Xiao, Y and Shi, D},
title = {Lactobacillus gallinarum improves broiler performance by enhancing antioxidant capacity and regulating intestinal microbiota.},
journal = {Poultry science},
volume = {104},
number = {10},
pages = {105537},
doi = {10.1016/j.psj.2025.105537},
pmid = {40752199},
issn = {1525-3171},
abstract = {The predominant objective in large-scale poultry farming has consistently been to enhance broiler. In this context, the supplementing of probiotics, specifically Lactobacilli, has emerged as a promising strategy to improve production efficiency. Numerous studies have demonstrated that Lactobacilli could modulate intestinal microbiota. To identify effective growth-promoting Lactobacilli, the present study replicated the "high body weight" phenotype of broiler chickens through fecal microbiota transplantation (FMT) and subsequently isolated target strains from FMT recipients exhibiting high body weight. The results demonstrated that Lactobacillus gallinarum CD-13 (CD-13) produced protease and exhibited inhibitory (P < 0.05) effects against pathogenic Gram-positive and Gram-negative bacteria. In vivo experimentation revealed that an average daily gain of broilers in the CD-13 group was increased by 17.72 %, along with enhanced (P < 0.05) duodenal villus height in the CD-13 group compared to the control group (Ctrl). Furthermore, the antioxidant capacity of broilers was improved, as evidenced by elevated levels of catalase (CAT) (P < 0.05) and glutathione peroxidase (GSH-Px) (P < 0.05) in the serum, while the level of malondialdehyde (MDA) was reduced (P < 0.05). 16S rRNA analysis revealed, the CD-13 group exhibited an increase (P < 0.05) in the diversity index of the intestinal microbiota, an elevated Bacteroidota/Firmicutes ratio, and the relative abundance of Bacteroides, whereas a decrease in the relative (P < 0.05) abundance of Alistipes compared with the Ctrl group. In conclusion, CD-13 demonstrated the capacity to enhance broiler growth performance through modulation of the intestinal microbiota and improvement of antioxidant capacity, thereby reducing of intestinal inflammation. The findings of this investigation substantiated the probiotic properties of CD-13 and provided a theoretical foundation for its potential application as a probiotic additive in the poultry industry.},
}

@article {pmid40751371,
year = {2025},
author = {El-Salhy, M and Valeur, J and Brønstad, I and Gilja, OH and Hatlebakk, JG},
title = {Possible Role of Butyric Acid in Long-Term Symptom Relief in Irritable Bowel Syndrome Patients Following Fecal Microbiota Transplantation.},
journal = {Neurogastroenterology and motility},
volume = {},
number = {},
pages = {e70115},
doi = {10.1111/nmo.70115},
pmid = {40751371},
issn = {1365-2982},
support = {//Helse Vest/ ; },
abstract = {BACKGROUND: We previously found that the fecal levels of short-chain fatty acids (SCFAs) changed in irritable bowel syndrome (IBS) patients at 1 month and 1 year after fecal microbiota transplantation (FMT). This study analyzed SCFAs at 2 and 3 years after FMT in the same IBS patients included in those previous studies.

METHODS: This study randomized 113 IBS patients into placebo, 30-g, and 60-g groups, who received FMT with 30 g of their own feces and with 30 g and 60 g of the donor's feces, respectively. The patients completed four questionnaires to assess IBS symptoms, fatigue, and quality of life, and supplied fecal samples at the baseline and at 2 and 3 years after FMT. The fecal SCFA levels were measured using gas chromatography.

RESULTS: The butyric acid level was significantly increased at 2 and 3 years after FMT in the 30-g and 60-g groups, and was significantly higher than that in the placebo group. The total SCFA and acetic acid levels decreased significantly in the 30-g and 60-g groups at 2 and 3 years after FMT, while the propionic acid level decreased in the 60-g group at both time points. The butyric acid level was inversely correlated with IBS symptoms and fatigue.

CONCLUSION AND INFERENCES: The increased butyric acid levels in IBS patients at 2 and 3 years after FMT and their inverse correlation with both IBS symptoms and fatigue suggest that butyric acid contributes to the long-term improvement seen after FMT (www.

CLINICALTRIALS: gov: NCT03822299).},
}

@article {pmid40750814,
year = {2025},
author = {Wan, M and Li, Q and Xiao, Y and Zhou, D and Lei, Q and Wang, S},
title = {Gut microbiota from Mori fructus (Morus alba L.) polyphenols and polysaccharides-dosed mice activates the PPARα/PGC-1α signaling pathway to mitigate HFD-induced metabolic syndrome in mice.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {28137},
pmid = {40750814},
issn = {2045-2322},
support = {2020YFS0031//the Sichuan Province Science and Technology Support Program/ ; 21JR11RM044//the Science and Technology Planning Project of Gansu Province/ ; 2024QB-120//the Gansu Provincial University Young Doctoral Support Project/ ; XYBYZK2310//the Ph.D. Foundation Program of Long Dong University/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Metabolic Syndrome/metabolism/etiology ; *Polyphenols/pharmacology ; *Morus/chemistry ; Mice ; Signal Transduction/drug effects ; *Polysaccharides/pharmacology/administration & dosage ; *Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism ; Diet, High-Fat/adverse effects ; *PPAR alpha/metabolism ; Male ; Fecal Microbiota Transplantation ; Plant Extracts/pharmacology ; Disease Models, Animal ; Mice, Inbred C57BL ; },
abstract = {Mori Fructus, rich in polysaccharides and polyphenols, has long been used in East Asia as a functional food and medicinal agent. In traditional Chinese medicine, it is used to treat various ailments like wasting-thirst syndrome and constipation. Studies suggest its extract fractions may alleviate metabolic syndrome symptoms by affecting gut microbiota. To explore this, fecal microbiota transplantation (FMT) was used in an experiment. Pseudo-germ-free mice were created with antibiotics and given a high-fat, high-sugar diet (HFD) to induce metabolic syndrome. Then, fecal bacterial infusions were transplanted. Results showed significant improvement in metabolic syndrome parameters in the FMT-MFPS(fecal microbiota transplantation-Mori Fructus polyphenols plus polysaccharides) group. Dyslipidemia, liver, and kidney injuries were modulated in treated mice. The PPARα/PGC-1α signaling pathway was activated. These findings indicate Mori Fructus extract fractions prevent metabolic syndrome via gut microbiota modulation, with effects sustained through FMT, providing a reference for prevention.},
}

Animals
*Gastrointestinal Microbiome/drug effects
*Metabolic Syndrome/metabolism/etiology
*Polyphenols/pharmacology
*Morus/chemistry
Mice
Signal Transduction/drug effects
*Polysaccharides/pharmacology/administration & dosage
*Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism
Diet, High-Fat/adverse effects
*PPAR alpha/metabolism
Male
Fecal Microbiota Transplantation
Plant Extracts/pharmacology
Disease Models, Animal
Mice, Inbred C57BL

@article {pmid40750041,
year = {2025},
author = {Kenneth, MJ and Chen, JS and Fang, CY and Tsai, HC and Wu, CC and Hsu, TK and Chen, CC and Hsu, BM},
title = {Exploring the therapeutic potential of Bacteriophage-mediated modulation of Gut microbiota towards Colorectal Cancer.},
journal = {International journal of antimicrobial agents},
volume = {},
number = {},
pages = {107585},
doi = {10.1016/j.ijantimicag.2025.107585},
pmid = {40750041},
issn = {1872-7913},
abstract = {The rising incidence of colorectal cancer (CRC), particularly among young individuals, necessitates urgent preventive and therapeutic strategies to reduce mortality and financial burdens associated with CRC treatment. According to studies, gut dysbiosis is associated with CRC, indicating that restoration to a healthy gut microbiota can improve CRC outcomes. Conventional antibiotics can rapidly eliminate CRC-associated gut microbiota, however, their lack of taxonomic precision results in non-selective elimination of both pro-tumoral and antineoplastic bacteria. In this review, we explore the potential of phage therapy to specifically target and eliminate CRC-associated bacteria, thereby mitigating their role in CRC pathogenesis. Tailored phage therapy, including phage cocktails and Fecal Microbial Transplantation (FMT), has shown promise in treating various diseases. As the efficacy of FMT is met with safety concerns, we highlight in this review how fecal viral transplantation (FVT) offers a safer alternative by using filtered fecal samples devoid of intact bacteria that would cause adverse effects. As a relatively new field with complex host-phage interactions, FVT requires further research to fully understand its potential and safety profile. Despite its potential for modulating the gut microbiota and improving CRC treatment, phage therapy still requires more clinical studies and experimental evidence to further establish its efficacy and safety in CRC patients.},
}

@article {pmid40749821,
year = {2025},
author = {Tian, Y and Jin, W and Jin, X and Wang, Y and Wu, R and Yu, R and Jiang, J and Zhu, M},
title = {Fecal microbiota transplantation promotes hair growth through gut microbiome and metabolic regulation.},
journal = {Life sciences},
volume = {},
number = {},
pages = {123887},
doi = {10.1016/j.lfs.2025.123887},
pmid = {40749821},
issn = {1879-0631},
abstract = {BACKGROUND: Gut microbiota plays a role in the etiology of a number of skin illnesses. In this study, we aimed to determine the relationship between intestinal flora (and related metabolites) and Androgenetic Alopecia (AGA).

METHODS: Mendelian randomization (MR) analysis was used to explore the causal relationship between gut microbiota and AGA. Gut microbiota was detected by fecal 16S rRNA sequencing, and fecal metabolites were analyzed by non-targeted metabolomics. Senescence and inflammation levels in the colon and hair follicles of mice were detected by β-galactosidase assay kits and other staining methods. Hair growth was assessed by dermoscopy and hair growth scoring.

RESULTS: Mendelian randomization analysis revealed a significant correlation between Lactobacillaceae (OR = 0.981, 95 % CI: 0.969-0.992, p = 0.001) and Lactobacillus (OR = 0.985, 95 % CI: 0.973-0.997, p = 0.018) with AGA. A similar reduction in Lactobacillaceae and Lactobacillus was observed in the feces of AGA mice (p < 0.05). Fecal microbiota transplantation (FMT) increased Lactobacillaceae and Lactobacillus levels (p < 0.05), and Lactobacillus rhamnosus GG (LGG) reversed aging and inflammation in the gut and hair follicles, promoting hair growth.

CONCLUSION: There is an intestinal-skin axis regulation pattern in the pathological process of AGA, and the aging of intestinal tissues and the alteration of bacterial flora and related metabolites can affect hair follicle aging and inflammation.},
}

@article {pmid40747461,
year = {2025},
author = {Zhu, Z and Zhu, Y and Sun, Q and Xue, J and Xie, M and Yu, Y and Wang, B and Shangguan, W and Feng, Z and Wu, P},
title = {Pentosan polysulfate alleviates interstitial cystitis/bladder pain syndrome by modulating bile acid metabolism and activating the TGR5 receptor through gut microbiota regulation.},
journal = {Bladder (San Francisco, Calif.)},
volume = {12},
number = {2},
pages = {e21200036},
pmid = {40747461},
issn = {2327-2120},
abstract = {BACKGROUND: The disrupted gut microbiome has been found to be implicated in the development of interstitial cystitis/bladder pain syndrome (IC/BPS). Pentosan polysulfate (PPS) is an oral medication used for treating IC/BPS, acting as both an anti-inflammatory agent and a bladder barrier protector. However, the precise mechanisms by which the PPS-mediated modulation of the gut microbiome alleviates IC/BPS are not fully understood.

OBJECTIVE: This study aimed to identify the key gut microbiota species and metabolites involved in PPS's protective effects against IC/BPS.

METHODS: We employed a multifaceted approach, including 16S rDNA gene sequencing, antibiotic treatment, and fecal microbiota transplantation, to validate the dependency of PPS's protective effects on the gut microbiome. Furthermore, we performed a comprehensive metabolomic profiling using non-targeted metabolomics and liquid chromatography-tandem mass spectrometry.

RESULTS: PPS significantly elevated the abundance of the xylan-degrading bacteria, Eubacterium xylanophilum group, which, through its interaction with the gut microbiome, markedly reduced inflammation and barrier damage induced by cyclophosphamide in IC/BPS. In addition, PPS significantly increased the level of ursodeoxycholic acid (UDCA), a secondary bile acid, demonstrating a strong correlation with the abundance of the E. xylanophilum group. Ex vivo supplementation with UDCA mitigated lipopolysaccharide-induced inflammation and barrier disruption in SV-HUC-1 cells by activating the TGR5 receptor.

CONCLUSION: PPS exerts its protective effects against IC/BPS by modulating the gut microbiome and its metabolites.},
}

@article {pmid40747222,
year = {2025},
author = {Pamungkas, KMN and Lesmana Dewi, PIS and Alamsyah, AZ and Dewi, NLPY and Dewi, NNGK and Mariadi, IK and Sindhughosa, DA},
title = {Microbiome dysbiosis and immune checkpoint inhibitors: Dual targets in Hepatocellular carcinoma management.},
journal = {World journal of hepatology},
volume = {17},
number = {7},
pages = {106810},
pmid = {40747222},
issn = {1948-5182},
abstract = {Hepatocellular carcinoma (HCC), a primary malignancy of the liver and leading cause of cancer-related mortality worldwide, poses substantial therapeutic challenges, particularly in advanced and unresectable stages. Immune checkpoint inhibitors (ICIs) have emerged as critical therapeutic agents, targeting immune checkpoint pathways to restore antitumor immune responses. Combinations such as atezolizumab (anti-programmed cell death ligand 1 with bevacizumab (anti-vascular endothelial growth factor), as well as antibodies directed against cytotoxic T-lymphocyte associated protein 4 and programmed cell death protein 1 (e.g., ipilimumab and nivolumab), have demonstrated improved clinical outcome in selected patients. However, the overall efficacy of ICIs remains hindered by variable response rate and primary or acquired resistance. Recent evidence suggests that the gut microbiome plays a pivotal role in modulating host immune responses and may significantly influence the therapeutic efficacy of ICIs. Dysbiosis within the gut-liver axis has been implicated not only in pathogenesis and progression of HCC but also diminishing immunotherapy effectiveness. Emerging studies highlight the potential of microbiome-targeted interventions including dietary modulation, prebiotics, probiotics, and fecal microbiota transplantation to enhance ICIs responsiveness. This review explores the evolving interplay between the gut microbiota and immunotherapy in HCC, with a focus on microbiome-based strategies aimed at optimizing clinical outcomes.},
}

@article {pmid40745657,
year = {2025},
author = {Hu, J and Chen, H and Zhu, L and Tong, Y and Cheng, C and Yan, G and Shen, H},
title = {Baitouweng decoction modulates gut microbial production of indole-3-propionic acid and epithelial necroptosis to alleviate DSS-induced colitis in mice.},
journal = {Chinese medicine},
volume = {20},
number = {1},
pages = {119},
pmid = {40745657},
issn = {1749-8546},
support = {82205023//The National Natural Science Foundation of China/ ; },
abstract = {BACKGROUND: Ulcerative colitis (UC) is a kind of inflammatory disorder structuring in the colon. Baitouweng decoction (BD) derived from Treatise on Cold Damage (Shang-Han-Lun in Chinese) has been used for the treatment of UC in clinical practice for more than 2000 years. However, the clear mechanism of BD is still unknown. Our previous study revealed the regulation of BD on gut microbiota in colitis mice. This study aimed to investigate the crosstalk between intestinal flora and host immunity in the therapeutic effect of BD on colitis.

METHODS: The model of colitis in mice was established using dextran sulfate sodium in drinking water, and the treatment group received BD, 5-ASA, or indole-3-propionic acid (IPA). The disease symptoms were documented, and assessments were conducted on both local and systemic inflammation as well as intestinal barrier function. The gut microbiota structure was analyzed using 16S ribosomal RNA sequencing. The metabolomic assay was performed using ultra-high performance liquid chromatography and quadrupole time-of-flight mass spectrometry, and RNA-sequencing was used to explore the mechanism of IPA on colitis treatment.

RESULTS: BD could improve colitis mice's colonic injury and rebalance the gut microbiota dysbiosis. Fecal microbiota transplantation experiments confirmed that the therapeutic effects of BD depend on the intestinal flora, while antibiotic treatment abrogated the effect of BD. The concentration of IPA, a microbial tryptophan metabolite, was upregulated after BD-treated. IPA was further evaluated for its effect on the development of colitis and it was identified as an inhibitor of necroptosis of intestinal epithelial cells.

CONCLUSIONS: Our findings suggest that BD could alleviate colitis by regulating the gut microbiota-metabolism homeostasis to inhibit the necroptosis of intestinal epithelial cells.},
}

@article {pmid40743285,
year = {2025},
author = {Herman, C and Bolyen, E and Simard, A and Gehret, L and Caporaso, JG},
title = {Assessing microbiome engraftment extent following fecal microbiota transplant with q2-fmt.},
journal = {PLoS computational biology},
volume = {21},
number = {7},
pages = {e1013299},
doi = {10.1371/journal.pcbi.1013299},
pmid = {40743285},
issn = {1553-7358},
abstract = {We present q2-fmt, a QIIME 2 plugin that provides diverse methods for assessing the extent of microbiome engraftment following fecal microbiota transplant. The methods implemented here were informed by a recent literature review on approaches for assessing FMT engraftment, and cover aspects of engraftment including Community Coalescence, Indicator Features, and Resilience. q2-fmt is free for all use, and detailed documentation illustrating worked examples on a real-world data set are provided in the project's documentation.},
}

@article {pmid40742160,
year = {2025},
author = {Bo, T and Song, G and Zhang, M and Xu, X and Duan, J and She, H and Fang, Y and Li, W and Wen, J and Liu, J and Wang, D and Lei, F},
title = {Gut microbiota contribute to high-altitude adaptation in tree sparrows.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0063025},
doi = {10.1128/msystems.00630-25},
pmid = {40742160},
issn = {2379-5077},
abstract = {UNLABELLED: The intricate relationship between gut microbiota and various physiological functions in animals has emerged as a focal point in understanding host adaptability. Unlike the native birds of the Qinghai-Tibet Plateau (QTP), the tree sparrow (Passer montanus) is believed to have colonized the plateau within the last few thousand years. Given the vast expanse and harsh conditions of the plateau, the role of gut microbiota in facilitating the tree sparrow's adaptation to this high-altitude habitat remains largely unexplored and holds significant scientific interest. Therefore, we employed a multidisciplinary approach combining amplicon sequencing, transcriptome analysis, and fecal microbiota transplantation (FMT) to investigate the functional role of gut microbiota in high-altitude tree sparrows across different seasons. Results indicate that the gut microbiota of tree sparrows exhibits seasonal and altitude-dependent changes, with an increase in Lactobacillus in winter, which may promote heat production to cope with the cold. FMT experiments confirmed that "high-altitude gut microbiota" enhances the expression of heat-related proteins (avUCP) and upregulates heat-related genes syt1 and chodl. These findings suggest an adaptive strategy whereby tree sparrows utilize their gut microbiota to modulate energy metabolism, ultimately conserving energy in the resource-limited high-altitude environment.

IMPORTANCE: This study provides one evidence that gut microbiota mediates high-altitude adaptation in tree sparrow. By integrating multi-omics and fecal transplantation in tree sparrows (Passer montanus)-a species invading the Qinghai-Tibet Plateau within millennia-we reveal seasonally dynamic microbial strategies critical for survival in extreme environments. These findings establish gut microbiota as a key driver of rapid altitudinal adaptation, offering new insights into how microbial functions enable vertebrate range expansion into challenging ecosystems. The mechanistic framework also informs conservation strategies for wildlife facing climate-driven habitat shifts.},
}

@article {pmid40741477,
year = {2025},
author = {Ma, L and Zhang, MH and Xu, YF and Hao, YX and Niu, XX and Li, Y and Xing, HC},
title = {Fecal microbiota transplantation: A promising treatment strategy for chronic liver disease.},
journal = {World journal of gastroenterology},
volume = {31},
number = {28},
pages = {105089},
pmid = {40741477},
issn = {2219-2840},
mesh = {Humans ; *Fecal Microbiota Transplantation/adverse effects/methods ; *Gastrointestinal Microbiome ; Treatment Outcome ; Animals ; *Dysbiosis/therapy/microbiology ; *Liver Diseases/therapy/microbiology ; Liver/pathology/microbiology ; Chronic Disease ; Clinical Trials as Topic ; },
abstract = {Chronic liver disease has become a global health crisis, with increasing incidence and mortality rates placing a substantial burden on healthcare systems worldwide. A key factor in the progression of chronic liver disease is intestinal microbiota dysbiosis, which influences liver function via the intricate liver-gut axis. This axis plays a central role in various physiological processes, and disruptions in microbial composition can exacerbate liver pathology. Fecal microbiota transplantation (FMT) has emerged as a promising therapeutic strategy, with the potential to restore the composition and metabolic functions of the intestinal microbiota. Supported by encouraging findings from clinical trials and animal studies, FMT has demonstrated therapeutic benefits, including improvements in clinical symptoms, objective indicators, and long-term prognosis. These benefits encompass reductions in hepatic lipid deposition and inflammation, mitigation of complications in advanced liver disease, promotion of hepatitis B e antigen seroconversion, and enhancement of cognitive function. Although clinical evidence remains preliminary, current data underscore the transformative potential of FMT in managing chronic liver diseases. Nonetheless, challenges persist, including the need for standardized procedures, variability among donors, potential risks, and concerns regarding long-term safety. This review provides a comprehensive evaluation of the current literature on the efficacy and safety of FMT, while exploring future research directions to expand its application in liver disease management.},
}

Humans
*Fecal Microbiota Transplantation/adverse effects/methods
*Gastrointestinal Microbiome
Treatment Outcome
Animals
*Dysbiosis/therapy/microbiology
*Liver Diseases/therapy/microbiology
Liver/pathology/microbiology
Chronic Disease
Clinical Trials as Topic

@article {pmid40741168,
year = {2025},
author = {Gu, C and Du, H and Li, N and Zhou, Y and Li, S and Sun, Y and Han, Y and Xu, X and Li, X},
title = {The gut-bone axis in osteoporosis: a multifaceted interaction with implications for bone health.},
journal = {Frontiers in endocrinology},
volume = {16},
number = {},
pages = {1569152},
pmid = {40741168},
issn = {1664-2392},
mesh = {Humans ; *Osteoporosis/metabolism/microbiology ; *Gastrointestinal Microbiome/physiology ; *Bone and Bones/metabolism ; Animals ; },
abstract = {With the accelerated aging of the population, degenerative orthopedic diseases, particularly osteoporosis, have become a major public health challenge, threatening bone health and affecting the quality of life. Existing anti-osteoporosis regimens remain rather unitary or poorly adhered, which also limits the maintenance of bone health to some extent. Given the increasingly elucidated prominence of gut-related factors in osteoblasts/osteoclasts and bone formation/metabolism/maintenance, focusing on intestinal microecology and then targeting the distal bone tissue via the gut-bone axis have been recognized as a feasible intervention strategy. This review systematically summarized the interaction of the gut-bone axis while highlighting the physicochemical barriers formed by intestinal intrinsic structures, the gut microbiota, and related molecules for bone health maintenance through the immune and endocrine pathways. Meanwhile, we emphasized the ideal anti-osteoporotic property and individual achievability of methods like fecal microbiota transplantation, probiotic and prebiotic supplementation, and dietary pattern modification. The conceptual framework of the gut-bone axis plus X was innovatively proposed, given the potential synergy among different organs in disease characterization and pathogenesis, which may help better explain the etiology and manage other co-morbidities concurrent with or secondary to osteoporosis. Since the intersection of orthopedics with other subjects, we also supported the application of nano-biomaterials, bacterial synthetic biology, and novel small molecules in anti-osteoporosis, which is expected to unlock broader prospects for the multidisciplinary integration of the gut-bone axis.},
}

Humans
*Osteoporosis/metabolism/microbiology
*Gastrointestinal Microbiome/physiology
*Bone and Bones/metabolism
Animals

@article {pmid40739711,
year = {2025},
author = {Xu, Y and Zhu, Y and Wu, X and Peng, W and Zhong, Y and Cai, Y and Chen, W and Liu, L and Tan, B and Chen, T},
title = {Gut Microbiota-Derived Acetate Ameliorates Endometriosis via JAK1/STAT3-Mediated M1 Macrophage Polarisation.},
journal = {Microbial biotechnology},
volume = {18},
number = {8},
pages = {e70202},
doi = {10.1111/1751-7915.70202},
pmid = {40739711},
issn = {1751-7915},
support = {8216140922//National Natural Science Foundation of China/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; Female ; *Endometriosis/therapy/microbiology/metabolism ; Mice ; Humans ; Fecal Microbiota Transplantation ; *STAT3 Transcription Factor/metabolism ; *Janus Kinase 1/metabolism ; *Macrophages/metabolism/immunology ; Disease Models, Animal ; *Acetates/metabolism ; Signal Transduction ; Feces/microbiology/chemistry ; },
abstract = {Endometriosis (EMs) is a common inflammatory disorder in women of reproductive age, severely impacting patients' quality of life and fertility. Current hormonal therapies offer limited efficacy, and surgical interventions often fail to prevent recurrence. Recent studies suggest a close association between gut microbiota and the pathophysiology of EMs, though the precise mechanisms remain unclear. To investigate the influence of gut microbiota on EMs, this study established an EMs mouse model and performed faecal microbiota transplantation (FMT) using samples from healthy donors (AH group) and EMs patients (AE group) into the model mice. Results demonstrated that compared to the model group (M group), FMT from healthy donors (AH group) significantly reduced ectopic lesion volume (658.3 ± 116.1 vs. 167.2 ± 112.8 mm[3], p < 0.01) and weight (0.7420 ± 0.1233 vs. 0.1885 ± 0.1239 mg, p < 0.01). Conversely, FMT from EMs patients exacerbated disease progression. Mechanistic studies revealed that healthy donor FMT attenuated EMs by remodelling the gut microbial composition (enhancing α-diversity and Lactobacillus abundance while suppressing Bacteroidetes), significantly elevating acetate levels in faeces and ectopic lesions, activating the JAK1/STAT3 signalling pathway within lesions, and thereby driving macrophage polarisation toward the M1 phenotype (by increased iNOS/CD86 expression and decreased Arg1/CD206 expression). Simultaneously, healthy donor FMT enhanced intestinal barrier integrity by upregulating tight junction proteins (ZO-1, Occludin, Claudin-1/5) and reducing levels of intestinal permeability markers (DAO, IFABP). In contrast, AE group FMT disrupted gut microbial ecology, reduced acetate production, failed to activate the JAK1/STAT3 pathway, promoted M2 macrophage polarisation and impaired intestinal barrier function. Collectively, this study elucidates for the first time that acetate, as a key gut microbiota metabolite, exerts anti-EMs effects by activating the JAK1/STAT3 signalling pathway to drive macrophage reprogramming toward the M1 phenotype, thereby positioning gut microbiota reconstruction as a novel therapeutic strategy for endometriosis.},
}

Animals
*Gastrointestinal Microbiome/physiology
Female
*Endometriosis/therapy/microbiology/metabolism
Mice
Humans
Fecal Microbiota Transplantation
*STAT3 Transcription Factor/metabolism
*Janus Kinase 1/metabolism
*Macrophages/metabolism/immunology
Disease Models, Animal
*Acetates/metabolism
Signal Transduction
Feces/microbiology/chemistry

@article {pmid40739580,
year = {2025},
author = {Song, J and Zhang, W and Wang, D},
title = {Gut microbiome in gastrointestinal neoplasms: from mechanisms to precision therapeutic strategies.},
journal = {Gut pathogens},
volume = {17},
number = {1},
pages = {57},
pmid = {40739580},
issn = {1757-4749},
abstract = {BACKGROUND: The incidence of Gastrointestinal Neoplasms (GI neoplasms) continues to increase globally. Colorectal cancer (CRC), in particular, has emerged as the second leading cause of cancer-related mortality worldwide. Now, Specific pathogenic bacteria, such as Fusobacterium nucleatum (F. nucleatum) and Helicobacter pylori (H. pylori), critically promote tumorigenesis through multiple mechanisms, including the induction of genotoxic damage, host metabolic reprogramming, and remodeling of the tumor immune microenvironment. Notably, a dysbiotic Gut Microbiome (GM) state significantly compromises patient response rates to cancer therapeutics. This review aims to systematically analyze the core molecular mechanism of GM affecting tumor development and explore the precise intervention strategies guided by clinical translation.

METHODS: This systematic review adhered to the PRISMA-2020 guidelines. We conducted a comprehensive literature search in PubMed (2008-2025) using key terms including "Gut Microbiome", "Gastrointestinal Neoplasms", "Fecal Microbiota Transplantation (FMT)", "immunotherapy resistance", "precision-based interventions", and "emerging research frontiers". Preclinical and clinical studies investigating the mechanisms, diagnostic applications, and therapeutic interventions of the GM in GI neoplasms were included.

RESULTS: This review systematically elucidates the tripartite mechanisms by which the GM influences the initiation and progression of GI neoplasms. And we innovatively proposed the "Proinflammation-metabolism-Immune framework (Dysbiosis of the GM jointly leads to the occurrence, development and metastasis of GI neoplasms by driving three interrelated processes: chronic inflammation (Proinflammation), reshaping the Metabolism of the host and TME(Metabolism), and inhibiting or altering the host Immune surveillance (Immune))" To deepen the understanding of host-microbe interactions. Based on this framework, we focused on discussing the therapeutic strategy targeting GM and confirmed its significant impact on the efficacy of anti-cancer treatment. Although these strategies have demonstrated clinical potential, current research is still mainly confined to preclinical models and the early clinical trial stage. To address this, we outline future directions: Integrating emerging technologies like multi-omics and artificial intelligence will enable dynamic monitoring and real-time modulation of microbial activity. This integration aims to establish a novel paradigm for microbiome-based personalized precision medicine.

DISCUSSION: This review systematically clarifies that GM is a key target for optimizing the treatment of GI neoplasms. Future research should integrate multi-omics and AI technologies for dynamic microbial monitoring and modulation, paving the way for microbiome-based precision medicine. Overcoming challenges in standardization and clinical translation is essential.},
}

@article {pmid40737908,
year = {2025},
author = {An, K and Yan, D and Lv, X and Liu, Y and Xia, Z},
title = {T-2 toxin induces gut and liver injury through triggering gut microbiota dysbiosis.},
journal = {Poultry science},
volume = {104},
number = {10},
pages = {105577},
doi = {10.1016/j.psj.2025.105577},
pmid = {40737908},
issn = {1525-3171},
abstract = {T-2 toxin (T-2), a foodborne mycotoxin, causes gut and liver injury in organisms. However, its effects on intestine in ducks and the mediating role of gut microbiota in pathogenesis remain unclear. This study investigated the involvement of gut microbiota in T-2-induced enterotoxicity and hepatotoxicity in ducks. Thirty 1-day-old ducklings were divided into control (CON) and T-2-exposed (400 μg/kg BW/day via oral gavage) groups for two weeks. Alterations in gut microbiota composition and barrier function were assessed. To further elucidate the role of microbiota, antibiotics mixture (ABX) treatment and fecal microbiota transplantation (FMT) were employed. Results revealed that T-2 exposure induced ileal dysbiosis characterized by increased relative abundance of Firmicutes, Candidatus Arthromitus, and Lactococcus, decreased Corynebacterium abundance with diminished α-diversity. For gut physical barrier function, ileal villi heights and mRNA levels of mucin2, Occludin, zonula occludens-1 were significantly downregulated by T-2, and serum concentration of lipopolysaccharide was increased. Notably, ABX treatment prevented T-2-induced gut barrier disruption, completely suppressed hepatic inflammation via toll-like receptor 4 (TLR4) pathway inhibition. Hepatic lipid accumulation induced by T-2 was significantly attenuated by ABX treatment. Furthermore, FMT confirmed the essential role of T-2-altered microbiota in recapitulating pathological features including intestinal leakage, hepatic inflammation and steatosis, and upregulated TLR4 pathway and lipid metabolism genes (angiopoietin-like 4, carnitine palmitoyltransferase 1B, perilipin 1) expression. These findings establish gut microbiota as a critical mediator in T-2-induced multiorgan toxicity, providing new insights into the potential therapeutic strategies.},
}

@article {pmid40736248,
year = {2025},
author = {Huang, X and Wu, R and Liang, X and Yu, Z and Qin, P and Wang, Z and Guo, P and Zeng, Y and Yan, Z and Xiao, W and Ma, Y},
title = {Streptococcus salivarius-derived ilexgenin A alleviates pneumonia through the gut-lung axis.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0073125},
doi = {10.1128/msystems.00731-25},
pmid = {40736248},
issn = {2379-5077},
abstract = {The alteration of gut microbiota during critical illness is associated with adverse clinical outcomes. This connection between intestinal dysbiosis and poor outcomes has prompted the idea that restoring healthy microbial communities could offer a novel approach to life-support treatment for patients with severe pneumonia. In this study, using 16S rRNA sequencing and fecal microbiota transplantation (FMT), we demonstrated that alterations in intestinal microbiota structure during pneumonia exacerbate disease outcomes. A notable feature of these alterations is the reduction in the relative levels of Streptococcus salivarius (S. salivarius). In combination with metabolomics analysis, we found that the administration of S. salivarius increased the level of ilexgenin A (IA) in mice, which enhances the resistance of mice to Pseudomonas aeruginosa (P. aeruginosa)-induced pneumonia. Mechanistically, IA regulates lipopolysaccharide-induced overexpression of macrophage inflammation through Toll-like receptor 4 (TLR4)-mediated NF-κB and MAPK signaling pathways. Our findings reveal the role of the microbial-immune axis in pneumonia, highlighting the potential of S. salivarius and IA in providing promising treatment strategies for pneumonia.IMPORTANCEOne of the major challenges faced by the clinical microbiome research community is to convert the connections between dysbiosis and negative clinical outcomes into rationalized and targeted therapeutic interventions. In the present work, 30 fecal samples from pneumonia and non-pneumonia patients were subjected to FMT and 16S rRNA analysis. The results revealed that a characteristic feature of gut microbiota dysbiosis in pneumonia hosts is the reduction of S. salivarius. Supplementation with S. salivarius can effectively enhance the resistance of mice to P. aeruginosa pneumonia. Moreover, we confirmed the anti-inflammatory effects of IA derived from S. salivarius both in vivo and in vitro. Thus, these findings enhance our understanding of how gut microbiota influences the outcomes of pneumonia and underscore the potential of S. salivarius as a precision microbial therapeutic for combating pneumonia.},
}

@article {pmid40741483,
year = {2024},
author = {Hunter, C and Dia, K and Boykins, J and Perry, K and Banerjee, N and Cuffee, J and Armstrong, E and Morgan, G and Banerjee, HN and Banerjee, A and Bhattacharya, S},
title = {An investigation for phylogenetic characterization of human pancreatic cancer microbiome by 16S rDNA sequencing and bioinformatics techniques.},
journal = {Journal of solid tumors},
volume = {14},
number = {1},
pages = {1-9},
pmid = {40741483},
issn = {1925-4067},
abstract = {Pancreatic cancer is a significant public health concern, with increasing incidence rates and limited treatment options. Recent studies have highlighted the role of the human microbiome, particularly the gut microbiota, in the development and progression of this disease. Microbial dysbiosis, characterized by alterations in the composition and function of the gut microbiota, has been implicated in pancreatic carcinogenesis through mechanisms involving chronic inflammation, immune dysregulation, and metabolic disturbances. Researchers have identified specific microbial signatures associated with pancreatic cancer, offering potential biomarkers for early detection and prognostication. By leveraging advanced sequencing and bioinformatics tools, scientists have delineated differences in the gut microbiota between pancreatic cancer patients and healthy individuals, providing insights into disease pathogenesis and potential diagnostic strategies. Moreover, the microbiome holds promise as a therapeutic target in pancreatic cancer treatment. Interventions aimed at modulating the microbiome, such as probiotics, prebiotics, and fecal microbiota transplantation, have demonstrated potential in enhancing the efficacy of existing cancer therapies, including chemotherapy and immunotherapy. These approaches can influence immune responses, alter tumor microenvironments, and sensitize tumors to treatment, offering new avenues for improving patient outcomes and overcoming therapeutic resistance. Overall, understanding the complex interplay between the microbiome and pancreatic cancer is crucial for advancing our knowledge of disease mechanisms and identifying innovative therapeutic strategies. Here we report phylogenetic analysis of the 16S rDNA microbial sequences of the pancreatic cancer mice microbiome and corresponding age matched healthy mice microbiome. We successfully identified differentially abundant microbiota in pancreatic cancer.},
}

@article {pmid40735439,
year = {2025},
author = {Wang, Q and Han, Y and Pang, L and Zhou, Z and Dai, L},
title = {Gut microbiome remodeling in chronic kidney disease: implications of kidney replacement therapies and therapeutic interventions.},
journal = {Frontiers in medicine},
volume = {12},
number = {},
pages = {1620247},
pmid = {40735439},
issn = {2296-858X},
abstract = {The escalating global burden of end-stage renal disease (ESRD), driven by aging populations and rising metabolic comorbidities, underscores the urgent need for innovative therapeutic strategies. Emerging evidence highlights the gut microbiome as a pivotal modulator of renal pathophysiology through the gut-kidney axis, with microbial dysbiosis exacerbating gut microbial metabolites (e.g., uremic toxins), systemic inflammation, and multi-organ damage. This narrative review explores the divergent impacts of kidney replacement therapies (KRT)-hemodialysis (HD) and peritoneal dialysis (PD)-on gut microbiota dynamics: HD is associated with Firmicutes and Proteobacteria enrichment, reduced butyrate-producing taxa (e.g., Faecalibacterium, Roseburia), and systemic microbial translocation; whereas PD-driven glucose absorption and iron supplementation foster pathogenic proliferation (e.g., Enterobacteriaceae) and impair short-chain fatty acid (SCFA) metabolism. Current interventions, including probiotics, prebiotics, plant-based diets (PBDs), and fecal microbiota transplantation (FMT), demonstrate potential in mitigating dysbiosis and uremic toxin accumulation. PBDs reduce inflammatory markers (IL-6, CRP) and lower all-cause mortality risk by 24% in PD patients; synbiotics (e.g., Lactobacillus casei + galactooligosaccharides) reduce serum p-cresyl sulfate by 20% in HD patients; and FMT increases levels of short-chain fatty acids (propionate, butyrate) and lowers trimethylamine N-oxide (TMAO) concentrations in streptozotocin-induced diabetic nephropathy mouse models. However, clinical translation remains challenged by small sample sizes, heterogeneous outcomes, and a lack of hard endpoints. Future research must prioritize standardized protocols, personalized microbial profiling, and synergistic integration of dietary and microbiome-targeted therapies. Bridging mechanistic insights with clinical validation will advance precision medicine in ESRD management, offering transformative potential for patients burdened by this therapeutic impasse.},
}

@article {pmid40735351,
year = {2025},
author = {Dean, EA and Roy, A and Lin, RY and Gharaibeh, RZ and Li, DM and Gauthier, J and Jobin, C and Wingard, JR},
title = {Gut Faecalibacterium abundance in patients with plasma cell disorders is associated with survival after autologous HSCT.},
journal = {Blood neoplasia},
volume = {2},
number = {3},
pages = {100114},
pmid = {40735351},
issn = {2950-3280},
abstract = {The gut microbiota (GM) has been linked to the development, progression, and response to therapy in plasma cell neoplasms (PCNs). The primary goal of this study was to investigate the relationship between the composition of the GM before and during autologous hematopoietic stem cell transplant (HSCT) with clinical outcomes of patients with PCNs. We focused on the genus Faecalibacterium, which includes the most abundant anaerobic commensal bacterium in the GM. Fecal samples were collected prospectively before, mid (at 1 week from the start of intervention), and end (at engraftment) of intervention (liberalized vs neutropenic diet) and subjected to 16S ribosomal DNA sequencing. Eighty-three patients were enrolled. Their median age was 64 (range, 31-79) years. Fifty-four patients received HSCT as part of frontline therapy and 29 for relapsed/refractory disease. With median follow-up time for survivors (n = 82) of 32 (range, 0.7-61) months, the median progression-free survival (PFS) was 40 months. Higher preintervention Faecalibacterium abundance was associated with improved PFS (hazard ratio [HR], 0.92; 95% confidence interval [CI], 0.86-0.99; P = .02). Faecalibacterium abundance was found to decrease early after transplant (P < .01). Although the administration of high-dose melphalan (200 mg/m[2]) was significantly associated with PFS in both univariable (HR, 0.38, 95% CI, 0.19-0.75; P = .006) and multivariable (HR, 0.42; 95% CI, 0.20-0.87; P = .02) analyses, preintervention Faecalibacterium abundance remained independently associated with PFS (HR, 0.93; 95% CI, 0.86-0.99; P = .04) on multivariable analysis. In conclusion, lower preintervention Faecalibacterium abundance was associated with inferior PFS.},
}

@article {pmid40733607,
year = {2025},
author = {Shrivastav, K and Nasser, H and Ikeda, T and Nema, V},
title = {Possible Crosstalk and Alterations in Gut Bacteriome and Virome in HIV-1 Infection and the Associated Comorbidities Related to Metabolic Disorder.},
journal = {Viruses},
volume = {17},
number = {7},
pages = {},
doi = {10.3390/v17070990},
pmid = {40733607},
issn = {1999-4915},
mesh = {Humans ; *Gastrointestinal Microbiome ; *HIV Infections/virology/complications/microbiology ; *Virome ; *Metabolic Diseases/virology/microbiology ; Dysbiosis ; HIV-1 ; Comorbidity ; },
abstract = {Improved antiretroviral therapy (ART) has significantly increased the life expectancy of people living with HIV (PLWH). At the same time, other complications like metabolic syndrome (MetS) are coming up as new challenges to handle. This review aims to explore the emerging evidence of gut microbiome and virome alterations in human immunodeficiency virus-1 (HIV-1) infection and associated metabolic disorders, such as type-2 diabetes (T2DM) and cardiovascular disease (CVD), with a focus on their interplay, contribution to immune dysfunction, and potential as therapeutic targets. We conducted a comprehensive review of the current literature on gut bacteriome and virome changes in HIV-1-infected individuals and those with metabolic comorbidities emphasizing their complex interplay and potential as biomarkers or therapeutic targets. HIV-1 infection disrupts gut microbial homeostasis, promoting bacterial translocation, systemic inflammation, and metabolic dysregulation. Similarly, metabolic disorders are marked by reduced beneficial short-chain fatty acid-producing bacteria and an increase in pro-inflammatory taxa. Alterations in the gut virome, particularly involving bacteriophages, may exacerbate bacterial dysbiosis and immune dysfunction. Conversely, some viral populations have been associated with immune restoration post-ART. These findings point toward a dynamic and bidirectional relationship between the gut virome, bacteriome, and host immunity. Targeted interventions such as microbiome modulation and fecal virome transplantation (FVT) offer promising avenues for restoring gut homeostasis and improving long-term outcomes in PLWH.},
}

Humans
*Gastrointestinal Microbiome
*HIV Infections/virology/complications/microbiology
*Virome
*Metabolic Diseases/virology/microbiology
Dysbiosis
HIV-1
Comorbidity

@article {pmid40732941,
year = {2025},
author = {Marano, G and Rossi, S and Sfratta, G and Acanfora, M and Anesini, MB and Traversi, G and Lisci, FM and Rinaldi, L and Pola, R and Gasbarrini, A and Sani, G and Gaetani, E and Mazza, M},
title = {Gut Microbiota in Women with Eating Disorders: A New Frontier in Pathophysiology and Treatment.},
journal = {Nutrients},
volume = {17},
number = {14},
pages = {},
doi = {10.3390/nu17142316},
pmid = {40732941},
issn = {2072-6643},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; Female ; *Feeding and Eating Disorders/microbiology/physiopathology/therapy ; Dysbiosis/microbiology/physiopathology/therapy ; Probiotics/therapeutic use ; Prebiotics/administration & dosage ; Fecal Microbiota Transplantation ; },
abstract = {Emerging evidence highlights the critical role of the gut microbiota in the development and progression of eating disorders (EDs), particularly in women, who are more frequently affected by these conditions. Women with anorexia nervosa, bulimia nervosa, and binge eating disorder exhibit distinct alterations in gut microbiota composition compared to healthy controls. These alterations, collectively termed dysbiosis, involve reduced microbial diversity and shifts in key bacterial populations responsible for regulating metabolism, inflammation, and gut-brain signaling. The gut microbiota is known to influence appetite regulation, mood, and stress responses-factors closely implicated in the pathogenesis of EDs. In women, hormonal fluctuations related to menstruation, pregnancy, and menopause may further modulate gut microbial profiles, potentially compounding vulnerabilities to disordered eating. Moreover, the restrictive eating patterns, purging behaviors, and altered dietary intake often observed in women with EDs exacerbate microbial imbalances, contributing to intestinal permeability, low-grade inflammation, and disturbances in neurotransmitter production. This evolving understanding suggests that microbiota-targeted therapies, such as probiotics, prebiotics, dietary modulation, and fecal microbiota transplantation (FMT), could complement conventional psychological and pharmacological treatments in women with EDs. Furthermore, precision nutrition and personalized microbiome-based interventions tailored to an individual's microbial and metabolic profile offer promising avenues for improving treatment efficacy, even though these approaches remain exploratory and their clinical applicability has yet to be fully validated. Future research should focus on sex-specific microbial signatures, causal mechanisms, and microbiota-based interventions to enhance personalized treatment for women struggling with eating disorders.},
}

Humans
*Gastrointestinal Microbiome/physiology
Female
*Feeding and Eating Disorders/microbiology/physiopathology/therapy
Dysbiosis/microbiology/physiopathology/therapy
Probiotics/therapeutic use
Prebiotics/administration & dosage
Fecal Microbiota Transplantation

@article {pmid40732937,
year = {2025},
author = {Zhang, G and Dou, Y and Xie, H and Pu, D and Wang, L and Wang, R and Han, X},
title = {Sea Cucumber Egg Oligopeptides Ameliorate Cognitive Impairments and Pathology of Alzheimer's Disease Through Regulating HDAC3 and BDNF/NT3 via the Microbiota-Gut-Brain Axis.},
journal = {Nutrients},
volume = {17},
number = {14},
pages = {},
doi = {10.3390/nu17142312},
pmid = {40732937},
issn = {2072-6643},
support = {DLUXK-2024-YB-006//Dalian University/ ; },
mesh = {Animals ; *Alzheimer Disease/pathology/metabolism ; *Gastrointestinal Microbiome/drug effects ; Mice ; *Brain-Derived Neurotrophic Factor/metabolism ; *Cognitive Dysfunction/drug therapy ; *Histone Deacetylases/metabolism ; *Oligopeptides/pharmacology ; *Sea Cucumbers/chemistry ; Disease Models, Animal ; Brain/metabolism/pathology/drug effects ; Male ; Fecal Microbiota Transplantation ; Neuroprotective Agents/pharmacology ; Fatty Acids, Volatile/metabolism ; Mice, Inbred C57BL ; *Eggs ; *Brain-Gut Axis/drug effects ; Feces/microbiology ; },
abstract = {BACKGROUND: Oligopeptides from sea cucumber eggs (SCEPs) are rarely studied for their neuroprotective effects.

METHODS: Therefore, we prepared SCEPs via simulated gastrointestinal digestion and then administered them to an Alzheimer's disease (AD) mouse model via gavage. Behavior tests, gut-brain histopathology and fecal microbiota transplantation (FMT) experiments were conducted, and gut microbiota and metabolite short-chain fatty acids (SCFAs) were evaluated via 16sRNA gene sequencing and LC-MS.

RESULTS: The results showed that both the SCEP and FMT groups experienced improvements in the cognitive impairments of AD and showed reduced levels of Aβ, P-Tau, GFAP, and NFL in the brain, especially in the hippocampus. SCEP remodeled the gut microbiota, increasing the relative abundances of Turicibacter and Lactobacillus by 2.7- and 4.8-fold compared with the model at the genus level. In the SCEP and FMT treatments, four SCFA-producing bacteria obtained from gut microbiota profiling showed consistent trends, indicating that they may be involved in mediating the neuroprotective effects of SCEP. Mechanically, SCEP regulated the SCFA distribution in feces, blood, and the brain, greatly increased the content of SCFAs in the brain up to 2000 μg/mg, eased gut-brain barrier dysfunction, inhibited HDAC3 overexpression, and upregulated BDNF/NT3 levels.

CONCLUSIONS: This study provides a promising candidate for preventing AD and a reference for applying SCEP.},
}

Animals
*Alzheimer Disease/pathology/metabolism
*Gastrointestinal Microbiome/drug effects
Mice
*Brain-Derived Neurotrophic Factor/metabolism
*Cognitive Dysfunction/drug therapy
*Histone Deacetylases/metabolism
*Oligopeptides/pharmacology
*Sea Cucumbers/chemistry
Disease Models, Animal
Brain/metabolism/pathology/drug effects
Male
Fecal Microbiota Transplantation
Neuroprotective Agents/pharmacology
Fatty Acids, Volatile/metabolism
Mice, Inbred C57BL
*Eggs
*Brain-Gut Axis/drug effects
Feces/microbiology

@article {pmid40732886,
year = {2025},
author = {Dipalma, G and Marinelli, G and Ferrante, L and Di Noia, A and Carone, C and Colonna, V and Marotti, P and Inchingolo, F and Palermo, A and Tartaglia, GM and Del Fabbro, M and Inchingolo, AM and Inchingolo, AD},
title = {Modulating the Gut Microbiota to Target Neuroinflammation, Cognition and Mood: A Systematic Review of Human Studies with Relevance to Fibromyalgia.},
journal = {Nutrients},
volume = {17},
number = {14},
pages = {},
doi = {10.3390/nu17142261},
pmid = {40732886},
issn = {2072-6643},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Fibromyalgia/therapy/microbiology/psychology ; Probiotics/administration & dosage/therapeutic use ; *Cognition ; Prebiotics/administration & dosage ; *Affect ; *Neuroinflammatory Diseases/therapy/microbiology ; Fecal Microbiota Transplantation ; },
abstract = {AIM: This systematic review aims to evaluate the effectiveness of microbiota-modulating interventions (such as probiotics, prebiotics, and fecal microbiota transplantation) in reducing cognitive symptoms, pain, and neuroinflammation in human studies relevant to fibromyalgia (FM). The review will investigate the role of gut-brain axis modulation through these interventions and explore the potential therapeutic benefits for FM management.

MATERIALS AND METHODS: A comprehensive search was conducted in electronic databases including PubMed, Scopus, and the Cochrane Library for studies published from 1 January 2015 to 30 April 2025. Studies were eligible if they were randomized controlled trials (RCTs), pilot studies, or observational studies assessing the impact of microbiota-targeted interventions (probiotics, prebiotics, fecal microbiota transplantation) on cognitive function, pain, or neuroinflammation in patients with FM. Studies were excluded if they involved animal models, lacked relevant outcome measures, or were not peer-reviewed. Although only a subset of the included studies directly involved FM patients, all were selected for their relevance to symptom domains (e.g., pain, cognition, mood) and mechanisms (e.g., neuroinflammation, gut-brain axis dysfunction) that are central to FM. A total of 11 human studies were included in the final qualitative synthesis.

RESULTS: Preliminary findings from the included studies suggest that microbiota-targeted interventions, particularly probiotics and prebiotics, show promise in reducing cognitive symptoms, pain, and neuroinflammation in FM patients. Improvements in mood and quality of life were also reported, indicating potential benefits for overall well-being. However, heterogeneity in study designs, sample sizes, and outcome measures limit the ability to draw definitive conclusions.

CONCLUSIONS: This systematic review highlights the potential of microbiota modulation as a therapeutic strategy for managing FM symptoms, particularly cognitive dysfunction and neuroinflammation.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Fibromyalgia/therapy/microbiology/psychology
Probiotics/administration & dosage/therapeutic use
*Cognition
Prebiotics/administration & dosage
*Affect
*Neuroinflammatory Diseases/therapy/microbiology
Fecal Microbiota Transplantation

@article {pmid40732657,
year = {2025},
author = {Maisetta, G and Moneta, S and Tuvo, B and Giordano, C and Petrocelli, PA and Tincani, G and Campani, D and Ghinolfi, D and Falcone, M and Bruschi, F and Lupetti, A},
title = {Three Autochthonous Cases of Amoebic Liver Abscess Clustered in a Small Village of Tuscany (Central Italy), a Non-Endemic Area.},
journal = {Pathogens (Basel, Switzerland)},
volume = {14},
number = {7},
pages = {},
doi = {10.3390/pathogens14070609},
pmid = {40732657},
issn = {2076-0817},
mesh = {Humans ; *Liver Abscess, Amebic/diagnosis/parasitology/epidemiology/pathology ; Italy/epidemiology ; Male ; Middle Aged ; *Entamoeba histolytica/isolation & purification/genetics ; Female ; Adult ; Feces/parasitology ; Aged ; },
abstract = {Amebiasis is a rare condition in industrialised countries but is epidemiologically growing. Clinical manifestations may range from asymptomatic to invasive disease. An amebic abscess can be the result of extraintestinal amebiasis, and it is associated with relatively high morbidity and mortality. We present three indigenous cases of amoebic liver abscesses observed within a few weeks (October-November 2023) in patients living in a small area near Lucca in Tuscany, Central Italy. Fever accompanied by abdominal pain and liver abscess was observed in all three patients, and one of them presented necrotising colitis and pleural effusion, too. The parasitological diagnosis was performed by microscopy and confirmed with real-time PCR in liver abscess drainage fluid and stools.},
}

Humans
*Liver Abscess, Amebic/diagnosis/parasitology/epidemiology/pathology
Italy/epidemiology
Male
Middle Aged
*Entamoeba histolytica/isolation & purification/genetics
Female
Adult
Feces/parasitology
Aged

@article {pmid40732223,
year = {2025},
author = {Li, W and Huang, D and Luo, Z and Zhou, T and Jin, Z},
title = {Yinchenhao Decoction Mitigates Cholestatic Liver Injury in Mice via Gut Microbiota Regulation and Activation of FXR-FGF15 Pathway.},
journal = {Pharmaceuticals (Basel, Switzerland)},
volume = {18},
number = {7},
pages = {},
doi = {10.3390/ph18070932},
pmid = {40732223},
issn = {1424-8247},
support = {82004417//National Natural Science Foundation of China/ ; 2021M702214//China Postdoctoral Science Foundation/ ; 2024//the 2024 Shanghai Public Health Research Special Project/ ; },
abstract = {Objective: Yinchenhao decoction (YCHD), a classical herbal formula comprising Artemisia capillaris, Gardenia jasminoides, and Rheum palmatum, has been clinically used for over 1000 years to treat cholestasis. However, its mechanism of action remains undefined. This study aimed to elucidate YCHD's therapeutic mechanisms against cholestasis, with a focus on the gut microbiota-mediated regulation of the farnesoid X receptor (FXR)-fibroblast growth factor 15 (FGF15) pathway. Methods: An alpha-naphthyl isothiocyanate (ANIT)-induced cholestasis mouse model was established. Mice received YCHD (3/9 g/kg) for 7 days. 16S rRNA sequencing, targeted LC/MS (bile acid (BA) quantification), untargeted GC/MS (fecal metabolite detection), qPCR/Western blot (FXR pathway analysis), fecal microbiota transplantation (FMT), and antibiotic depletion were employed to dissect the gut-liver axis interactions. Results: YCHD alleviated cholestatic liver injury by reducing serum biomarkers, restoring BA homeostasis via FXR-FGF15 activation, and suppressing hepatic Cyp7a1-mediated BA synthesis. It remodeled gut microbiota, enriched FXR-activating secondary BAs (CDCA, DCA, CA), and restored the intestinal barrier integrity. Antibiotic cocktail abolished YCHD's efficacy, while FMT from YCHD-treated mice enhanced its therapeutic effects, confirming microbiota dependency. Conclusions: YCHD mitigates cholestasis through gut microbiota-driven FXR activation and direct hepatobiliary regulation. These findings bridge traditional medicine and modern pharmacology, highlighting microbiome modulation as a therapeutic strategy for cholestatic liver diseases.},
}

@article {pmid40730543,
year = {2025},
author = {Du, L and Ding, X and Zhang, W and Huang, L and Lü, H and Jian, T and Li, J and Gai, Y and Meng, X and Niu, G and Chen, J and Li, W},
title = {Anthocyanins from blueberry and blackberry ameliorate metabolic syndrome by Prevotella histicola and acetic acid.},
journal = {NPJ science of food},
volume = {9},
number = {1},
pages = {158},
doi = {10.1038/s41538-025-00526-4},
pmid = {40730543},
issn = {2396-8370},
support = {KYCX24-1240//Postgraduate Research & Practice Innovation Program of Jiangsu Province/ ; 82004018//National Natural Science Foundation of China/ ; 81973463//National Natural Science Foundation of China/ ; 32170377//National Natural Science Foundation of China/ ; },
abstract = {Metabolic syndrome (MetS) is a globally prevalent disorder and poses a significant threat to human health and social harmony. Consumption of anthocyanins has been proven to improve disrupted gut microbiota and obesity in mice and humans. However, the potential specific gut microbiota and metabolites that might mediate these beneficial effects on MetS remain unknown. Here, the MetS-mice model, induced by a high-fat diet (HFD), was employed to investigate the specific effects of ACNs. Additionally, 16S rRNA sequencing and targeted metabolomics analysis of short-chain fatty acids (SCFAs) were utilized to evaluate the influence on gut microbiota composition and SCFAs levels. More importantly, we also utilized antibiotics to construct a pseudo-germ-free mouse model for fecal microbiota transplantation (FMT) to further confirm the regulation of gut microbiota by ACNs and demonstrating that the related effects on MetS could be transferable through FMT. Our data demonstrated that the amelioration of MetS by ACNs might be achieved through modulation of the gut microbiota, which was validated through FMT, and the related benefits could be transferable by FMT. Furthermore, acetic acid and Prevotella histicola might be key microbial metabolites and bacteria, respectively, in this process. These findings highlight the diet-gut-metabolites-diseases system crosstalk and provide new research perspectives for plant-derived ingredients with poor bioavailability.},
}

@article {pmid40728956,
year = {2025},
author = {Qiao, Y and Cheng, R and Li, X and Zheng, H and Guo, J and Wei, L and Gao, T and Bi, H},
title = {Plateau Environment, Gut Microbiota, and Depression: A Possible Concealed Connection?.},
journal = {Current issues in molecular biology},
volume = {47},
number = {7},
pages = {},
doi = {10.3390/cimb47070487},
pmid = {40728956},
issn = {1467-3045},
support = {Grant No. 82171863//the Natural Science Foundation of China/ ; 2020-ZJ-T08//the Innovation Platform Program of Qinghai Province/ ; None//the Tianfu Emei Project of Sichuan Province/ ; },
abstract = {Plateau environments present unique mental health challenges owing to stressors including hypoxia, low temperatures, and intense ultraviolet (UV) radiation. These factors induce structural and functional alterations in the gut microbiota, disrupting gut-brain axis homeostasis and contributing to the higher prevalence of depression in plateau regions relative to flatland areas. For example, studies report that 28.6% of Tibetan adults and 29.2% of children/adolescents on the Qinghai-Tibet Plateau experience depression, with increasing evidence linking this trend to alterations in the gut microbiota. Dysbiosis contributes to depression through three interconnected mechanisms: (1) Neurotransmitter imbalance: Reduced bacterial diversity impairs serotonin synthesis, disrupting emotional regulation. (2) Immune dysregulation: Compromised gut barrier function allows bacterial metabolites to trigger systemic inflammation via toll-like receptor signaling pathways. (3) Metabolic dysfunction: Decreased short-chain fatty acid levels weaken neuroprotection and exacerbate hypothalamic-pituitary-adrenal axis stress responses. Current interventions-including dietary fiber, probiotics, and fecal microbiota transplantation-aim to restore microbiota balance and increase short-chain fatty acids, alleviating depressive symptoms. However, key knowledge gaps remain in understanding the underlying mechanisms and generating population-specific data. In conclusion, existing evidence indicates an association between plateau environments, the gut microbiota, and depression, but causal relationships and underlying mechanisms require further empirical investigation. Integrating multiomics technologies to systematically explore interactions among high-altitude environments, the microbiota and the brain will facilitate the development of precision therapies such as personalized nutrition and tailored probiotics to protect mental health in high-altitude populations.},
}

@article {pmid40693962,
year = {2025},
author = {Mutengo, M and Dashti, A and Liptáková, M and Mulunda, NR and Chabala, FW and Hayashida, K and Chinyanta, S and Chisanga, K and Mwansa, J and Köster, PC and Santín, M and Sotillo, J and Sánchez, S and Carmena, D},
title = {High prevalence of Enterocytozoon bieneusi (microsporidia) in asymptomatic schoolchildren, Zambia.},
journal = {Medical mycology},
volume = {63},
number = {7},
pages = {},
doi = {10.1093/mmy/myaf065},
pmid = {40693962},
issn = {1460-2709},
support = {//Health Institute Carlos III (ISCIII)/ ; PI19CIII/00029//Spanish Ministry of Economy and Competitiveness/ ; FI20CIII/00002//PFIS/ ; //Spanish Ministry of Science and Innovation and Universities/ ; //Women Program of the Women for Africa Foundation/ ; },
mesh = {Humans ; Zambia/epidemiology ; *Enterocytozoon/genetics/isolation & purification/classification ; Child ; Male ; *Microsporidiosis/epidemiology/microbiology ; Female ; Adolescent ; Prevalence ; Feces/microbiology ; Child, Preschool ; Genetic Variation ; DNA, Fungal/genetics ; *Asymptomatic Infections/epidemiology ; Genotype ; Sequence Analysis, DNA ; Polymerase Chain Reaction ; },
abstract = {Microsporidia are single-celled, fungi-related eukaryotic intracellular parasites able to infect a wide diversity of invertebrate and vertebrate hosts. Among them, Enterocytozoon bieneusi and Encephalitozoon spp. (including Enc. cuniculi, Enc. hellem, and Enc. intestinalis) are known causative agents of infectious diseases in immunocompromised individuals, including HIV/AIDS patients and organ transplant recipients. Additionally, asymptomatic microsporidial infections seem more frequent than initially anticipated and might represent an overlooked public health threat. Here, we provide novel data on the occurrence and genetic diversity of microsporidial infections in individual stool samples (n = 247) collected from apparently healthy schoolchildren (age range: 5-18 years; male/female ratio: 1.1) in Lusaka, Zambia. Stool DNA samples were analysed by PCR and Sanger sequencing methods. A basic epidemiological questionnaire was used to retrieve data on variables potentially linked with higher odds of harbouring E. bieneusi infections. A high prevalence rate was found for E. bieneusi (9.3%, 23/247; 95% CI: 6.0-13.6), whereas Enc. intestinalis was much less frequent (0.4%, 1/247; 95% CI: 0.01-2.2). Four known (D, S2, S6, and Type IV) and three novel (HhZbEb1, HhZbEb2, and HhZbEb3) genotypes were identified within E. bieneusi. Genotype D was the predominant genotype found (30.8%, 4/13), followed by genotypes Type IV, HhZbEb2, and HhZbEb3 (15.4%, 2/13 each), and genotypes S2, S6, and HhZbEb1 (7.7%, 1/13 each). The only Encephalitozoon-positive sample was identified as Enc. intestinalis. Subclinical infections by E. bieneusi were common in the investigated paediatric population. Infected children could act as disregarded spreaders of microsporidial pathogens at the community level, thus representing a potential public health concern.},
}

Humans
Zambia/epidemiology
*Enterocytozoon/genetics/isolation & purification/classification
Child
Male
*Microsporidiosis/epidemiology/microbiology
Female
Adolescent
Prevalence
Feces/microbiology
Child, Preschool
Genetic Variation
DNA, Fungal/genetics
*Asymptomatic Infections/epidemiology
Genotype
Sequence Analysis, DNA
Polymerase Chain Reaction

@article {pmid40734779,
year = {2024},
author = {Lo, K and Kavarian, P and Wang, B and Parsana, R and Durazo-Arvizu, R and Sun, F and Michail, S},
title = {Fecal bile acid profiles before and after fecal microbial transplant in pediatric onset ulcerative colitis.},
journal = {Gut microbes reports},
volume = {1},
number = {1},
pages = {},
pmid = {40734779},
issn = {2993-3935},
abstract = {Fecal bile acids (BAs) are key metabolites altered in patients with inflammatory bowel disease (IBD), therefore serving as potential targets of fecal microbial transplant (FMT). To compare changes in fecal BA composition and corresponding microbial transformation pathways in pediatric ulcerative colitis (UC) patients before and after FMT for up to 48 weeks. Fecal BAs, as well as enzymes and bacteria related to BA metabolism were measured in 28 healthy children, and 48 children with mild to moderate UC before and after FMT. Several primary BAs were higher in UC patients at baseline, and subsequently decreased over the 48 weeks following FMT. In particular, the primary BA cholic acid (CA) was higher in UC children at baseline (11.73 pg/mg) compared to healthy controls (8.47 pg/mg), decreased to 10.82 pg/mg at 4 weeks post FMT (p = 0.001) then 10.07 pg/mg at 48 weeks (p = 0.077). Following FMT, the ratio of secondary to primary BAs became more similar to healthy children. The genes coding for bile salt hydrolase, 7α/β-hydroxysteroid dehydrogenase, and bile acid induced operon enzymes were lower in UC patients at baseline, with the majority of them increasing following FMT. Similarly, many of the bacterial genera involved in bile acid metabolism had corresponding increases after FMT.},
}

@article {pmid40728532,
year = {2025},
author = {Zhu, L and Song, B and Zhang, R and Wang, C and He, X and Cao, Y and Li, G},
title = {Gut microbiota in sexual function: exploring new avenues.},
journal = {Sexual medicine reviews},
volume = {},
number = {},
pages = {},
doi = {10.1093/sxmrev/qeaf039},
pmid = {40728532},
issn = {2050-0521},
support = {2022xkjT020//Basic and Clinical Collaborative Research Program of Anhui Medical University/ ; 82201777//The National Natural Science Foundation of China/ ; },
abstract = {INTRODUCTION: The gut microbiota, which is recognized for its crucial role in regulating numerous physiological processes, harbors a relationship with sexual function that has remained relatively understudied.

OBJECTIVES: This narrative review aims to integrate the existing evidence regarding the association between the gut microbiota and sexual function. Additionally, it endeavors to discuss the research challenges and delineate the future directions within this burgeoning field.

METHODS: A comprehensive analysis was carried out on both pre-clinical and clinical studies. The scope of the analysis encompassed: (1) the associations between the composition of the gut microbiota and various forms of sexual dysfunctions, (2) the risk factors for sexual dysfunction that are associated with alterations in the microbiota, and (3) the potential interventions that target the regulation of the gut microbiota.

RESULTS: In the context of erectile dysfunction and hypoactive sexual desire disorder, several investigations have identified specific changes in the gut microbiota. Additionally, risk factors for sexual dysfunction, such as mental health disorders, obesity, diabetes, hypertension, and thyroid dysfunction, are also influenced by the gut microbiota. Promising intervention strategies include dietary modification, supplementation with probiotics or prebiotics, fecal microbiota transplantation, and bioengineering approaches.

CONCLUSION: The current body of evidence has established a link between gut microbial dysbiosis and the pathophysiology of various sexual health issues. Despite the fact that our understanding and assessment of the impact of gut microbes on the sexual function of the host are still in their infancy, continued advancements may unveil novel potential targets for the management of sexual health.},
}

@article {pmid40727459,
year = {2025},
author = {Xue, J and Zhou, Q},
title = {Effects of Emodin on Lung Inflammation and Intestinal Microbes in Chronic Obstructive Pulmonary Disease.},
journal = {Journal of inflammation research},
volume = {18},
number = {},
pages = {9795-9809},
pmid = {40727459},
issn = {1178-7031},
abstract = {INTRODUCTION: The impact of COPD on human health is enormous. Emodin, which has anti-inflammatory, anti-cancer, spasmolysis, and laxative effects, has not been systematically investigated within a study with regard to the treatment of COPD.

METHODS: In this study, we conducted Experiment 1 to evaluate the effects of emodin on COPD. Emodin was purchased from Shanghai Yuanye Biotechnology Co. Ltd. (batch number: T17A10F95418). Pathological changes in lung tissue and the average lung lining interval were used to evaluate the severity of emphysema. Inflammatory cell counts in alveolar lavage fluid and the ratio of neutrophils and lymphocytes were used to observe the level of inflammation. The level of HMGB1-RAGE expression was determined via PCR. Moreover, we compared changes in the metabolites of the intestinal microbial community following an intervention with emodin. In Experiment 2, we observed the effect of fecal on the inflammatory response in COPD mice. A mouse dual intervention model was established using flora depletion and COPD modeling. We evaluated the general health of the model mice, specific pathological changes in lung tissue, the average lung lining interval, inflammatory cell counts within the alveolar lavage fluid, and HMGB1-RAGE pathway expression.

RESULTS: Our results demonstrated that emodin statistically significantly improved lung tissue inflammation in COPD mice, and that butanoic acid was the main differential metabolite in intestinal bacteria. Transplanting the feces of the emodin group mice in Experiment 1 to the model mice evaluated in Experiment 2 reduced the infiltration of inflammatory cells and down-regulated the HMGB1-RAGE inflammation pathway.

CONCLUSION: Our findings provide important information for guiding future research directions.},
}

@article {pmid40725913,
year = {2025},
author = {Ugwu, OP and Okon, MB and Alum, EU and Ugwu, CN and Anyanwu, EG and Mariam, B and Ogenyi, FC and Eze, VHU and Anyanwu, CN and Ezeonwumelu, JOC and Egba, SI and Uti, DE and Onohuean, H and Aja, PM and Ugwu, MN},
title = {Unveiling the therapeutic potential of the gut microbiota-brain axis: Novel insights and clinical applications in neurological disorders.},
journal = {Medicine},
volume = {104},
number = {30},
pages = {e43542},
doi = {10.1097/MD.0000000000043542},
pmid = {40725913},
issn = {1536-5964},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; Probiotics/therapeutic use ; *Nervous System Diseases/therapy/microbiology ; *Dysbiosis/therapy/complications ; *Brain ; Fecal Microbiota Transplantation/methods ; Prebiotics/administration & dosage ; *Brain-Gut Axis/physiology ; },
abstract = {Over the last several years, the gut microbiota-brain axis has been the focus of medical study, demonstrating the bidirectional nature of gut and brain communication and the resulting influence on neurological and mental health. Trillions of microorganisms, particularly those found in the gastrointestinal tract, contribute the most to the pathophysiology recovery of organs that are critical to human health, such as digestive processes and metabolism, immune responses, and even cognitive function. Dysbiosis (a disturbance in the microbiome balance) has been identified as one of the risk factors for neuropsychiatric illnesses such as depression, anxiety, autism spectrum disorder, Parkinson's disease, and Alzheimer's disease. Therapeutic strategies aimed at the gut microbiota, such as probiotics, dietary modifications, prebiotics, and fecal microbiota transplantation, will eventually offer ways to alleviate symptoms associated with these disorders by restoring microbial balance, modulating the immune response, and influencing the production of major neurotransmitters. Innovative drug carriers, such as microbially-derived nanoparticles and probiotics that target particular parts of the gut or microbial communities, may improve pharmaceutical treatment efficacy and specificity. The resolution of difficulties such as ethical concerns, unexpected repercussions, and peak performance optimization in a clinical setting is critical for the advancement of this subject.},
}

Humans
*Gastrointestinal Microbiome/physiology
Probiotics/therapeutic use
*Nervous System Diseases/therapy/microbiology
*Dysbiosis/therapy/complications
*Brain
Fecal Microbiota Transplantation/methods
Prebiotics/administration & dosage
*Brain-Gut Axis/physiology

@article {pmid40725626,
year = {2025},
author = {Augustynowicz, G and Lasocka, M and Szyller, HP and Dziedziak, M and Mytych, A and Braksator, J and Pytrus, T},
title = {The Role of Gut Microbiota in the Development and Treatment of Obesity and Overweight: A Literature Review.},
journal = {Journal of clinical medicine},
volume = {14},
number = {14},
pages = {},
doi = {10.3390/jcm14144933},
pmid = {40725626},
issn = {2077-0383},
abstract = {The gut microbiota, dominated by bacteria from the Firmicutes, Bacteroidetes, Proteobacteria, and Actinobacteria phyla, plays an essential role in fermenting indigestible carbohydrates, regulating metabolism, synthesizing vitamins, and maintaining immune functions and intestinal barrier integrity. Dysbiosis is associated with obesity development. Shifts in the ratio of Firmicutes to Bacteroidetes, particularly an increase in Firmicutes, may promote enhanced energy storage, appetite dysregulation, and increased inflammatory processes linked to insulin resistance and other metabolic disorders. The purpose of this literature review is to summarize the current state of knowledge on the relationship between the development and treatment of obesity and overweight and the gut microbiota. Current evidence suggests that probiotics, prebiotics, synbiotics, and fecal microbiota transplantation (FMT) can influence gut microbiota composition and metabolic parameters, including body weight and BMI. The most promising effects are observed with probiotic supplementation, particularly when combined with prebiotics, although efficacy depends on strain type, dose, and duration. Despite encouraging preclinical findings, FMT has shown limited and inconsistent results in human studies. Diet and physical activity are key modulators of the gut microbiota. Fiber, plant proteins, and omega-3 fatty acids support beneficial bacteria, while diets low in fiber and high in saturated fats promote dysbiosis. Aerobic exercise increases microbial diversity and supports growth of favorable bacterial strains. While microbiota changes do not always lead to immediate weight loss, modulating gut microbiota represents an important aspect of obesity prevention and treatment strategies. Further research is necessary to better understand the mechanisms and therapeutic potential of these interventions.},
}

@article {pmid40724502,
year = {2025},
author = {Lazăr, DC and Chiriac, SD and Drăghici, GA and Moacă, EA and Faur, AC and Avram, MF and Turi, VR and Nicolin, MR and Goldiș, A and Salehi, MA and Jipa, R},
title = {Gastric Cancer and Microbiota: Exploring the Microbiome's Role in Carcinogenesis and Treatment Strategies.},
journal = {Life (Basel, Switzerland)},
volume = {15},
number = {7},
pages = {},
doi = {10.3390/life15070999},
pmid = {40724502},
issn = {2075-1729},
abstract = {Gastric cancer (GC) remains a major global health burden, with high morbidity and mortality rates, particularly in regions with prevalent Helicobacter pylori (H. pylori) infection. While H. pylori has long been recognized as a primary carcinogenic agent, recent research has underscored the broader contribution of the gastric microbiota to gastric carcinogenesis. Alterations in the microbial community, or dysbiosis, contribute to chronic inflammation, immune modulation, and epithelial transformation through a range of mechanisms, including disruption of mucosal integrity, activation of oncogenic signaling pathways (e.g., PI3K/Akt, NF-κB, STAT3), and epigenetic alterations. Furthermore, microbial metabolites, such as short-chain fatty acids, secondary bile acids, and lactate, play dual roles in either promoting or suppressing tumorigenesis. Oral and gut-derived microbes, translocated to the gastric niche, have been implicated in reshaping the gastric microenvironment and exacerbating disease progression. The composition of the microbiota also influences responses to cancer immunotherapy, suggesting that microbial profiles can serve as both prognostic biomarkers and therapeutic targets. Emerging strategies, such as probiotics, dietary interventions, and fecal microbiota transplantation (FMT), offer new avenues for restoring microbial balance and enhancing therapy response. This review synthesizes current knowledge on the complex interplay between microbiota and gastric cancer development and emphasizes the potential of microbiome modulation in both preventive and therapeutic frameworks.},
}

@article {pmid40723882,
year = {2025},
author = {Neagu, AI and Bostan, M and Ionescu, VA and Gheorghe, G and Hotnog, CM and Roman, V and Mihaila, M and Stoica, SI and Diaconu, CC and Diaconu, CC and Ruta, SM and Bleotu, C},
title = {The Impact of the Microbiota on the Immune Response Modulation in Colorectal Cancer.},
journal = {Biomolecules},
volume = {15},
number = {7},
pages = {},
doi = {10.3390/biom15071005},
pmid = {40723882},
issn = {2218-273X},
mesh = {Humans ; *Colorectal Neoplasms/immunology/microbiology/therapy ; *Gastrointestinal Microbiome/immunology ; Animals ; Probiotics/therapeutic use ; Fecal Microbiota Transplantation ; },
abstract = {Colorectal cancer (CRC) is a multifactorial disease increasingly recognized for its complex interplay with the gut microbiota. The disruption of microbial homeostasis-dysbiosis-has profound implications for intestinal barrier integrity and host immune function. Pathogenic bacterial species such as Fusobacterium nucleatum, Escherichia coli harboring polyketide synthase (pks) island, and enterotoxigenic Bacteroides fragilis are implicated in CRC through mechanisms involving mucosal inflammation, epithelial barrier disruption, and immune evasion. These pathogens promote pro-tumorigenic inflammation, enhance DNA damage, and suppress effective anti-tumor immunity. Conversely, commensal and probiotic bacteria, notably Lactobacillus and Bifidobacterium species, exert protective effects by preserving epithelial barrier function and priming host immune responses. These beneficial microbes can promote the maturation of dendritic cells, stimulate CD8[+] T cell cytotoxicity, and modulate regulatory T cell populations, thereby enhancing anti-tumor immunity. The dichotomous role of the microbiota underscores its potential as both a biomarker and a therapeutic target in CRC. Recent advances in studies have explored microbiota-modulating strategies-ranging from dietary interventions and prebiotics to fecal microbiota transplantation (FMT) and microbial consortia-as adjuncts to conventional therapies. Moreover, the composition of the gut microbiome has been shown to influence the responses to immunotherapy and chemotherapy, raising the possibility of microbiome-informed precision oncology therapy. This review synthesizes the current findings on the pathogenic and protective roles of bacteria in CRC and evaluates the translational potential of microbiome-based interventions in shaping future therapeutic paradigms.},
}

Humans
*Colorectal Neoplasms/immunology/microbiology/therapy
*Gastrointestinal Microbiome/immunology
Animals
Probiotics/therapeutic use
Fecal Microbiota Transplantation

@article {pmid40723792,
year = {2025},
author = {Guo, H and Tang, X and He, X and Weng, Y and Zhang, Q and Fang, Q and Zhang, L},
title = {A Comprehensive Review of the Role of the Microbiota-Gut-Brain Axis via Neuroinflammation: Advances and Therapeutic Implications for Ischemic Stroke.},
journal = {Biomolecules},
volume = {15},
number = {7},
pages = {},
doi = {10.3390/biom15070920},
pmid = {40723792},
issn = {2218-273X},
support = {KJXW2023013//Xingwei Kejiao science and technology project of Suzhou/ ; SSD2024058//Suzhou Basic Research Pilot Project/ ; 82001125//National Natural Science Foundation of China/ ; BK20180201//Natural Science Foundation of Jiangsu Province/ ; 23KJB320016//The Natural Science Foundation of the Jiangsu Higher Education Institutions of China/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome ; *Ischemic Stroke/microbiology/therapy/metabolism ; Animals ; *Brain/metabolism ; *Neuroinflammatory Diseases/microbiology/metabolism/therapy ; Probiotics/therapeutic use ; *Brain-Gut Axis ; Fecal Microbiota Transplantation ; },
abstract = {The human gastrointestinal tract harbors a complex and diverse microbial community. Emerging evidence has revealed bidirectional communication between the gut microbiome and the central nervous system, termed the "microbiota-gut-brain axis". This axis serves as a critical regulator of glial cell function, positioning it as an essential target for ameliorating the onset and progression of ischemic stroke. In this review, we discuss the developments in the relationship between ischemic stroke and neuroinflammation via MGBA. The gut microbiome plays a critical role in signaling to microglia, astrocytes, and other immune components within this axis. We also summarize the interactions between the gut microbiota and glial cells under both healthy and ischemic stroke conditions. Additionally, we also focus on the role of microbiota-derived metabolites and neurotransmitters in ischemic stroke. Furthermore, we investigate the potential of targeting the intestinal and blood-brain barriers to improve MGBA. Finally, we evaluate the preclinical and clinical evidence for dietary interventions, probiotics, prebiotics, and fecal microbiota transplantation in ischemic stroke. A comprehensive understanding of the MGBA is essential for developing MGBA-based treatment for ischemic stroke.},
}

Humans
*Gastrointestinal Microbiome
*Ischemic Stroke/microbiology/therapy/metabolism
Animals
*Brain/metabolism
*Neuroinflammatory Diseases/microbiology/metabolism/therapy
Probiotics/therapeutic use
*Brain-Gut Axis
Fecal Microbiota Transplantation

@article {pmid40723178,
year = {2025},
author = {Tudorache, M and Treteanu, AR and Gradisteanu Pircalabioru, G and Lixandru-Petre, IO and Bolocan, A and Andronic, O},
title = {Gut Microbiome Alterations in Colorectal Cancer: Mechanisms, Therapeutic Strategies, and Precision Oncology Perspectives.},
journal = {Cancers},
volume = {17},
number = {14},
pages = {},
doi = {10.3390/cancers17142294},
pmid = {40723178},
issn = {2072-6694},
abstract = {Colorectal cancer (CRC) is one of the most prevalent and lethal oncological diseases worldwide, with a concerning rise in incidence, particularly in developing countries. Recent advances in genetic sequencing have revealed that the gut microbiome plays a crucial role in CRC development. Mechanisms such as chronic inflammation, metabolic alterations, and oncogenic pathways have demonstrated that dysbiosis, a disruption of the gut microbiome, is linked to CRC. Associations have been found between tumor progression, treatment resistance, and pathogenic microbes such as Fusobacterium nucleatum and Escherichia coli. A promising approach for CRC prevention and treatment is microbiome manipulation through interventions such as probiotics, prebiotics, fecal microbiota transplantation, and selective antibiotics. This article explores how gut microbiome alterations influence CRC pathogenesis and examines microbiome modulation strategies currently used as adjuncts to traditional treatments. Advances in artificial intelligence, single-cell and spatial transcriptomics, and large-scale initiatives such as the ONCOBIOME Project are paving the way for the identification of microbiome-derived biomarkers for early CRC detection and personalized treatment. Despite promising progress, challenges such as interindividual variability, causal inference, and regulatory hurdles must be addressed. Future integration of microbiome analysis into multi-omics frameworks holds great potential to revolutionize precision oncology in CRC management.},
}

@article {pmid40722867,
year = {2025},
author = {Akinrimisi, OI and Maasen, K and Scheijen, JLJM and Nemet, I and Nieuwdorp, M and Schalkwijk, CG and Hanssen, NMJ},
title = {Does Gut Microbial Methylglyoxal Metabolism Impact Human Physiology?.},
journal = {Antioxidants (Basel, Switzerland)},
volume = {14},
number = {7},
pages = {},
doi = {10.3390/antiox14070763},
pmid = {40722867},
issn = {2076-3921},
support = {09150172210019/NWO_/Dutch Research Council/Netherlands ; 2021T055//Hartstichting/ ; },
abstract = {Methylglyoxal (MGO) is a highly reactive dicarbonyl associated with oxidative stress, inflammation, and chronic diseases, particularly diabetic vascular complications and atherosclerosis through the formation of advanced glycation end products (AGEs). In the setting of human/host diseases, the formation of MGO has mainly been considered as the byproduct of glycolysis. Gut microbes play an important role in the development of cardiometabolic diseases. Here, we discuss a possibility that gut microbes can modulate the MGO pool within the host through (i) the alternation of the host metabolism, and (ii) direct MGO synthesis and/or detoxification by human commensal microorganisms. We also explore how dietary MGO impacts the composition of the gut microbiota and their potential role in modulating host health. This paradigm is highly innovative, with the current literature providing observations supporting this concept. Targeting the gut microbiome is emerging as an approach for treating cardiometabolic diseases through dietary, pre-, pro-, and postbiotic interventions, faecal microbiota transplantations, and the use of small molecule inhibitors of microbial enzymes. This can be a novel strategy to reduce MGO stress in the setting of cardiometabolic diseases and lowering the burden of diabetic complications and cardiovascular disease.},
}

@article {pmid40722839,
year = {2025},
author = {Carrossa, G and Misenti, V and Faggin, S and Giron, MC and Antonini, A},
title = {The Small Intestinal Microbiota and the Gut-Brain Axis in Parkinson's Disease: A Narrative Review.},
journal = {Biomedicines},
volume = {13},
number = {7},
pages = {},
doi = {10.3390/biomedicines13071769},
pmid = {40722839},
issn = {2227-9059},
abstract = {Researchers are increasingly focusing on understanding the microbiota's influence on disease susceptibility and overall health. The vast number of microorganisms in our gastrointestinal tract and their extensive surface area underscore their undeniable impact on well-being. Viewing the gut microbiome as a distinct pool of microbial genetic information that interacts with the human genome highlights its pivotal role in genetically predisposed diseases. Investigating this complex crosstalk may lead to the development of novel therapeutic strategies-such as targeting dysbiosis-to complement conventional treatments and improve patient care. Parkinson's disease (PD) is a multifactorial condition originating from a combination of genetic and environmental risk factors. Compelling evidence points to the enteric nervous system as an initial site of pathological processes that later extend to the brain-a pattern known as the 'body-first' model. Furthermore, most patients with PD exhibit both qualitative and quantitative alterations in the composition of the gut microbiota, including dysbiosis and small intestinal overgrowth. Nonetheless, the existing literature predominantly addresses fecal microbiota, while knowledge of upper intestinal sections, like the duodenum, remains scarce. Given the potential for microbiota modulation to impact both motor and gastrointestinal symptoms, further research exploring the therapeutic roles of balanced diets, probiotics, and fecal transplants in PD is warranted.},
}

@article {pmid40722483,
year = {2025},
author = {Dragasevic, S and Nikolic, A and Zgradic, S and Stojkovic Lalosevic, M and Stojkovic, S and Matovic Zaric, V and Lukic, S and Glisic, T and Kmezic, S and Saponjski, D and Popovic, D},
title = {Dysbiosis of Gut Microbiota in Microscopic Colitis: Diagnostic and Therapeutic Implications.},
journal = {Diagnostics (Basel, Switzerland)},
volume = {15},
number = {14},
pages = {},
doi = {10.3390/diagnostics15141733},
pmid = {40722483},
issn = {2075-4418},
abstract = {Microscopic colitis (MC) is an idiopathic inflammatory bowel disease characterized by watery, non-bloody diarrhea and histopathological changes but normal endoscopic findings. Increasing evidence now suggests that alterations in the gut microbiota contribute to the pathogenesis of MC. In this narrative review, we summarize evidence from nine case-control studies examining microbial composition using sequencing technology. The research presented here illustrates reduced alpha diversity, high dysbiosis, and pro-inflammatory oral-associated taxa enrichment, such as Veillonella dispar, and loss of protective microbes such as Akkermansia muciniphila and Bacteroides stercoris. These microbial changes have the potential to be non-invasive diagnostic biomarkers that can differentiate MC from other etiologies. In addition, the characterization of gut microbiota in MC can guide personalized therapeutic strategies, such as directed probiotic therapy or fecal microbiota transplantation, to help restore microbial balance. These microbial patterns can be applied to guide the creation of diagnostic biomarkers and personalized therapy. Despite differences in sample types and sequencing methods, general microbial trends highlight the need for further longitudinal and standardized investigations.},
}

@article {pmid40721426,
year = {2025},
author = {Yang, Y and Ye, M and Song, Y and Xing, W and Zhao, X and Li, Y and Shen, J and Zhou, J and Arikawa, K and Wu, S and Song, Y and Xu, N},
title = {Gut microbiota and SCFAs improve the treatment efficacy of chemotherapy and immunotherapy in NSCLC.},
journal = {NPJ biofilms and microbiomes},
volume = {11},
number = {1},
pages = {146},
doi = {10.1038/s41522-025-00785-9},
pmid = {40721426},
issn = {2055-5008},
support = {2020YFC2003700//National Key R&D Plan/ ; ZD2021CY001//Shanghai Municipal Science and Technology Major Project/ ; 20Z11901000, 20DZ2261200, 20XD1401200, 22Y11900800//Science and Technology Commission of Shanghai Municipality/ ; SHDC2020CR5010-002//Clinical Research Plan of SHDC/ ; shslczdzk02201//Shanghai Municipal Key Clinical Specialty/ ; ZY(2021-2023)-0207-01//Shanghai Municipal Health Commission and Shanghai Municipal Administrator of Traditional Chinese Medicine/ ; 81401877, 82130001, and 82272243//National Natural Science Foundation of China/ ; 81401877, 82130001, and 82272243//National Natural Science Foundation of China/ ; },
mesh = {*Gastrointestinal Microbiome ; Humans ; *Carcinoma, Non-Small-Cell Lung/therapy/microbiology/drug therapy ; *Immunotherapy/methods ; Animals ; *Lung Neoplasms/therapy/microbiology/drug therapy ; Mice ; *Fatty Acids, Volatile/metabolism ; Fecal Microbiota Transplantation ; RNA, Ribosomal, 16S/genetics ; Treatment Outcome ; *Bacteria/classification/genetics/isolation & purification/metabolism ; Female ; Male ; Metagenomics ; Middle Aged ; Aged ; Dysbiosis/microbiology ; Antineoplastic Agents/therapeutic use ; },
abstract = {The role of gut dysbiosis in shaping immunotherapy responses is well-recognized, yet its effect on the therapeutic efficacy of chemotherapy and immunotherapy combinations remains poorly understood. We analyzed gut microbiota in non-small cell lung cancer (NSCLC) patients treated with chemo-immunotherapy, comparing responders and non-responders using 16S rRNA sequencing. Responders showed higher microbial richness and abundance of specific genera like Faecalibacterium and Subdoligranulum, and the phylum Firmicutes. Support vector machine (SVM), a machine learning model based on microbial composition, predicted treatment efficacy with the area under the curve (AUC) values of 0.763 for genera and 0.855 for species. Metagenomic analysis revealed significant differences in metabolic pathways, with responders exhibiting higher short-chain fatty acids (SCFAs) production. Fecal microbiota transplantation (FMT) and SCFAs supplementation in mouse models enhanced treatment efficacy by promoting effector T cell activity in tumors. Our study suggests that gut microbiota, through SCFAs production, regulates chemo-immunotherapy efficacy, offering new strategies to improve NSCLC treatment outcomes.},
}

*Gastrointestinal Microbiome
Humans
*Carcinoma, Non-Small-Cell Lung/therapy/microbiology/drug therapy
*Immunotherapy/methods
Animals
*Lung Neoplasms/therapy/microbiology/drug therapy
Mice
*Fatty Acids, Volatile/metabolism
Fecal Microbiota Transplantation
RNA, Ribosomal, 16S/genetics
Treatment Outcome
*Bacteria/classification/genetics/isolation & purification/metabolism
Female
Male
Metagenomics
Middle Aged
Aged
Dysbiosis/microbiology
Antineoplastic Agents/therapeutic use

@article {pmid40716617,
year = {2025},
author = {Yi, D and Li, T and Xiao, Y and Li, X and Shao, B and Wu, Z and Hao, Q and Zhang, F and Zhang, X and Yang, G and Zhang, C and Deng, H and Sun, X and Wang, N},
title = {Hydroxytyrosol improved insulin resistance in male offspring born to high-fat diet dams by remodeling gut microbiota.},
journal = {The Journal of nutritional biochemistry},
volume = {},
number = {},
pages = {110041},
doi = {10.1016/j.jnutbio.2025.110041},
pmid = {40716617},
issn = {1873-4847},
abstract = {Maternal obesity during pregnancy and lactation critically influences offspring metabolic programming, increasing insulin resistance (IR) risk through gut microbiome alterations. This study investigated whether hydroxytyrosol (HT), a polyphenol, could exert metabolic benefits through intergenerational regulation of gut microbiota. Through dietary intervention and fecal microbiota transplantation experiments in pregnant and lactating C57BL/6J dams, combined with 16S rRNA sequencing and interaction analysis, we found that maternal high-fat diet (60% fat for energy) during gestation and lactation caused obesity and IR associated phenotypes in male offspring at 4 weeks of age, but not in female young pups. Oral gavage of HT (50 mg/kg) during pregnancy and lactation alleviated abnormal adipocyte hypertrophy, hyperplasia, and excessive leptin secretion in male offspring born to obese dams. Additionally, HT reduced systemic insulin intolerance, hyperglycemia, and hyperinsulinemia, decreased liver index and liver injury, attenuated hepatocyte ballooning, hepatic oxidative stress, and systemic inflammation, and restored hepatic PI3K/AKT signaling in male offspring. Furthermore, HT recovered intestinal barrier function and gut microbiota homeostasis in male offspring, especially the community structure represented by β-diversity, microbial dysbiosis index and SCFAs content. Importantly, the beneficial effects of maternal HT ingestion on offspring IR were closely associated with gut microbiota remodeling and could be transmitted through intergenerational microbial inheritance between mothers and offspring. Together, our study indicated that the intergenerational transmission of microbiota may underlie maternal obesity-induced IR and that HT intake could be a promising intervention.},
}

@article {pmid40716471,
year = {2025},
author = {Mkilima, T},
title = {Synthetic Biology Approaches for Restoring Gut Microbial Balance and Engineering Disease-Specific Microbiome Therapeutics.},
journal = {Microbial pathogenesis},
volume = {},
number = {},
pages = {107931},
doi = {10.1016/j.micpath.2025.107931},
pmid = {40716471},
issn = {1096-1208},
abstract = {The human gut microbiome plays a pivotal role in regulating digestion, immune function, and metabolic homeostasis. Disruption of this microbial equilibrium, known as dysbiosis, is increasingly linked to chronic conditions including inflammatory bowel disease (IBD), obesity, diabetes, and neurodegenerative disorders. Conventional interventions, such as probiotics and faecal microbiota transplantation (FMT), often yield inconsistent results due to individual microbiome variability and limited ecological stability. Engineered artificial microbial consortia (AMCs) have emerged as a next-generation strategy for precision modulation of the gut microbiome. This review critically examines cutting-edge advances in synthetic biology, CRISPR-based genome editing, metabolic engineering, and multi-omics integration that underpin the rational design of AMCs targeted to disease-specific microbial dysfunctions. Notably, this work presents an ecological precision engineering framework that integrates regional microbiome ecotypes, diet-responsive modular design, and adaptive metabolic modelling to ensure cross-population compatibility and stability. Enabling technologies, such as gut-on-a-chip platforms, high-throughput co-culture screening, and ecological modelling, are explored in the context of optimising AMC performance across diverse host environments. Furthermore, the review highlights the potential for AMC-based therapeutics to be equitably scaled through regionally adapted templates, thereby extending microbiome-based healthcare to low-resource settings. By bridging ecological diversity and therapeutic specificity, this review presents a globally relevant roadmap for developing reproducible, adaptable, and inclusive microbiome interventions within the broader framework of precision medicine.},
}

@article {pmid40720392,
year = {2025},
author = {Solis, AJ and Zucchi, P and Romo, JA},
title = {Biofilm Assay for Clostridioides difficile with Applications for Drug Discovery.},
journal = {Journal of visualized experiments : JoVE},
volume = {},
number = {221},
pages = {},
doi = {10.3791/67913},
pmid = {40720392},
issn = {1940-087X},
mesh = {*Biofilms/drug effects/growth & development ; *Clostridioides difficile/drug effects/physiology ; *Drug Discovery/methods ; *Anti-Bacterial Agents/pharmacology ; Humans ; Clostridium Infections/microbiology/drug therapy ; },
abstract = {Clostridioides difficile is a gastrointestinal bacterial pathogen able to take advantage of a dysbiotic microbiota environment to proliferate, secrete toxins, and damage the intestinal epithelium. A subset of C. difficile infection (CDI) patients will experience antibiotic (15%-30%) or fecal microbiota transplant (FMT) (<10%) treatment failure. Therefore, the development of additional therapeutic interventions is of critical importance. The role of C. difficile biofilms in recurrence is unclear. However, biofilms in other organisms are responsible for chronic and relapsing disease, suggesting this could also be the case in recurrent CDI. We hypothesize that biofilms of C. difficile present a valuable therapeutic target. The goal of the protocol presented here is to adapt a biofilm formation assay for the identification of repositionable compounds with activity against established C. difficile biofilms. The protocol refines a robust and reproducible assay for forming biofilms, couples it to a metabolic assay, and applies it to drug discovery. This protocol outlines the biofilm formation assay, biomass and metabolic activity readouts, drug susceptibility testing, drug screening of a repositioning library, and representative results.},
}

*Biofilms/drug effects/growth & development
*Clostridioides difficile/drug effects/physiology
*Drug Discovery/methods
*Anti-Bacterial Agents/pharmacology
Humans
Clostridium Infections/microbiology/drug therapy

@article {pmid40715107,
year = {2025},
author = {Lei, W and Zhou, K and Lei, Y and Li, Q and Zhu, H},
title = {Gut microbiota shapes cancer immunotherapy responses.},
journal = {NPJ biofilms and microbiomes},
volume = {11},
number = {1},
pages = {143},
pmid = {40715107},
issn = {2055-5008},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; *Neoplasms/therapy/immunology/microbiology ; *Immunotherapy/methods ; Tumor Microenvironment/immunology ; Probiotics/therapeutic use ; Animals ; Fecal Microbiota Transplantation ; },
abstract = {The gut microbiota significantly influences cancer immunotherapy efficacy by modulating immune responses, remodeling the tumor microenvironment (TME), and producing key metabolites. Strategies such as FMT, probiotics, and dietary interventions show promise in enhancing responses to ICIs and ACTs while reducing immune-related adverse events (irAEs). This review summarizes clinical and preclinical findings and discusses microbiota-based interventions and future directions for precision immunotherapy.},
}

Humans
*Gastrointestinal Microbiome/immunology
*Neoplasms/therapy/immunology/microbiology
*Immunotherapy/methods
Tumor Microenvironment/immunology
Probiotics/therapeutic use
Animals
Fecal Microbiota Transplantation

@article {pmid40719366,
year = {2025},
author = {Wang, X and Wang, N and Gao, T and Zhang, Y and Fu, Z and Zhao, Y and Huang, Y and Zheng, X and Gao, X and Lu, L and Yang, L},
title = {Symptom-specific gut microbial and metabolic profiles in ADHD reveal SCFA deficiency as a Key pathogenic mechanism.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2537755},
doi = {10.1080/19490976.2025.2537755},
pmid = {40719366},
issn = {1949-0984},
abstract = {Previous evidence links gut microbiota to attention-deficit/hyperactivity disorder (ADHD) through the gut-brain axis. However, the specific microbiota contributing to symptoms remain unclear. To characterize the gut microbial profile related to different symptoms and explore the mediation mechanism between microbiota alterations and the core ADHD symptoms, we conducted shotgun metagenomic sequencing and fecal metabolomics analysis on 94 ADHD patients and 94 age- and gender-matched controls. Microbial characteristics of three subgroups exhibiting different ADHD core symptom presentations were analyzed. We developed a metabolic model and conducted causal mediation analyses to examine how metabolites connect the microbiota to the symptoms. Fecal microbiota transplantation in mice was employed to validate the findings. The redundancy analysis identified ADHD symptoms as environmental gradients and explained the changes in beta diversity (F = 1.345, pFDR = 0.015). Greater gut microbial alterations were observed in combined presentations (ADHD-C). Several beneficial bacteria involved in short-chain fatty acid synthesis were found to be downregulated, with Lactobacillus sanfranciscensis notably linked to all three core symptoms (p.adj = 1.04E-13; p.adj = 5.07E-07; p.adj = 2.61E-05). Various taxa, functional pathways, and metabolites associated with specific ADHD symptom domains were identified. Imidazoleacetic acid partially mediated the effects between Lactobacillus sanfranciscensis and inattention (p = 0.012). In mice subjected to feces from ADHD patients with a low abundance of Lactobacillus sanfranciscensis, treatment with this strain greatly improved both hyperactivity (t = 2.665, p = 0.0237) and inattention (t = 2.389, p = 0.0380), while acetate supplementation only alleviated inattention (t = 2.362, p = 0.0398). Our findings suggest that different ADHD symptoms were related to common and different gut microbiota and metabolites. Fecal microbiota transplantation in mice validated the hypothesis that gut microbial composition affects ADHD symptoms through metabolic alterations. This study provides more insight into the mechanisms underlying metabolic disturbances in ADHD and elucidates the role of gut microbiota in these processes.},
}

@article {pmid40717663,
year = {2025},
author = {Liu, Y and Wang, Z and Zhang, Y and Zhao, T and Zhang, Q and Huang, W and Lu, B},
title = {Dietary cholesterol impairs cognition via gut microbiota-derived deoxycholic acid in obese mice.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2537753},
doi = {10.1080/19490976.2025.2537753},
pmid = {40717663},
issn = {1949-0984},
abstract = {Dietary cholesterol is often found in a high-fat diet (HFD) and excessive intake is harmful to cognitive function. The gut microbiome constitutes an environmental factor influenced by diet, which regulates cognitive function via the gut-brain axis. The present study explored the role of dietary cholesterol in HFD-induced cognitive impairment and the participation of the gut microbiota and metabolites. Here, we found that dietary cholesterol promoted cognitive impairment in HFD-fed mice, which was associated with an increase in gut microbiota containing 7α-dehydroxylase, including Lachnospiraceae bacterium, Dorea sp. Clostridium sp. and elevated levels of deoxycholic acid (DCA) in the hippocampus. Upon dietary cholesterol intake, the activity of gut microbiota in mice to produce DCA is increased. Fecal microbiota transplantation confirmed that the cognitive impairment-promoting process was driven by gut microbiota. Reducing circulating bile acid levels with cholestyramine improved cognitive decline in mice, whereas hippocampal administration of DCA worsened cognitive function. Pharmacological inhibition of hippocampal apical sodium bile acid transporter reduces neuronal DCA accumulation and improves neuronal apoptosis as well as cognitive impairments in mice. Overall, this study revealed that dietary cholesterol promotes HFD-induced cognitive impairment by inducing the production of DCA through gut microbiota metabolism.},
}

@article {pmid40714355,
year = {2025},
author = {Nóbrega, R and Costa, CFFA and Cerqueira, Ó and Inês, A and Carrola, JS and Gonçalves, C},
title = {Association between gut microbiota and pediatric obesity: A systematic review.},
journal = {Nutrition (Burbank, Los Angeles County, Calif.)},
volume = {140},
number = {},
pages = {112875},
doi = {10.1016/j.nut.2025.112875},
pmid = {40714355},
issn = {1873-1244},
abstract = {OBJECTIVES: Pediatric obesity is a multifactorial public health problem with increasing prevalence. Among the many contributing factors, the intestinal microbiota has emerged as a key area of investigation due to its potential role in metabolism, immunity, and energy regulation. Understanding and modulating the gut microbiota may offer novel therapeutic strategies. This systematic review aims to explore the relationship between the intestinal microbiota composition and obesity in pediatric age.

METHODS: The review followed PRISMA recommendations. Two databases (PubMed and Scopus) were consulted in May 2024 for research and two independent reviewers screened abstracts, following extraction of relevant data. Risk of bias was assessed using the Cochrane Collaboration's RoB 2 and ROBIN-I tools.

RESULTS: This review included a set of 70 studies, of which 23 were clinical trials and 47 were cross-sectional studies. They all analyzed the intestinal microbiota using fecal DNA sequencing, comparing microbial and metabolomic profiles between normal-weight children and overweight children. The effects of current interventions, such as the use of probiotics, supplementation, physical activity, and fecal microbiota transplantation, are also explored. Despite variability in findings, certain genera-such as Akkermansia, Bifidobacterium, Blautia, and Faecalibacterium-emerged as frequently associated with obesity-related traits. The Firmicutes/Bacteroidetes ratio showed inconsistent associations.

CONCLUSIONS: Pediatric obesity is associated with distinct changes in gut microbiota composition and function. While promising, the current evidence is heterogeneous. Future research should focus on longitudinal designs and standardized methodologies to clarify the role of diet, physical activity, and microbiota-based therapies in obesity prevention and management.},
}

@article {pmid40713811,
year = {2025},
author = {Sun, B and Yuan, J and Zhang, X and Ma, X and Hao, Z and Wang, L and Li, Y and Zhang, L and Li, L},
title = {Metaproteomics Reveals Community Coalescence Outcomes in Co-Cultured Human Gut Microbiota.},
journal = {Proteomics},
volume = {},
number = {},
pages = {e70009},
doi = {10.1002/pmic.70009},
pmid = {40713811},
issn = {1615-9861},
support = {32370050//National Natural Science Foundation of China/ ; 82371559//National Natural Science Foundation of China/ ; },
abstract = {The human gut microbiome exhibits characteristics of complex ecosystems, including the ability to resist and compete with exogenous species or communities. Understanding the microbiome response that emerges from such competitive interactions is crucial, particularly for applications like fecal microbiota transplantation (FMT), where the success of treatment largely depends on the outcome of these microbial competitions. During these processes, microbial communities undergo coalescence, a phenomenon where distinct microbial communities combine and interact, leading to complex ecological outcomes that are still being uncovered. In this study, we examined the coalescent dynamics of 10 different pairs of human gut microbiota by co-culturing the plateau-phase communities of individual samples in vitro, and highlighted the critical role of metaproteomics in elucidating the competitive dynamics of co-cultured human fecal samples. Results showed that microbiome changes observed after coalescent co-culture were not straightforwardly an approximate average of the initial taxonomic or functional compositions of the two samples. Instead, both coalescent microbiotas behaved as cohesive structures, influencing the competitive outcome toward one of them. Although co-cultured communities usually exhibited high degrees of taxonomic similarities to one of its parental samples, we found that 23% of the observed proteins still showed differential expression or abundance at the metaproteomic level. Interestingly, and somewhat counterintuitively, no specific microbial ecological characteristic could linearly determine which of the two initial microbiotas would act as the driving microbiota. Instead, we observed that the outcomes of the microbial co-cultures resembled a "rock-paper-scissors"-like dynamic. Through an analysis of co-colonizing species in such "rock-paper-scissors"-like triangle, we discovered that co-colonizing species that contributed to winning each between-community competition differed from one community pair to another. This suggests that no single species or function consistently dominates across all situations; instead, this involves more complex mechanisms, which require further in-depth investigation in future studies. Our findings demonstrate that the complex competitive interactions between microbial communities make predicting success through a single parameter challenging, whereas pre-co-culturing shows promise as an effective method for predicting outcomes in ecological therapies such as FMT. SUMMARY: This study underscores the critical importance of integrating metaproteomics with microbial systems ecology to gain a functional understanding of microbial coalescence. By addressing the ecological question of how two communities compete when they are brought into contact, we investigated the metaproteomic responses of pairs of coalescent co-cultured human gut microbiotas. Our results revealed significant insights: post-co-culture microbiota changes were not merely a simple average of the initial compositions but instead exhibited distinct shifts toward one of the original samples. Notably, due to the observed rock-paper-scissors-like cycle of winning, we argue that no single microbial ecological characteristic could straightforwardly predict which of the two samples would dominate as the driving microbiota. Overall, our findings suggest that during coalescence, microbial communities behave as cohesive structures both taxonomically and functionally, influencing competitive dynamics and ecosystem complexity, indicating that an in vitro coalescence pretest may help predict the success of therapies like FMT.},
}

@article {pmid40713799,
year = {2025},
author = {Soleimani Samarkhazan, H and Nouri, S and Maleknia, M and Aghaei, M},
title = {"The microbiome in graft-versus-host disease: a tale of two ecosystems".},
journal = {Journal of translational medicine},
volume = {23},
number = {1},
pages = {832},
pmid = {40713799},
issn = {1479-5876},
mesh = {*Graft vs Host Disease/microbiology/therapy ; Humans ; *Microbiota ; Hematopoietic Stem Cell Transplantation ; Animals ; *Ecosystem ; Fecal Microbiota Transplantation ; Dysbiosis ; },
abstract = {Graft-versus-host disease (GVHD), a life-threatening complication of allogeneic hematopoietic stem cell transplantation (HSCT), is shaped by a dynamic interplay between two microbial ecosystems: the recipient's disrupted microbiome and the donor's transplanted microbiota. This narrative review unravels the "tale of two ecosystems," exploring how pre-transplant chemotherapy, radiation, and antibiotics induce recipient dysbiosis-marked by loss of beneficial taxa (Clostridia, Faecalibacterium) and dominance of pathobionts (Enterococcus). These shifts impair barrier integrity, fuel systemic inflammation, and skew immune responses toward pro-inflammatory T-cell subsets, exacerbating GVHD. Conversely, emerging evidence implicates donor microbiota in modulating post-transplant immune reconstitution, though its role remains underexplored. Therapeutic strategies, including probiotics, prebiotics, and fecal microbiota transplantation (FMT), demonstrate promise in restoring microbial balance, enhancing short-chain fatty acid (SCFA)-driven immune regulation, and reducing GVHD severity. However, challenges such as strain-specific efficacy, safety in immunocompromised hosts, and protocol standardization persist. By bridging microbial ecology and immunology, this review underscores the microbiome's transformative potential in redefining GVHD management and advocates for personalized, microbiome-targeted interventions to improve HSCT outcomes.},
}

*Graft vs Host Disease/microbiology/therapy
Humans
*Microbiota
Hematopoietic Stem Cell Transplantation
Animals
*Ecosystem
Fecal Microbiota Transplantation
Dysbiosis

@article {pmid40713743,
year = {2025},
author = {Wang, L and Li, M and Dong, Y and Wang, J and Qin, S and Li, L and Li, B and Wang, B and Cao, H},
title = {Magnoflorine alleviates colitis-induced anxiety-like behaviors by regulating gut microbiota and microglia-mediated neuroinflammation.},
journal = {Microbiome},
volume = {13},
number = {1},
pages = {172},
doi = {10.1186/s40168-025-02158-y},
pmid = {40713743},
issn = {2049-2618},
support = {82270574, 82070545 and 81970477//National Natural Science Foundation of China/ ; 82270574, 82070545 and 81970477//National Natural Science Foundation of China/ ; 22ZYYJQ02//Tianjin Medical University General Hospital Fund for Distinguished Young Scholars/ ; 21JCYBJC00810//Diversified Fund Project of the Natural Science Foundation of Tianjin, China/ ; TJYXZDXK-002A//Tianjin Key Medical Discipline (Specialty) Construction Project/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; Mice ; *Anxiety/drug therapy/etiology/microbiology ; *Microglia/drug effects/metabolism ; *Aporphines/pharmacology/therapeutic use ; *Colitis, Ulcerative/drug therapy/microbiology/complications ; Ziziphus/chemistry ; Male ; *Colitis/complications/drug therapy/microbiology ; Disease Models, Animal ; Mice, Inbred C57BL ; *Neuroinflammatory Diseases/drug therapy ; Humans ; },
abstract = {BACKGROUND: Inflammatory bowel disease (IBD) and anxiety are often comorbid and are interconnected through the microbiota-gut-brain axis. Therapeutic medications for anxiety are often constrained by adverse effects that limit their long-term use. Therefore, recent research has focused on identifying natural, safe drugs for anxiety, and elucidating the precise mechanisms underlying the interplay between drugs and the gut-brain axis in modulating mood.

RESULTS: We revealed a significant association between active ulcerative colitis (UC) and anxiety. The results of Mendelian randomization analysis suggested that UC has a causal relationship with anxiety, but not depression. We identified Ziziphus jujuba, a natural plant, as a dual therapeutic agent for both UC and anxiety using the Batman database. Magnoflorine, the predominant compound found in Ziziphus jujuba, exhibits promising therapeutic properties for the treatment of UC and anxiety disorders. We found that magnoflorine not only alleviated colitis but also reduced colitis-induced anxiety behaviors through the gut microbiota. Mechanistically, magnoflorine increased the abundance of Odoribacteraceae and Ruminococcus and regulated bile acid metabolism, especially hyodeoxycholic acid (HDCA) in mice with colitis. HDCA supplementation alleviated both colitis and colitis-induced anxiety. HDCA inhibited the binding of lipopolysaccharide to the TLR4/MD2 complex, thereby inhibiting microglial activation and alleviating neuroinflammation.

CONCLUSION: Our study revealed that magnoflorine alleviated colitis-induced anxiety-like behaviors by regulating the gut microbiota and microglia-mediated neuroinflammation, which has the potential to treat patients with IBD and anxiety disorders. Video Abstract.},
}

Animals
*Gastrointestinal Microbiome/drug effects
Mice
*Anxiety/drug therapy/etiology/microbiology
*Microglia/drug effects/metabolism
*Aporphines/pharmacology/therapeutic use
*Colitis, Ulcerative/drug therapy/microbiology/complications
Ziziphus/chemistry
Male
*Colitis/complications/drug therapy/microbiology
Disease Models, Animal
Mice, Inbred C57BL
*Neuroinflammatory Diseases/drug therapy
Humans

@article {pmid40713718,
year = {2025},
author = {Pisani, A and Petito, V and Paciello, F and Emoli, V and Masi, L and Hizam, VM and Puca, P and Montuoro, R and Chierico, FD and Putignani, L and Grassi, C and Galli, J and Taglialatela, M and Caristo, ME and Ianiro, G and Lopetuso, LR and Cammarota, G and Gasbarrini, A and Fetoni, AR and Scaldaferri, F},
title = {Intestinal inflammation and microbiota modulation impact cochlear function: emerging insights in gut-ear axis.},
journal = {Cell communication and signaling : CCS},
volume = {23},
number = {1},
pages = {357},
doi = {10.1186/s12964-025-02338-1},
pmid = {40713718},
issn = {1478-811X},
mesh = {Animals ; *Gastrointestinal Microbiome ; *Cochlea/physiopathology/pathology ; Female ; Mice, Inbred C57BL ; Mice ; *Inflammation/pathology ; Humans ; Dysbiosis ; Fecal Microbiota Transplantation ; Colitis, Ulcerative/microbiology ; Myeloid Differentiation Factor 88/metabolism ; *Intestines/microbiology/pathology ; },
abstract = {BACKGROUND: Although several evidence demonstrates a "gut-microbiota-brain axis", suggesting a bidirectional communication between gut microbiota and the central nervous system, less is known about a possible link between the gut and the peripheral nervous system, including the inner ear.

METHODS: Here, we investigated the impact of intestinal inflammation and the modulation of gut microbiota through fecal microbiota transplantation on hearing sensitivity. Female C57BL/6 mice were assigned to four groups: control (Ctrl), DSS-induced colitis (DSS), FMT from patients with active ulcerative colitis (FMT aUC), and FMT from patients with ulcerative colitis in remission (FMT rUC). Auditory function was evaluated by auditory brainstem responses (ABR). Morphological and molecular analyses on cochlear tissues were performed using immunofluorescence, histological staining, and Western blot to assess inflammation, oxidative stress, and blood-labyrinth barrier integrity. Donor microbiota composition was characterized by 16S rRNA sequencing, and systemic inflammation was evaluated by measuring serum lipopolysaccharide (LPS) levels.

RESULTS: We found that intestinal dysbiosis is associated with functional, morphological, and molecular alterations in the cochlea, such as increased oxidative stress, inflammation, and altered blood-labyrinth barrier permeability. This leads to macrophage infiltration and immune response activation through the MyD88/NF-κB pathway. Notably, these effects were exacerbated by FMT from subjects with aUC, while FMT from patients with rUC provided a protective effect on cochlear functions.

CONCLUSIONS: Overall, our findings suggest that gut inflammation, microbiota alteration, or its therapeutic modulation can impact inner ear pathology: worsening gut inflammatory status negatively affects hearing sensitivity, while the restoration of gut microbiota positively impacts auditory function.},
}

Animals
*Gastrointestinal Microbiome
*Cochlea/physiopathology/pathology
Female
Mice, Inbred C57BL
Mice
*Inflammation/pathology
Humans
Dysbiosis
Fecal Microbiota Transplantation
Colitis, Ulcerative/microbiology
Myeloid Differentiation Factor 88/metabolism
*Intestines/microbiology/pathology

@article {pmid40712381,
year = {2025},
author = {Li, Q and Wang, G and Zhao, J and Chen, W and Tian, P},
title = {Gut microbiota and myelination: Crosstalk across the lifespan and microbiota-based modulation strategies.},
journal = {Microbiological research},
volume = {300},
number = {},
pages = {128286},
doi = {10.1016/j.micres.2025.128286},
pmid = {40712381},
issn = {1618-0623},
abstract = {Myelin, a lipid-rich sheath that insulates axons, is essential for efficient neural signal transmission and the modulation of neural circuits. Its formation, maintenance, and regeneration are tightly regulated processes that shape neurodevelopment, cognition, and emotional stability. Recent evidence positions the gut microbiota as a critical modulator of myelination, orchestrating metabolic signaling, immune homeostasis, and neuroinflammatory responses. Notably, the synchronized development and remodeling of gut microbiota and myelin across key life stages suggest a dynamic and bidirectional interplay essential for sustaining neurological health. Disruptions in this axis are increasingly recognized as contributing factors in dysmyelination-related disorders, including autism spectrum disorder, Alzheimer's disease, and multiple sclerosis. Harnessing microbiota-targeted interventions-such as fecal microbiota transplantation, dietary modulation, and probiotic therapies-holds promise for restoring myelin integrity and mitigating disease pathology. This review provides a comprehensive synthesis of the gut microbiota-myelin interface, delineating mechanistic insights and translational opportunities for microbiome-based therapeutic strategies in neuroprotection.},
}

@article {pmid40711721,
year = {2025},
author = {Shoukry, AEA and Rahhal, A and Constantinou, C},
title = {The role of the gut microbiota and metabolites in heart failure and possible implications for treatment.},
journal = {Heart failure reviews},
volume = {},
number = {},
pages = {},
pmid = {40711721},
issn = {1573-7322},
abstract = {The prevalence of heart failure has increased significantly in recent years, prompting investigations into novel contributory factors. Among these, alterations in the gut microbiota composition have garnered attention due to their potential association with heart failure. Disruption in the bacterial environment associated with heart failure is characterized by heightened levels of Proteobacteria and Firmicutes and decreased levels of Bifidobacteria and Bacteroides. Reduced blood supply weakens the gut barrier, facilitating the transportation of bacteria and metabolites into the bloodstream. This breach can trigger an immune response and inflammation, subsequently contributing to the pathogenesis of heart failure through the generation of harmful organic compounds in the gastrointestinal tract and bloodstream. Specific metabolites, including short-chain fatty acids, trimethylamine, and trimethylamine N-oxide also contribute to the development of heart failure. Management of heart failure includes pharmacological management, surgery, and lifestyle modifications including recommendations for the consumption of a diet high in fruits and low in animal products. Heart failure can be managed by modulating the gut microbiota. Clinical interventions include antibiotics, prebiotics, and dietary changes. However, other approaches including fecal microbial transplantation, probiotics, and natural phytochemicals are still under study in animal models. This review highlights the significant yet underexplored link between gut microbiota and heart failure, suggesting that further research could lead to new therapeutic strategies and dietary recommendations to mitigate heart failure progression.},
}

@article {pmid40709504,
year = {2025},
author = {Sheng, H and Xu, W and He, Y and Cai, Y and Wang, Z and Tao, X and Qiu, L and Wei, H},
title = {Amelioration of hypercholesterolemia by Lactiplantibacillus plantarum GLPL02 via regulating intestinal flora and cholesterol metabolism.},
journal = {Journal of the science of food and agriculture},
volume = {},
number = {},
pages = {},
doi = {10.1002/jsfa.70078},
pmid = {40709504},
issn = {1097-0010},
support = {82360114//National Natural Science Foundation of China/ ; 82160791//National Natural Science Foundation of China/ ; },
abstract = {BACKGROUND: In recent years, hypercholesterolemia has become one of the important risk factors for death around the world. Lactic acid bacteria (LAB), especially Lactiplantibacillus plantarum, exhibit strain-specific property of cholesterol-lowering activity. However, the metabolic mechanism involved in lipid-lowering capacity and regulation of intestinal flora of L. plantarum has not been well elucidated comprehensively.

RESULTS: The present study aimed to screen out cholesterol-lowering lactic acid bacteria from healthy lean individuals, evaluate their cholesterol-lowering effect and disclose its mechanism of amelioration of hypercholesterolemia in mice fed a high-cholesterol diet (HCD). Upon probiotic properties evaluation, the cholesterol removal rate of Lactiplantibacillus plantarum GLPL02 was 53.58%, and cholesterol degradation rate was 39.39%. In the systematic exploration of a model of HCD-induced mice and fecal microbiota transplantation, L. plantarum GLPL02 was found to reduce plasma lipid profiles (total cholesterol, triglycerides and low-density lipoprotein-cholesterol) and glucose tolerance, alleviate liver damage and steatosis, positively regulate intestinal flora related to cholesterol metabolism, upregulate genes relevant to decomposition (CYP7A1) and transportation (LDLR, ABCG5/8 and NPC1L1) of cholesterol, and downregulate genes relevant to synthesis (SREBP-2 and HMGCR), thereby improving hypercholesterolemia. Meanwhile, acetate and butyrate affected cholesterol metabolism in HepG2 cell through regulating cholesterol metabolism. Therefore, L. plantarum GLPL02 ameliorated hypercholesterolemia by regulating intestinal flora and genes related to cholesterol metabolism.

CONCLUSION: The present study indicates that L. plantarum GLPL02 and short-chain fatty acids (propionate, butyrate) ameliorated hypercholesterolemia and offers new insights into the role of L. plantarum in systemic cholesterol reduction from the perspective of microbiota-short-chain fatty acid interactions. © 2025 Society of Chemical Industry.},
}

@article {pmid40709417,
year = {2025},
author = {Lee, SB},
title = {[Expanding Role of Gastroenterologists in Acute Gastrointestinal Graft-versus-Host Disease: From Diagnosis and Management to Microbiome-Based Strategies].},
journal = {The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi},
volume = {85},
number = {3},
pages = {268-273},
doi = {10.4166/kjg.2025.049},
pmid = {40709417},
issn = {2233-6869},
mesh = {Humans ; *Graft vs Host Disease/diagnosis/therapy/pathology/drug therapy ; Hematopoietic Stem Cell Transplantation/adverse effects ; *Gastrointestinal Microbiome ; Fecal Microbiota Transplantation ; Pyrimidines ; Acute Disease ; Antibodies, Monoclonal, Humanized/therapeutic use ; Pyrazoles/therapeutic use ; Nitriles ; },
abstract = {Acute graft-versus-host disease (GVHD) is a major complication following allogeneic hematopoietic stem cell transplantation. Steroid-refractory cases have poor outcomes, so an accurate diagnosis, particularly differentiation from cytomegalovirus colitis, is critical. Ruxolitinib is the standard second-line therapy, while Vedolizumab has shown potential in gut-specific modulation. Recent studies have reported that reduced microbiome diversity and the loss of short-chain fatty acid-producing bacteria are linked to acute GVHD severity and mortality. Fecal microbiota transplantation may offer benefit in selected steroid-refractory cases, but the evidence remains limited and variable. Gastroenterologists play an essential role in diagnosis and microbiome-guided care. A personalized approach incorporating microbial biomarkers may improve the future outcomes.},
}

Humans
*Graft vs Host Disease/diagnosis/therapy/pathology/drug therapy
Hematopoietic Stem Cell Transplantation/adverse effects
*Gastrointestinal Microbiome
Fecal Microbiota Transplantation
Pyrimidines
Acute Disease
Antibodies, Monoclonal, Humanized/therapeutic use
Pyrazoles/therapeutic use
Nitriles

@article {pmid40708926,
year = {2025},
author = {Zhang, Y and Dong, Y and Sun, C and Zhang, L and Zhang, Y and Wang, D and Chen, Q and Yao, J and Wu, Y and Wang, T},
title = {Shouhui Tongbian Capsule ameliorates 5-fluorouracil induced constipation in mice by modulating gut microbiota and activating PI3K/AKT/AQP3 signaling pathway.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1596881},
pmid = {40708926},
issn = {1664-302X},
abstract = {OBJECTIVE: Shouhui Tongbian Capsule (SHTC) has been clinically applied to treat various types of constipation, including chemotherapy-induced constipation. However, the pharmacological mechanism by which it regulates intestinal peristalsis and treats constipation is unclear. In this study, we aimed to investigate the underlying mechanism of SHTC on chemotherapy-induced constipation through regulating of gut microbiota and PI3K/AKT/AQP3 signaling pathway.

METHODS: Chemotherapy-induced constipation was induced with 5-Fluorouracil in C57BL/6 mice. SHTC was administrated with different dosages (100, 200, 400 mg/kg) for 12 days. The intestinal tissues were collected for the measurements of intestinal propulsion rate, time of first black stool, and expressions of colonic aquaporin. 16S rRNA sequencing, short-chain fatty acids (SCFAs) profiling, and fecal microbiota transplantation (FMT) were performed to confirm whether gut microbiota is a key target for SHTC. Finally, the expressions of proteins or genes related to PI3K/AKT/AQP3 pathway were detected.

RESULTS: SHTC markedly improved the pathological manifestations associated with constipation and restored the deregulated gut microbiota. The mice that were given fecal supernatant from SHTC-treated mice showed significant improvement in constipation symptoms. Additionally, SHTC increased the level of acetic acid and upregulated the expression of AQP3, with activation of PI3K/AKT. Furthermore, the blockade of PI3K reversed the beneficial effect of acetic acid on the expression of AQP3.

CONCLUSION: Our findings indicated that SHTC effectively relieved 5-FU-induced constipation in mice, mainly by regulating homeostasis of gut microbiota and activating PI3K/AKT/AQP3 pathway, making it a potential protective agent against chemotherapy-induced constipation.},
}

@article {pmid40708753,
year = {2025},
author = {Zheng, YM and Ye, MM and Zhang, HY and Luo, DP and Liu, T and He, XX and Chen, XY and Wu, LH},
title = {Retrospective review: single- and multidonor washed microbiota transplantation have equivalent efficacy in the treatment of autism.},
journal = {Frontiers in cellular and infection microbiology},
volume = {15},
number = {},
pages = {1606417},
pmid = {40708753},
issn = {2235-2988},
mesh = {Humans ; Retrospective Studies ; Male ; *Fecal Microbiota Transplantation/methods ; Female ; Feces/microbiology ; Child ; Treatment Outcome ; *Autism Spectrum Disorder/therapy/microbiology ; Child, Preschool ; Gastrointestinal Microbiome ; Adolescent ; *Autistic Disorder/therapy ; },
abstract = {BACKGROUND: Autism spectrum disorder (ASD) is a serious neurodevelopmental disorder with no effective treatment. This study explored the short-term clinical effects of washed microbiota transplantation (WMT) with different numbers of donors on autism.

METHODS: Consecutive ASD patients treated with two continuous WMT courses from March 2020 to March 2022 at the First Affiliated Hospital of Guangdong Pharmaceutical University were retrospectively assessed. Basic information, aberrant behavior checklist (ABC) scores, childhood autism rating scale (CARS) scores, sleep disturbance scale for children (SDSC) scores, adverse reactions, and feces were collected.

RESULTS: Forty-four patients were included (single-donor group: 17 patients; multidonor group: 27 patients). The CARS, ABC and SDSC scores didn't differ between the two groups before treatment. After two courses, the scores for the 44 patients were lower than those at baseline (P<0.05), with no severe adverse reactions observed. After the first course, the mean ABC (P=0.049) and SDSC (P=0.019) scores were significantly different between the single-donor and multidonor groups, but the difference disappeared after two courses. The alpha-diversity of the faecal flora in the effective-group was greater than that in the ineffective-group (Shannon index P=0.0018). Lactobacillus was the predominant genus in the effective group, whereas Faecalibacterium, Campylobacter, and Sphingomonas were predominant genera in the ineffective group.

CONCLUSION: After two WMT courses, the symptoms of ASD improved, with good short-term treatment efficacy. The ASD symptom improvement did not differ between the single-donor and multidonor groups. Changes in the alpha-diversity and abundance of the faecal microbiota after WMT may be related to treatment efficacy.},
}

Humans
Retrospective Studies
Male
*Fecal Microbiota Transplantation/methods
Female
Feces/microbiology
Child
Treatment Outcome
*Autism Spectrum Disorder/therapy/microbiology
Child, Preschool
Gastrointestinal Microbiome
Adolescent
*Autistic Disorder/therapy

@article {pmid40707990,
year = {2025},
author = {Drevland, OM and de Muinck, EJ and Trosvik, P and Hammerstad, M and Kvitne, KE and Midtvedt, K and Åsberg, A and Robertsen, I},
title = {Microbiome-derived reactivation of mycophenolate explains variations in enterohepatic recirculation in kidney transplant recipients.},
journal = {Microbiome},
volume = {13},
number = {1},
pages = {169},
pmid = {40707990},
issn = {2049-2618},
support = {315792//Norges Forskningsråd/ ; 315792//Norges Forskningsråd/ ; },
mesh = {*Mycophenolic Acid/pharmacokinetics/analogs & derivatives/metabolism ; *Kidney Transplantation ; Humans ; *Gastrointestinal Microbiome/drug effects ; Male ; Female ; *Immunosuppressive Agents/pharmacokinetics/therapeutic use ; Middle Aged ; Feces/microbiology ; Adult ; Transplant Recipients ; Glucuronidase/metabolism/genetics ; Glucuronides/metabolism ; Metagenomics/methods ; *Enterohepatic Circulation ; },
abstract = {BACKGROUND: The pivotal role of microbes in drug metabolism is increasingly recognized, as variation in the gut microbiome composition between individuals has been shown to impact systemic drug exposure, efficacy and toxicity. Mycophenolate mofetil (MMF) is a cornerstone in immunosuppressive therapy following solid organ transplantation. However, dosing and tolerance are challenged by significant pharmacokinetic variability among patients, largely due to variable degrees of enterohepatic recirculation of mycophenolic acid (MPA), the active moiety of MMF. It is hypothesized that the variability in MPA recirculation is driven by gut microbiome-derived β-glucuronidase (β-GUS) mediated cleavage of MPA-glucuronide (MPAG) excreted in the bile. Here, we investigated the bidirectional interaction between MPA and the gut microbiome in kidney transplant recipients, using a combination of in vivo and in vitro data.

RESULTS: We compared the fecal microbiomes of kidney transplant recipients (n = 21) both pre- and post-transplantation to healthy individuals (n = 15) using shotgun metagenomic sequencing. We also determined the individual microbiome-derived reactivation rate of MPAG to MPA and show a strong positive correlation between this reactivation rate and the degree of MPA enterohepatic recirculation in vivo. Through metagenomic analysis, the reactivation rate of MPA was linked to specific gut microbial species. In particular, specific β-GUS gene variants associated with Faecalibacterium prausnitzii showed a strong impact on the conversion of MPAG to MPA. Furthermore, our study confirmed a significant shift in microbial composition post-transplantation and revealed notable fluctuations in species such as F. prausnitzii and Akkermansia muciniphila across different time points after transplantation. Lastly, we provide evidence that the microbiome-derived reactivation rate of MPA is linked to specific beta-glucuronidase alleles.

CONCLUSIONS: We highlight for the first time that the ex vivo determined reactivation rate of MPA explains the variation of enterohepatic recirculation, emphasizing the important role of F. prausnitzii in this process. More broadly, our findings suggest that the gut microbiome significantly influences the degree of enterohepatic recirculation of MPA, providing valuable insights that could be relevant for optimizing individualized immunosuppressive drug dosing in transplant patients. Video Abstract.},
}

*Mycophenolic Acid/pharmacokinetics/analogs & derivatives/metabolism
*Kidney Transplantation
Humans
*Gastrointestinal Microbiome/drug effects
Male
Female
*Immunosuppressive Agents/pharmacokinetics/therapeutic use
Middle Aged
Feces/microbiology
Adult
Transplant Recipients
Glucuronidase/metabolism/genetics
Glucuronides/metabolism
Metagenomics/methods
*Enterohepatic Circulation

@article {pmid40707965,
year = {2025},
author = {Wang, X and Xiao, ZJ and Xue, CZ and Wu, WT and Yang, JH and Yan, C and Wang, Y and Kui, Y and Luo, WB and Du, X and Zan, RN and Shang, RJ and Li, S and Na, R and Han, S and Li, SZ},
title = {Clinical confirmation of an infection with Echinococcus multilocularis (Mongolian genotype): first case report of human alveolar echinococcosis in Inner Mongolia, China.},
journal = {Infectious diseases of poverty},
volume = {14},
number = {1},
pages = {74},
pmid = {40707965},
issn = {2049-9957},
support = {82404325//National Natural Science Foundation of China/ ; GWVI-11.1-12//Three-Year Initiative Plan for Strengthening Public Health System Construction in Shanghai (2023-2025) Key Discipline Project/ ; },
mesh = {*Echinococcus multilocularis/genetics/isolation & purification/classification ; Humans ; Female ; China ; Middle Aged ; Animals ; Genotype ; *Echinococcosis/parasitology/diagnosis ; Phylogeny ; *Echinococcosis, Hepatic/parasitology/diagnosis/surgery ; Fatal Outcome ; Dogs ; Liver Transplantation ; },
abstract = {BACKGROUND: Alveolar echinococcosis (AE), caused by the larval stage of Echinococcus multilocularis, poses a substantial global health challenge due to its high mortality profile. This study reports the inaugural human infection of echinococcosis caused by the Mongolian genotype of E. multilocularis in China, also the first reported indigenous AE case in Inner Mongolia.

CASE PRESENTATION: A 58-year-old female pastoralist from Inner Mongolia, who had no endemic region exposure history but prolonged occupational contact with dogs, presented with severe AE. Clinical examinations revealed a massive hepatic lesion exceeding 10 cm in diameter, accompanied by elevated eosinophils (0.90 × 10[9]/L) and basophils (0.08 × 10[9]/L). Despite undergoing liver transplantation, the patient succumbed postoperatively. Histopathological confirmation and molecular phylogenetics identified the Mongolian genotype of E. multilocularis infection, distinct from the predominant Asian genotype in China. Potential evidence of zoonotic transmission was discovered through genotype-matched E. multilocularis detection in corsac fox (Vulpes corsac) feces from the grasslands along the shores of Hulun Lake (Hulun Buir City, northeastern Inner Mongolia, China).

CONCLUSIONS: This report provides the primary evidence of a locally acquired human AE infection in China caused by the Mongolian genotype of Echinococcus multilocularis. The discovery of this case challenges historical classifications of echinococcosis endemic areas. The findings call for revised AE-endemic identification criteria, improved AE diagnostic protocols, and enhanced AE surveillance in the Inner Mongolia region to generate further epidemiological evidence and information on disease progression.},
}

*Echinococcus multilocularis/genetics/isolation & purification/classification
Humans
Female
China
Middle Aged
Animals
Genotype
*Echinococcosis/parasitology/diagnosis
Phylogeny
*Echinococcosis, Hepatic/parasitology/diagnosis/surgery
Fatal Outcome
Dogs
Liver Transplantation

@article {pmid40398302,
year = {2025},
author = {Yu, M and Xu, M and Wang, G and Feng, J and Zhang, M},
title = {Effect of cecal microbiota transplantation on peripheral 5-hydroxytryptamine and breast muscle glucose metabolism in long-photoperiod broilers.},
journal = {Poultry science},
volume = {104},
number = {8},
pages = {105225},
pmid = {40398302},
issn = {1525-3171},
mesh = {Animals ; *Chickens/physiology/metabolism/microbiology ; *Glucose/metabolism ; Male ; *Serotonin/metabolism ; *Photoperiod ; *Gastrointestinal Microbiome ; *Fecal Microbiota Transplantation/veterinary ; *Muscle, Skeletal/metabolism ; Random Allocation ; Cecum/microbiology ; },
abstract = {Prolonged light periods resulted in up-regulation of cecal 5-hydroxytryptamine (5-HT) synthesis and secretion, disorders of breast muscle glucose metabolism and alteration in gut microbiota composition. The present study was conducted to investigate the effects of cecal microbiota on peripheral 5-HT metabolism and breast muscle glucose metabolism in broiler chickens underlying prolonged light periods. A total of 144 5-day-old male Arbor Acres (AA) broiler chickens were randomly divided into four treatment groups i.e., 12 hours light: 12 hours dark (12L:12D) photoperiod group, 18 hours light: 6 hours dark (18L:6D) photoperiod group, 18L:6D photoperiod with phosphate buffered saline (PBS) solution administration group (18L:6D+PBS) and 18L:6D photoperiod with cecal microbiota transplantation (CMT) group (18L:6D+CMT) for 14 days. The results demonstrated that the 18L:6D photoperiod increased breast muscle rate (P < 0.05) but induced the morphological damage of breast muscle, dysregulation of breast muscle glucose metabolism and higher peripheral 5-HT synthesis (P < 0.05). In contrast, CMT significantly improved breast muscle weight and breast muscle ratio while reducing the breast muscle injury. Furthermore, CMT alleviated glucose metabolism dysregulation, as evidenced by significant reductions in serum glucose (P < 0.05), insulin (INS) (P < 0.05), homeostasis model assessment of insulin resistance (HOMA-IR) (P < 0.05), and the lactic acid-to-pyruvate ratio (L/P) (P < 0.05), as well as an increase in muscle glycogen concentrations (P < 0.05). Additionally, the expression of glycogen synthase (GS), pyruvate dehydrogenase (PDH) and glucose transporter-4 (GLUT4) up-regulated, while the expression of glycogen phosphorylase L (PYGL), hexokinase (HK), 6-phosphofructokinase (PFK), pyruvate kinase (PK) and lactate dehydrogenase (LDH) down-regulated (P < 0.05) in breast muscle of CMT-treated broiler chickens. Notably, both peripheral 5-HT concentrations and cecal 5-HT synthesis was significantly reduced (P < 0.05) in the 18L:6D+CMT group. In summary, these findings indicate that CMT promotes breast muscle rate, reduces breast muscle injury, alleviates breast muscle glucose metabolism disorder in broiler chickens exposed to prolonged light periods. Moreover, peripheral 5-HT metabolism may serve as a key pathway through which cecal microbiota regulates skeletal muscle glucose metabolism.},
}

Animals
*Chickens/physiology/metabolism/microbiology
*Glucose/metabolism
Male
*Serotonin/metabolism
*Photoperiod
*Gastrointestinal Microbiome
*Fecal Microbiota Transplantation/veterinary
*Muscle, Skeletal/metabolism
Random Allocation
Cecum/microbiology

@article {pmid39758049,
year = {2025},
author = {Bartha, V and Boutin, S and Schüßler, DL and Felten, A and Fazeli, S and Kosely, F and Luft, T and Wolff, D and Frese, C and Schoilew, K},
title = {Exploring the Influence of Oral and Gut Microbiota on Ulcerative Mucositis: A Pilot Cohort Study.},
journal = {Oral diseases},
volume = {31},
number = {6},
pages = {1776-1788},
doi = {10.1111/odi.15246},
pmid = {39758049},
issn = {1601-0825},
support = {//Deutsche Gesellschaft für Präventivzahnmedizin e. V. and CP GABA/ ; },
mesh = {Humans ; Pilot Projects ; Female ; Male ; Middle Aged ; *Gastrointestinal Microbiome ; Adult ; Feces/microbiology ; *Mouth Mucosa/microbiology ; Saliva/microbiology ; *Stomatitis/microbiology ; Aged ; Cohort Studies ; *Oral Ulcer/microbiology ; *Mucositis/microbiology ; RNA, Ribosomal, 16S/genetics ; Hematopoietic Stem Cell Transplantation/adverse effects ; },
abstract = {AIM: Comparing oral and gut microbiome profiles between patients with and without ulcerative mucositis during allogeneic stem cell transplantation (aSCT).

MATERIALS AND METHODS: Specimens from oral mucosa, saliva, and stool were collected pre-(T0) and post- (T0 +28d ± 14d) aSCT (T1). Microbiome structure differences were analyzed by 16S-rRNA-gene sequencing, and associations to patients' clinical characteristics were investigated.

RESULTS: Ten of 25 included patients developed ulcerations. The α-diversity decreased between T0 and T1, independent of ulcerations. PERMANOVA revealed differences in beta diversity between T1 stool samples from patients with and without ulcerations. At T1, saliva samples of patients with ulcerations showed an increase of Mycoplasma salvarius, while commensals decreased in saliva and mucosal swabs. The gut microbiome of both groups showed an overabundance of Enterococcus spp., associated with inflammatory conditions. Salival α-diversity of older and overweight patients decreased slower, whereas in mucosal swabs mucositis or impaired renal function was associated with a higher decline. Female gender and history of periodontitis were associated with increased stool microbiome changes, while self-reported probiotics intake was related to reduced changes.

CONCLUSIONS: Ulcerations appeared in 40% of the patients. Distinct microbial changes, including increased abundance of Mycoplasma salivarius in saliva and decreased abundance of commensals, marked those with ulcerations.

TRIAL REGISTRATION: The study was registered in the German Register for Clinical Studies (DRKS00032882).},
}

Humans
Pilot Projects
Female
Male
Middle Aged
*Gastrointestinal Microbiome
Adult
Feces/microbiology
*Mouth Mucosa/microbiology
Saliva/microbiology
*Stomatitis/microbiology
Aged
Cohort Studies
*Oral Ulcer/microbiology
*Mucositis/microbiology
RNA, Ribosomal, 16S/genetics
Hematopoietic Stem Cell Transplantation/adverse effects

@article {pmid40706525,
year = {2025},
author = {Gutting, T and Brobeil, A and Strach, L and Stricker, E and Boxberger, M and Trierweiler-Hauke, B and Heine, C and Michl, P and Luntz, S and Robert, B and Göbel, F and Weis, C and Pfützner, A},
title = {Sealing efficiency and safety of a polyurethane-based fecal management system in intensive care-Results from a real-world study.},
journal = {Australian critical care : official journal of the Confederation of Australian Critical Care Nurses},
volume = {38},
number = {5},
pages = {101296},
doi = {10.1016/j.aucc.2025.101296},
pmid = {40706525},
issn = {1036-7314},
abstract = {OBJECTIVE: Fecal management systems (FMSs) are critical for preventing skin irritations and anal dermatitis in intensive care. A polyurethane-based system (hygh-tec® [Advanced Medical Balloons]) has been introduced in the European Union and United States. This real-world observational study aimed to evaluate the sealing efficiency and safety of the system in routine care.

METHODS: Thirty-nine patients were included in the descriptive analysis (18 females and 21 males; mean age: 66.4 ± 10.5 years; body mass index: 28.8 ± 11.7 kg/m[2]). Intensive care nurses documented findings related to sealing efficiency, anal lesions, and adverse events during their shifts.

RESULTS: Sealing efficiency was assessed from 1110 shift reports. The mean device usage duration was 10.8 days (range: 3-31 days). No visible perianal contamination was noted in 76.0% of shift reports (n = 844). Relevant leakage was documented in 10.7% of cases and was independent of body mass index, anal sphincter muscle tone, and reason for admission. Stool consistency and patient vigilance had minimal influence. There were no device-related adverse events, and the incidence of anal lesions was 0.8% over 31 days of use.

CONCLUSION: The polyurethane-based FMS demonstrated excellent sealing efficiency, tolerability, and safety. Controlled studies are needed to confirm these findings and evaluate economic implications. FMSs can improve both work quality and patient safety.},
}

@article {pmid40705333,
year = {2025},
author = {Woodworth, MH and Babiker, A and Prakash-Asrani, R and Mehta, CC and Steed, DB and Ashley, A and Koundakjian, D and Acharya, A and Grooms, L and Bower, CW and Suchindran, DR and Trehan, T and Halpin, AL and Spalding Walters, M and Reddy, SC and Samore, MH and Roghmann, MC and Hayden, MK and Van Riel, J and Burd, EM and Lohsen, S and Satola, SW and Fridkin, SK},
title = {Microbiota Transplantation Among Patients Receiving Long-Term Care: The Sentinel REACT Nonrandomized Clinical Trial.},
journal = {JAMA network open},
volume = {8},
number = {7},
pages = {e2522740},
doi = {10.1001/jamanetworkopen.2025.22740},
pmid = {40705333},
issn = {2574-3805},
mesh = {Humans ; Female ; Male ; *Fecal Microbiota Transplantation/methods/adverse effects ; Aged ; Middle Aged ; *Long-Term Care/methods ; },
abstract = {IMPORTANCE: Intestinal multidrug-resistant organism (MDRO) colonization is highly prevalent in long-term acute care hospital (LTACH) patients and is associated with MDRO infection and transmission. However, there are no therapies approved by the US Food and Drug Administration to reduce intestinal MDRO colonization.

OBJECTIVE: To determine the safety and acceptability of fecal microbiota transplantation (FMT) in LTACH patients.

This single-center, open-label nonrandomized clinical trial was conducted from April to December 2023 at an LTACH in the Southeastern US with median 50-patient census and 28-day length of stay. Patients with MDRO colonization were identified by perirectal prevalence sampling. Patients colonized with at least 1 target MDRO were approached for informed consent for FMT. FMT recipients were compared with untreated controls with MDRO colonization. Data were analyzed from August 2024 to May 2025.

INTERVENTION: Healthy donor fecal microbiota (50-100 g stool and 250 mL normal saline with 9% glycerol) instilled via gastrostomy tube or enema without antibiotic or bowel preparation conditioning.

MAIN OUTCOMES AND MEASURES: The primary outcome was frequency and severity of adverse events. Solicited adverse events were recorded for 7 days. Unsolicited adverse events were recorded for 6 months. Four weekly perirectal MDRO cultures were performed after FMT.

RESULTS: A total of 42 patients, including 10 (mean [SD] age, 63.8 (14.5) years; 7 [70%] female) who received FMT and 32 contemporaneous controls (mean [SD] age, 64.0 [13.7] years; 13 [41%] female) were assessed. In 2 prevalence surveys, 23 of 32 (72%) and 26 of 34 (77%) perirectal cultures grew at least 1 MDRO. Among the FMT group, 5 patients received FMT via gastrostomy alone, 4 via enema alone, and 1 with both routes more than 30 days apart. No serious adverse events were attributed to FMT, and post-FMT solicited adverse events were mild. At final visit, all perirectal cultures from FMT recipients grew at least 1 MDRO. Post hoc analyses found numerically fewer FMT recipients had positive blood culture results (0 individuals vs 6 individuals [19%]; P = .31), pathogen intestinal dominance (2 of 8 individuals [25%] vs 4 of 8 individuals [50%]; P = .61), and 7 fewer days of antibiotic therapy per 1000 patient days (median [IQR], 12.6 [0-25.2] days vs 19.7 [6.5-36.1] days; P = .38) compared with controls in the 6 months after prevalence survey, although these differences were not statistically significant. Accounting for higher baseline FMT recipient antibiotic use, difference-in-differences analysis estimated 26 (95% CI, -64 to 12) fewer days of antibiotic therapy per 1000 patient-days after FMT, although this difference was also not statistically significant.

CONCLUSIONS AND RELEVANCE: In this nonrandomized pilot clinical trial, FMT was acceptable for LTACH patients without related serious adverse events. Although not powered to test these outcomes, this study found potential reductions in bacteremia, intestinal pathogen domination, and antibiotic use associated with FMT, suggesting FMT should be evaluated in larger, randomized trials.

TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT05780801.},
}

Humans
Female
Male
*Fecal Microbiota Transplantation/methods/adverse effects
Aged
Middle Aged
*Long-Term Care/methods

@article {pmid40703681,
year = {2025},
author = {Hlavaty, M and Brezina, J and Osadcha, T and Fabian, O and Vajsova, A and Drastich, P and Cahova, M and Bajer, L},
title = {Serological Markers of Intestinal Barrier Function and Inflammation as Potential Predictors of Recurrent Primary Sclerosing Cholangitis.},
journal = {Clinical and experimental gastroenterology},
volume = {18},
number = {},
pages = {171-178},
pmid = {40703681},
issn = {1178-7023},
abstract = {The impairment of intestinal barrier function is implicated in primary sclerosing cholangitis, but the clinical evidence is scarce. Therefore, we performed a cross-sectional study to evaluate serological markers of inflammation and intestinal permeability (Reg3a, iFABP, Zonulin, Calprotectin) in patients after liver transplantation (LT) for PSC. The cohort included 26 subjects with PSC recurrence (rPSC), 87 subjects without PSC recurrence (non-rPSC), and a unique control group consisting of post-LT patients (n = 113) transplanted due to alcohol cirrhosis. Generalized Linear Models were calculated to assess the association between serological markers of intestinal barrier function or inflammation (IP_Models) and PSC diagnosis per se (IP_Model_1), non-rPSC (IP_Model_2) or rPSC incidence (IP_Model_3) and compared with models (ST_Models) based on validated PSC markers (ALP, GGT, bilirubin). The increased probability of PSC occurrence (IP_Model_1, p < 0.001, AIC = 182) was associated with higher serum Reg3a concentration, while a negative association was found for iFABP, BMI, and age. The probability of non-recurrence (IP_Model_2, p < 0.001, AIC = 167) was associated with lower Reg3a concentration, older age, and BMI. The performance of IP_Models_1,2 and ST_models_1,2 was comparable. rPSC prediction was less precise by both models (IP_Model_3 p = 0.063, AIC = 92; ST_Model_3 p < 0.001, AIC = 108). rPSC incidence was positively associated with fecal calprotectin and serum zonulin concentrations, while it was independent of Reg3a, iFABP, age or BMI. In conclusion, this pilot study suggests that impaired intestinal permeability is associated with the pathophysiology of rPSC. Our data could serve as a basis for testing in a larger independent validation cohort and, if confirmed, help to explain the mechanisms underlying the pathophysiology of PSC and the recurrence of this disease after transplantation.},
}

@article {pmid40703302,
year = {2025},
author = {Zhang, J and Ren, X and Li, B and Zhao, Z and Li, S and Zhai, W},
title = {Fecal microbiota transplantation is a promising therapy for kidney diseases.},
journal = {Frontiers in medicine},
volume = {12},
number = {},
pages = {1628722},
pmid = {40703302},
issn = {2296-858X},
abstract = {Kidney diseases, including acute kidney injury (AKI) and chronic kidney disease (CKD), pose growing global public health challenges. With the emergence and expanding understanding of the "microbiota-gut-kidney axis," increasing evidence indicates that intestinal barrier disruption, abnormal microbial metabolite production, and intestinal mucosal immune dysregulation play critical roles in the pathogenesis of various kidney diseases. Therapeutic modulation of the gut microbiota through probiotics, prebiotics, synbiotics, and natural products has shown potential for slowing kidney disease progression. Fecal microbiota transplantation (FMT), a direct method of reconstructing gut microbial communities, has demonstrated promise in CKD by targeting mechanisms such as inhibition of the renin-angiotensin system (RAS), attenuation of inflammation and immune activation, and restoration of intestinal barrier integrity. Although FMT has not yet been applied to AKI, its use in CKD subtypes, such as diabetic nephropathy, IgA nephropathy, membranous nephropathy, and focal segmental glomerulosclerosis, has shown encouraging preclinical and preliminary clinical results. This review systematically summarizes the current research on FMT in the context of kidney disease, evaluates its therapeutic mechanisms and feasibility, and highlights its limitations. Most studies remain in the preclinical stage, while available clinical trials are limited by small sample sizes, heterogeneous designs, and lack of standardization. To enhance the translational potential of FMT in nephrology, future studies should incorporate artificial intelligence for personalized intervention strategies and establish standardized protocols to ensure safety, efficacy, and reproducibility.},
}

@article {pmid40703229,
year = {2025},
author = {Yuan, C and Liu, L and Zeng, D and Yuan, J and Guo, L and Zhang, J},
title = {Exploring the influence of gut microbiota metabolites on vitiligo through the gut-skin axis.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1566267},
pmid = {40703229},
issn = {1664-302X},
abstract = {Vitiligo is an autoimmune skin disease with a complex pathogenesis closely linked to immune imbalance and oxidative stress. Currently, comprehensive curative treatments and effective relapse prevention strategies are lacking. Recently, the "gut-skin axis" hypothesis has offered new insights into the pathological mechanisms of vitiligo. Studies indicate that gut microbiota and their metabolic products significantly affect disease progression by regulating immune homeostasis and inflammatory responses in the host. This review systematically examines the effects of short-chain fatty acids, secondary bile acids, and tryptophan metabolites on the human immune system and the inflammatory milieu, and their direct impact on melanocytes. Furthermore, considering the reduced diversity of gut microbiota in individuals with vitiligo, this article also evaluates methods including probiotic intervention, the Mediterranean diet, and fecal microbiota transplantation, which may emerge as potential therapeutic strategies for vitiligo by restoring microbiota balance. Future multidimensional therapeutic strategies that target gut microbiota metabolites show promise for pioneering innovative approaches in vitiligo management.},
}

@article {pmid40701508,
year = {2025},
author = {Chen, WJ and Wang, JP and Zhou, JR and He, Y and An, DQ and Tian, TT and Liang, MT and Aikepa, D and Kahaer, M and Sun, YP},
title = {Efficacy and Mechanisms of Compound Bai Mao Yin in Regulating Uric Acid Transport and Improving the Intestinal Microbiota to Alleviate Hyperuricemia via the Enterorenal Axis.},
journal = {Microbial pathogenesis},
volume = {},
number = {},
pages = {107922},
doi = {10.1016/j.micpath.2025.107922},
pmid = {40701508},
issn = {1096-1208},
abstract = {BACKGROUND: The compound Bai Mao Yin (BMY) has demonstrated therapeutic efficacy in reducing uric acid (UA) levels; however, its underlying mechanisms remain unclear.

METHODS: The UA-lowering effects of BMY were evaluated in a cohort of 40 patients with hyperuricemia (HUA) who received BMY treatment for 90 days. Fecal samples were collected at baseline (day 0), mid-treatment (day 30), and post-treatment (day 90) for metagenomic sequencing to analyze changes in gut microbiota and identify potential BMY targets in HUA. These clinical findings were validated in a hyperuricemic mouse model induced by xanthine and potassium oxonate. Mouse fecal samples were analyzed via 16S rDNA (V3-V4 region) sequencing to assess microbiota shifts. Additionally, fecal microbiota transplantation (FMT) from BMY-treated mice to HUA mice and in vitro cell experiments using HK2 cells were conducted to investigate the roles of BMY and the reconstructed microbiota in UA metabolism, renal UA transport, and inflammation through upstream signaling pathways.

RESULTS: Clinical cohort studies demonstrated that the BMY effectively lowers UA levels in patients with HUA without inducing hepatorenal toxicity. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis of metagenomic data revealed that BMY modulates the gut microbiota and influences ATP-binding cassette transporters and UA metabolism-related pathways. In animal models, BMY increased the relative abundance of beneficial gut bacteria, reduced intestinal permeability, and regulated UA transporters in both intestinal and renal systems, contributing to UA reduction. In vitro assays showed that BMY directly decreased UA levels in the cell supernatant and suppressed interleukin-1β (IL-1β) and interleukin-6 (IL-6) expression by downregulating the TLR4/MYD88/NFκB signaling pathway, thereby alleviating inflammation.

CONCLUSIONS: Compound BMY was found to improve the intestinal microenvironment and modulate UA transport via the enterorenal axis, effectively reducing HUA.},
}

@article {pmid40701347,
year = {2025},
author = {Yun, F and Han, X and Wang, Z and Gao, Q and Xu, M and Liu, H and Fang, N and Zhang, Y and Li, Y and Gong, Y},
title = {Intermittent fasting ameliorates resistant hypertension through modulation of gut microbiota.},
journal = {Pharmacological research},
volume = {},
number = {},
pages = {107864},
doi = {10.1016/j.phrs.2025.107864},
pmid = {40701347},
issn = {1096-1186},
abstract = {Resistant hypertension (RH) remains a major cardiovascular challenge despite optimal pharmacological treatment. Intermittent fasting (IF) has demonstrated beneficial effects in various diseases, but its impact on RH and the underlying mechanisms remain unclear. In this study, we explored the effects of a 2-week IF regimen (16-hour fasting/8-hour eating) on RH patients and spontaneously hypertensive rats (SHRs) resistant to antihypertensive drugs. We found that IF significantly reduced blood pressure in RH patients, accompanied by a shift in the gut microbiota, including increased abundance of Akkermansia muciniphila and Adlercreutzia equolifaciens. These microbiota alterations were correlated with a decrease in lipopolysaccharide (LPS) and trimethylamine-N-oxide (TMAO) levels, and an increase in short-chain fatty acids (SCFAs). Furthermore, fecal microbiota transplantation (FMT) from drug-resistant SHRs successfully transferred both hypertension and impaired drug efficacy to recipient rats. Supplementation with Akkermansia muciniphila and Adlercreutzia equolifaciens significantly lowered blood pressure in SHR rats resistant to antihypertensive drugs. In RH patients, oral supplementation with Akkermansia muciniphila reduced blood pressure and normalized LPS, TMAO, and SCFA levels. Our findings provide both clinical and mechanistic evidence supporting IF and A. muciniphila supplementation as promising non-pharmacological approaches for managing resistant hypertension.},
}

@article {pmid40484213,
year = {2025},
author = {Zbóril, S and Schmidt, AP and Ramos Maia, DR and Sanches, TR and Neto, AND and Andrade, L and Oses, JP and Moreira, FP and Auler, JOC and Otsuki, DA},
title = {Treatment with mesenchymal stem cells in a porcine model of sepsis: Assessment of the central nervous system.},
journal = {Neuroscience letters},
volume = {862},
number = {},
pages = {138294},
doi = {10.1016/j.neulet.2025.138294},
pmid = {40484213},
issn = {1872-7972},
mesh = {Animals ; Swine ; *Mesenchymal Stem Cell Transplantation/methods ; *Sepsis/therapy/pathology/physiopathology ; Disease Models, Animal ; *Mesenchymal Stem Cells ; Cytokines/blood/cerebrospinal fluid ; Humans ; Hippocampus/pathology ; Hemodynamics ; },
abstract = {Sepsis remains a leading cause of intensive care unit admissions and a significant public health challenge worldwide. Despite efforts, the development of specific therapies for sepsis has been limited. Mesenchymal stem cell therapy, particularly with cells derived from the human umbilical cord (hUC-MSC), has shown promise in animal studies. This study evaluated the use of hUC-MSC in a porcine model of sepsis induced by fecal peritonitis, focusing on hemodynamic and metabolic effects, inflammatory response, and central nervous system impact. Twenty-two pigs were randomized into a control group receiving fluids, vasopressors, and antibiotics, and a treatment group receiving the same interventions plus hUC-MSC infusion. Hemodynamic parameters, acid-base status, cytokine levels in serum and cerebrospinal fluid (CSF), and neuron-specific enolase were assessed over 24 h. Histopathological analysis of the hippocampus was performed post-mortem. No significant differences were observed between groups regarding hemodynamic and metabolic parameters or serum cytokine levels. While interleukin-1β levels in CSF increased in all animals' post-sepsis induction, interleukin-10 levels were significantly higher in hUC-MSC-treated animals. Histopathological analysis revealed reduced congestion, vasodilation, and neuronal karyolysis in the hippocampus of the treatment group. These findings suggest that while hUC-MSC therapy does not significantly impact hemodynamics, metabolism, systemic inflammation, or mortality in septic shock, it may offer neuroprotective effects. Further studies are required to elucidate the mechanisms underlying these potential neuroprotective properties of hUC-MSC in sepsis.},
}

Animals
Swine
*Mesenchymal Stem Cell Transplantation/methods
*Sepsis/therapy/pathology/physiopathology
Disease Models, Animal
*Mesenchymal Stem Cells
Cytokines/blood/cerebrospinal fluid
Humans
Hippocampus/pathology
Hemodynamics

@article {pmid40699664,
year = {2025},
author = {Bonù, ML and Georgopulos, A and Ramera, M and Andreuccetti, J and Guerini, AE and Bozzola, AM and Morelli, V and Balduzzi, J and Katica, M and Cefaratti, M and Granello, L and Triggiani, L and Buglione, M and Magrini, SM and Marampon, F and Mondini, M and Parisi, S and Timon, G and Bellu, L and Rescigno, M and Arcangeli, S and Scorsetti, M},
title = {Microbiota Modulation of Radiosensitiveness and Toxicity in Gastrointestinal Cancers: What Radiation Oncologists Need to Know-A Review on Behalf of the Italian Association of Radiobiology (AIRB).},
journal = {Current issues in molecular biology},
volume = {47},
number = {4},
pages = {},
doi = {10.3390/cimb47040265},
pmid = {40699664},
issn = {1467-3045},
abstract = {The impact of the microbiota on radiation (RT)-induced toxicity and cancer response to radiotherapy is an emerging area of interest. In this review, we summarize the available preclinical and clinical evidence concerning microbiota modulation of RT toxicity and efficacy in the main gastrointestinal (GI) districts. A huge amount of data supports the clinical application of microbiota modulation, particularly through prebiotics and probiotics, to prevent or mitigate radiotherapy-induced toxicity in rectal cancer. Preclinical and clinical studies also support the observation of microbiota modulation to impact the toxicity and efficacy of treatment in esophageal cancer, hepatocellular carcinoma (HCC), and anal squamous cell carcinoma (ASCC). However, insufficient evidence remains to endorse microbiota modulation as a strategy to enhance tumor radiosensitivity in clinical practice. Well-designed studies focusing on prebiotics, probiotics, and fecal microbiota transplantation are needed across all GI sites to evaluate their potential to improve treatment efficacy, as suggested by promising preclinical findings. The impact of pre-treatment microbiota analyses should be addressed in prospective studies to verify the efficacy of patient-level tailored strategies. Additionally, the repurposing of radioprotective agents with innovative delivery systems, such as encapsulated amifostine, holds significant promise for mitigating small bowel toxicity, thereby enabling more effective RT treatment.},
}

@article {pmid40697274,
year = {2025},
author = {Wei, N and Dai, S and Li, W and Zhou, J and Chen, Y},
title = {Gut microbiota and sepsis-associated encephalopathy: pathogenesis and precision therapies.},
journal = {Frontiers in neuroscience},
volume = {19},
number = {},
pages = {1596467},
pmid = {40697274},
issn = {1662-4548},
abstract = {Sepsis is defined as a condition of immune dysregulation in response to an infection, and sepsis-associated encephalopathy (SAE) is often the initial symptom that manifests in patients with sepsis. This condition is characterized by its high mortality rates and the potential to cause significant disability among survivors. Despite its severity, the underlying pathophysiologic mechanisms that contribute to the development of SAE are not yet fully understood. Additionally, there are no established strict diagnostic criteria or potent treatment options available for this condition. However, an increasing body of evidence suggests that an imbalance in the gut microbiota is associated with SAE, potentially through the gut-brain axis (GBA). The GBA axis refers to the bidirectional communication between the gut microbiota and the central nervous system. In this review, we discuss the changes in the gut microbiota in SAE and the mechanisms of the GBA axis, involving neural, immune, endocrine, and neurotransmitter pathways. Finally, we conclude by evaluating the preclinical and clinical evidence for fecal microbiota transplantation and probiotics in SAE. Targeting the GBA axis will be an actionable target to ameliorate the development and progression of SAE.},
}

@article {pmid40697099,
year = {2025},
author = {Zhang, Y and Tu, M and Long, P and Zheng, J and Du, G and Xiao, S and Gao, C},
title = {Efficacy of probiotics pretreatment in Helicobacter pylori eradication therapy: a systematic review and meta-analysis of clinical outcomes.},
journal = {Annals of medicine},
volume = {57},
number = {1},
pages = {2533431},
doi = {10.1080/07853890.2025.2533431},
pmid = {40697099},
issn = {1365-2060},
mesh = {*Probiotics/therapeutic use/administration & dosage ; Humans ; *Helicobacter Infections/therapy/microbiology/drug therapy ; *Helicobacter pylori/drug effects ; Anti-Bacterial Agents/therapeutic use ; Treatment Outcome ; Gastrointestinal Microbiome/drug effects ; Randomized Controlled Trials as Topic ; },
abstract = {BACKGROUND: Probiotics inhibit Helicobacter pylori (H. pylori) growth and alter gut microbiome, in addition to alleviating the side effects of H. pylori eradication. It has also been reported that H. pylori be eradicated after fecal microbiota transplantation in some cases. However, whether probiotics used before H. pylori eradication improves the eradication rate remains unclear. This study evaluates their role through a systematic review and meta-analysis.

METHODS: We searched PubMed, EMBASE, the Cochrane Library, and the Conference Proceedings Citation Index up to January 31, 2024, to identify randomized controlled studies (RCTs) assessing the efficacy of probiotics used before H. pylori eradication. Meta-analyses of eradication rates were performed.

RESULTS: Twelve eligible RCTs with 2,144 participants were included. The intention-to-treat analysis revealed that the overall eradication rate of H. pylori was higher in the probiotics pretreatment group compared to the control group (80.34% vs. 70.49%), with a risk ratio (RR) of 1.14 (95% CI: 1.08 to 1.19; I[2] = 36%) and side effects were less (16.0% vs. 28.3%, RR = 0.59, 95% CI 0.41 to 0.84). The per-protocol analysis yielded similar results (86.43% vs. 76.88%, RR = 1.12, 95% CI: 1.08 to 1.17; I[2] = 57%). Subgroup analyses, considering factors like geographic location, eradication regimens, and probiotic combinations, consistently confirmed the benefits. Finally, probiotics pretreatment durations of 14 days or more, as well as the study designs pre vs. free and pre and combine vs. free, demonstrated significant effects. Shorter durations and other study designs with fewer studies did not show significant effects.

CONCLUSION: There is moderate to high evidence to suggest that probiotics pretreatment improves H. pylori eradication rate and reduces side effects. These findings highlight the potential value of gut microbiome modulation in H. pylori treatment and offer a new direction for addressing the challenges of antibiotic resistance and treatment failure.},
}

*Probiotics/therapeutic use/administration & dosage
Humans
*Helicobacter Infections/therapy/microbiology/drug therapy
*Helicobacter pylori/drug effects
Anti-Bacterial Agents/therapeutic use
Treatment Outcome
Gastrointestinal Microbiome/drug effects
Randomized Controlled Trials as Topic

@article {pmid40696369,
year = {2025},
author = {Song, S and Wen, X and Chen, F and Li, J and Shi, K and Lou, Y and Xu, A and Wen, C and Shao, T},
title = {Qu-zhuo-tong-bi decoction exerts gouty arthritis therapy by skewing macrophage polarization through butanoate metabolism.},
journal = {Chinese medicine},
volume = {20},
number = {1},
pages = {115},
pmid = {40696369},
issn = {1749-8546},
support = {82274302//National Natural Science Foundation of China/ ; 82074248//National Natural Science Foundation of China/ ; 2023C03040//Key Research and Development Program of Zhejiang Province/ ; },
abstract = {BACKGROUND: Qu-zhuo-tong-bi decoction (QZTBD), a traditional Chinese medicine (TCM), has demonstrated efficacy in the treatment of gouty arthritis. However, to date, the precise pharmacological mechanisms remain unclear.

PURPOSE: The study aims to ascertain the therapeutic effects and the underlying mechanisms of QZTBD in the treatment of gouty arthritis.

METHODS: The efficacy and safety of different doses of QZTBD were investigated in Uox-KO mice. Candidate active ingredients were identified using UHPLC-MS/MS. The potential therapeutic pathways of the active ingredients were predicted through network pharmacology. The mechanisms of QZTBD in alleviating gouty arthritis were explored via comprehensive analyses of gut microbiota, combined with RT-qPCR, western blot, immunofluorescence, ELISA, flow cytometry, and Seahorse assay. Fecal microbiota transplantation (FMT), bacterial culture experiment, butyrate-producing bacteria (BPB) and butyrate administration, and 2-DG intervention were conducted to explore the roles of BPB and butanoate metabolism in gout progression and therapeutic mechanisms of QZTBD. In vitro studies further validated the regulatory effects of butyrate and QZTBD on macrophage polarization through glycolysis modulation.

RESULTS: 18.0 g/kg/d of QZTBD effectively alleviated the symptoms of gouty arthritis with excellent hepatic and renal safety. UHPLC-MS/MS analysis and network pharmacology revealed that QZTBD exerts its effects on butanoate metabolism during gouty arthritis inflammation. QZTBD treatment increased the abundance of BPB, the levels of serum and colon butyrate, and the expression levels of Buk and But. The transplantation of QZTBD-treated microbiota reproduced the therapeutic effects of QZTBD. M1 macrophage polarization was suppressed after QZTBD intervention. The administration of BPB and butyrate attenuated gouty arthritis and orchestrated macrophage polarization. Inhibition of glycolysis regulated the phenotype of macrophage and attenuated inflammatory processes. In vitro analysis unveiled that QZTBD and butyrate modulated glycolysis to regulate macrophage polarization, thereby alleviating gouty arthritis.

CONCLUSION: QZTBD targeted butanoate metabolism to regulate macrophage polarization, thereby effectively alleviating intestinal inflammation and restoring immune homeostasis in gouty arthritis. These findings establish a mechanistic foundation for developing precision therapeutic strategies leveraging QZTBD to combat gouty arthritis.},
}

@article {pmid40693424,
year = {2025},
author = {Lu, HH and Nguyen, NTK and Panwar, R and Lin, CI and Cross, TL and Lin, SH},
title = {Ameliorating Gastrointestinal Symptoms in Children With Autism Spectrum Disorder by Modulating the Gut Microbiota: A Systematic Review and Meta-Analysis.},
journal = {Autism research : official journal of the International Society for Autism Research},
volume = {},
number = {},
pages = {},
doi = {10.1002/aur.70091},
pmid = {40693424},
issn = {1939-3806},
abstract = {Children with autism spectrum disorder (ASD) exhibit a high prevalence (55%) of gastrointestinal symptoms (GISs) and gut dysbiosis. Most studies involving children with ASD have focused on behavioral symptoms but not GISs. This systematic review and meta-analysis investigated the effects of gut microbiota-modulating interventions (GMMIs) on GISs and gut microbial composition in children with ASD. Five databases were searched for relevant domestic and international articles published from database inception until July 15, 2024. The meta-analysis included human trials wherein children with ASD received prebiotics, probiotics, synbiotics, or fecal microbiota transplantation. Intervention effects were measured on the basis of α-diversity, and genus- and phylum-level data were analyzed using a random-effects model and forest plots. This study included 19 trials (n = 1154). The results indicated that GMMIs significantly ameliorated GISs (p = 0.0017), reduced six-item Gastrointestinal Symptom Index scores by 1.86 points (p = 0.0187), and significantly increased the relative abundance of Bifidobacterium spp. (p = 0.0205). Longer interventions (≥ 8 weeks) were more effective in ameliorating GISs. Limitations in this investigation include the fact that the included studies neither incorporated any dietary control groups nor collected relevant dietary data, and the relatively small sample size (19 studies) may have hindered the identification of sources of heterogeneity in the pooled results. Overall, our findings suggest that GMMIs, especially probiotics, ameliorate GISs in children with ASD by modulating gut microbial composition, particularly by increasing the relative abundance of Bifidobacterium spp. These interventions may alleviate symptoms such as constipation, diarrhea, abnormal stool consistency and smell, flatulence, and abdominal pain. Our evidence supports that treatments involving GMMIs can be considered for children with ASD.},
}

@article {pmid40692142,
year = {2025},
author = {Chao, J and Tan, Z and Li, Z and Xu, C},
title = {The Role of the Microbiota-Gut-Brain Axis in Perinatal Depression: Novel Insights for Treatment.},
journal = {Current neuropharmacology},
volume = {},
number = {},
pages = {},
doi = {10.2174/011570159X380460250710061340},
pmid = {40692142},
issn = {1875-6190},
abstract = {Perinatal depression, a prevalent mood disorder complicating pregnancy and childbirth, poses significant threats to maternal health and neonatal development. While psychotherapy and antidepressants constitute current standard treatments, their clinical application faces substantial limitations during pregnancy and lactation, including safety concerns, treatment resistance, and poor adherence rates. These therapeutic constraints have spurred growing interest in novel gut-brain axis (GBA)-targeted interventions. Emerging evidence suggests that the gut microbiota communicates with the brain through a complex network of neural, immune, and endocrine pathways, playing a critical role in regulating mood, behavior, and cognitive functions. Interventions such as probiotics and fecal microbiota transplantation (FMT) are increasingly explored for their potential to restore microbial balance and alleviate depressive symptoms. This review aims to systematically examine the role of the GBA in the context of perinatal depression, offering novel insights to inform clinical treatment strategies. Furthermore, it evaluates the promise and limitations of microbiota-targeted interventions while discussing future directions for personalized microbiome therapeutics.},
}

@article {pmid40691891,
year = {2025},
author = {Song, H and Zhang, H and Qin, X and Liu, Y and Lai, Y and Yang, W and Zhang, L and Hu, W and Wang, X and Zeng, J and Liu, R},
title = {Gut microbiota dysbiosis and disturbed tryptophan metabolism mediate cognitive impairment in mice with circadian rhythm disruption.},
journal = {Brain research bulletin},
volume = {},
number = {},
pages = {111473},
doi = {10.1016/j.brainresbull.2025.111473},
pmid = {40691891},
issn = {1873-2747},
abstract = {Circadian rhythm disorder (CRD) is a risk factor for cognitive deficits, yet its mechanisms remain unclear. We previously found CRD model mice developed cognitive impairment mediated through gut microbiota disturbance, intestinal barrier damage, and microglia activation, but the signaling pathway was undefined. Here, we show CRD induces cognitive deficits and gut microbiota disturbance in mice. Fecal microbiota transplantation (FMT) from CRD mice to normal mice reproduced intestinal barrier damage, microglia activation, neuronal damage, and cognitive deficits. Notably, gut metabolite analysis revealed significant alterations, with tryptophan metabolism being particularly affected: tryptophan decreased by 26.9% and 5-hydroxytryptophan (5-HTP) by 30.7% (both P < 0.05). Dietary tryptophan supplementation restored serum tryptophan and 5-HTP levels, ameliorating the neuronal damage and cognitive deficits caused by CRD gut microbiota. Collectively, these findings indicate that disturbances in gut microbiota and metabolites play a key role in CRD-induced neurological damage in mice, suggesting targeting the gut microbiota or tryptophan metabolism may prevent CRD-induced cognitive dysfunction.},
}

@article {pmid40691449,
year = {2025},
author = {Vázquez-Castellanos, JF and Maciel, LF and Wauters, L and Gregory, A and Van Oudenhove, L and Geboers, K and Verbeke, K and Smokvina, T and Tack, J and Vanuytsel, T and Derrien, M and Raes, J},
title = {Probiotic-mediated modulation of gut microbiome in students exposed to academic stress: a randomized controlled trial.},
journal = {NPJ biofilms and microbiomes},
volume = {11},
number = {1},
pages = {140},
pmid = {40691449},
issn = {2055-5008},
mesh = {Humans ; *Probiotics/administration & dosage ; *Gastrointestinal Microbiome/drug effects ; *Stress, Psychological/microbiology ; *Students/psychology ; Male ; Female ; *Lacticaseibacillus rhamnosus/physiology ; RNA, Ribosomal, 16S/genetics ; Young Adult ; Adult ; Feces/microbiology ; *Bacteria/classification/genetics/isolation & purification ; Anxiety ; Metagenomics ; },
abstract = {Probiotics have been widely tested for their effect on mental well-being, albeit with heterogeneous outcomes. Direct and indirect effects through the gut microbiome might lie at the basis of these observations. Here, in a post-hoc analysis, we assessed the effect of 4-week consumption of a probiotic candidate strain on the gut microbiome in students exposed to academic stress. Healthy students were randomized to consume a fermented milk product with Lacticaseibacillus rhamnosus CNCM I-3690 (N = 39) or an acidified non-fermented milk product (N = 40) twice daily for 4 weeks before academic exams. The gut microbiome was analysed by Quantitative Microbiome Profiling based on 16S rRNA gene amplicon and shotgun metagenomic sequencing. Stress and anxiety were assessed using both objective and self-reported markers. Changes of alpha-diversity markers and community shifts from baseline (beta diversity) were lower in L. rhamnosus treated individuals over controls, suggesting lower overall changes of gut microbiota during psychological stress in the Probiotic group. The intake of L. rhamnosus CNCM I-3690 induced differential abundance of some species, such as the maintenance of the quantitative abundance of Ruminococcus bicirculans, and co-varied with species, which differed according to visits (i.e., stress level), suggesting a potential beneficial effect of the strain before the highest increase of stress level. The higher quantitative abundance of F. prausnitzii induced by the probiotic intake was associated with lowered self-reported anxiety levels before the exam. Functional analysis revealed minor changes upon intake of the probiotic strain. Taken together, using a quantitative framework, we found that L. rhamnosus CNCM I-3690 has a potential effect on gut microbiome response to stress, although further studies are needed to better understand the precise interaction.},
}

Humans
*Probiotics/administration & dosage
*Gastrointestinal Microbiome/drug effects
*Stress, Psychological/microbiology
*Students/psychology
Male
Female
*Lacticaseibacillus rhamnosus/physiology
RNA, Ribosomal, 16S/genetics
Young Adult
Adult
Feces/microbiology
*Bacteria/classification/genetics/isolation & purification
Anxiety
Metagenomics

@article {pmid40690011,
year = {2025},
author = {Nazir, MM and Ghaffar, W and Mustafa, G and Saeed, S and Ijaz, MU and Ashraf, A},
title = {Modulating depression through the gut-brain axis: the role of gut microbiota in therapeutic interventions.},
journal = {Naunyn-Schmiedeberg's archives of pharmacology},
volume = {},
number = {},
pages = {},
pmid = {40690011},
issn = {1432-1912},
abstract = {Depression is a multifactorial mental disorder increasingly linked to gut microbiota through the microbiota-gut-brain axis (MGBA). This review aims to explore how alterations in gut microbial composition influence depressive symptoms via neurochemical, immunological, and neuroendocrine pathways. Key mechanisms include microbial modulation of serotonin, dopamine, and GABA levels; systemic inflammation; hypothalamic-pituitary-adrenal (HPA) axis dysregulation; and vagus nerve signaling. Emerging evidence suggests that gut microbiota may also influence the efficacy of selective serotonin reuptake inhibitors (SSRIs), potentially via vagal pathways. Additionally, a distinct microbial signature has been observed in individuals with depression, with therapeutic probiotics targeting this dysbiosis showing beneficial effects. This review further evaluates the therapeutic potential of probiotics, prebiotics, fecal microbiota transplantation (FMT), and dietary interventions in managing depression. We highlight the need for microbiota-based biomarkers and personalized interventions in future clinical applications. Overall, this review underscores the therapeutic relevance of targeting the gut-brain axis in depression treatment.},
}

@article {pmid40686934,
year = {2025},
author = {Alaeddin, S and Chatterjee, A and Roberts, TL and Steiner-Lim, GZ and Jensen, SO and Gyengesi, E and Muench, G and Ho, V},
title = {Exploring the effects of faecal microbiota transplantation on cognitive function: A review of clinical trials.},
journal = {Brain, behavior, & immunity - health},
volume = {48},
number = {},
pages = {101049},
pmid = {40686934},
issn = {2666-3546},
abstract = {Faecal Microbiota Transplantation (FMT) is a widely used microbiota-modulation technique to treat recurrent Clostridioides difficile infections (rCDI). Rodent studies and clinical trials on probiotic interventions indicate that alterations in microbiota composition may impact cognitive function. To explore whether FMT influences cognitive function in humans, we conducted a systematic search and narrative synthesis and identified 14 studies examining its effects on cognition. A variety of cohort studies, single-arm trials, case reports and randomised, placebo-controlled trials have been conducted on different neurological patient cohorts, including those with Hepatic Encephalopathy, Parkinson's Disease, dementia, and Mild Cognitive Impairment. FMT has been shown to have a significant impact on cognitive function in these populations, accompanied by alterations in microbial composition and blood markers. Interestingly, success was influenced by the route of FMT administration, indicating greater efficacy of rectal cf. oral administration on microbiome composition and cognitive improvements. However, no clinical trials have yet examined the effects of FMT on cognitively healthy individuals. FMT appears to have potential as a therapeutic strategy for cognitive impairment, though further research with larger sample sizes is needed to explore its effects in both impaired and cognitively healthy populations.},
}

@article {pmid40686307,
year = {2025},
author = {Li, W and Xu, M and Cheng, M and Wei, J and Zhu, L and Deng, Y and Guo, F and Bi, F and Liu, M},
title = {Current Advances and Future Directions for Sensitizing Gastric Cancer to Immune Checkpoint Inhibitors.},
journal = {Cancer medicine},
volume = {14},
number = {14},
pages = {e71065},
doi = {10.1002/cam4.71065},
pmid = {40686307},
issn = {2045-7634},
support = {ZYJC21043//West China Hospital, Sichuan University/ ; 2023YFS0111//Sichuan Province Science and Technology Support Program/ ; },
mesh = {Humans ; *Stomach Neoplasms/therapy/immunology/drug therapy/mortality/pathology ; *Immune Checkpoint Inhibitors/therapeutic use/pharmacology ; Tumor Microenvironment/drug effects/immunology ; *Immunotherapy/methods ; Combined Modality Therapy ; Drug Resistance, Neoplasm ; *Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; },
abstract = {BACKGROUND: Immunotherapy combined with chemotherapy has become the standard treatment for HER2-negative gastric cancer (GC), but its clinical benefits remain limited, with a median progression-free survival (mPFS) of 6-8 months and median overall survival (mOS) of 15-18 months. These outcomes are particularly poor in patients with CPS < 1. The marked heterogeneity of GC, along with primary and secondary resistance, presents significant clinical challenges and underscores the urgent need for novel therapeutic strategies.

RECENT ADVANCES: To address these limitations, several combination therapies are being explored. Anti-VEGF therapy combined with immune checkpoint inhibitors (ICIs) has shown synergistic effects by enhancing immune cell infiltration and reducing tumor-mediated immunosuppression, thereby improving response rates and survival. Radiotherapy combined with ICIs also holds promise, with low-dose radiation remodeling the tumor microenvironment and high-dose radiation inducing immunogenic cell death. Other potential combinations include PD-1/PD-L1 inhibitors paired with targeted therapies against HER2, FGFR2, DKK1, PARP, LSD1, HDAC, and other emerging targets. Novel approaches such as hyperbaric oxygen therapy, oncolytic viruses, metabolic modulators, and fecal microbiota transplantation are also under investigation to further enhance immune responses.

CONCLUSION: These multimodal strategies represent a promising shift toward personalized, mechanism-driven immunotherapy sensitization. By targeting diverse pathways to overcome immune resistance, they aim to reshape the tumor microenvironment, restore immune responsiveness, and improve outcomes in GC. While many remain in early-stage development, accumulating evidence supports their potential. Future research should prioritize optimizing combination regimens, clarifying resistance mechanisms, and identifying predictive biomarkers through multi-omics and artificial intelligence to enable more precise, individualized immunotherapy.},
}

Humans
*Stomach Neoplasms/therapy/immunology/drug therapy/mortality/pathology
*Immune Checkpoint Inhibitors/therapeutic use/pharmacology
Tumor Microenvironment/drug effects/immunology
*Immunotherapy/methods
Combined Modality Therapy
Drug Resistance, Neoplasm
*Antineoplastic Combined Chemotherapy Protocols/therapeutic use

@article {pmid40685369,
year = {2025},
author = {Rahman, R and Marcolla, CS and Willing, BP},
title = {Fecal microbiota transplantation in pigs: current status and future perspective.},
journal = {Animal microbiome},
volume = {7},
number = {1},
pages = {76},
pmid = {40685369},
issn = {2524-4671},
support = {res0030386//Alberta Livestock and Meat Agency/ ; RGPIN-2019-06336//Natural Sciences and Engineering Research Council of Canada/ ; },
abstract = {Fecal microbiota transplantation (FMT) is gaining attention as a method to modulate the gut microbiome in pigs, with the goal of enhancing health and production outcomes. While some studies indicate that FMT can enhance growth performance and intestinal health in piglets, others report minimal or even negative effects. This variability highlights the need for standardized protocols and further research to optimize FMT for swine applications. Currently, the use of FMT in pigs is still in its early stages, with limited studies showing considerable methodological differences. Although some evidence supports the effectiveness of FMT, significant gaps remain in our understanding of its approach and underlying mechanisms. Therefore, this review summarizes the role and development of gut microbiota in pigs, analyzes existing FMT research in pigs, emphasizes the varying outcomes, illustrates the potential mechanisms of action based on human and animal studies and discusses the innovative potential of using co-evolved microbial communities as a transplant material. As our understanding of pig gut microbiome advances, FMT and related microbiome-based interventions could become valuable tools in pig production. However, ongoing research is essential to elucidate their mechanisms and develop reliable protocols.},
}

@article {pmid40685095,
year = {2025},
author = {Cheng, YY and Lin, CC and Tung, CS and Liu, CC and Liu, YP},
title = {The Effects of Autologous Fecal Microbiota Transplantation on Fear Memory and Anxiety Abnormalities Induced by Single Prolonged Stress -Implication of gut-brain axis regulation.},
journal = {Brain research bulletin},
volume = {},
number = {},
pages = {111472},
doi = {10.1016/j.brainresbull.2025.111472},
pmid = {40685095},
issn = {1873-2747},
abstract = {Increasing evidence suggests that alterations in the gut microbiota play a crucial role in the pathophysiology of psychiatric disorders, including post-traumatic stress disorder (PTSD). This implies that restoring gut microbiota might serve as a therapeutic strategy, with autologous fecal microbiota transplantation (FMT) being the most promising treatment due to its effectiveness and fewer pharmacological side effects. However, the hypothesis that adjusting gut microbiota may help to restore the impairment of fear memory is still less examined. To evaluate this hypothesis, we employed single prolonged stress (SPS) rat model to examine the impact of autologous FMT on PTSD-related fear memory extinction retention deficits and increased anxiety, and to investigate changes in the levels of gut microbiota, central monoamines, and plasma corticosterone. The correlations between gut microbiota and central serotonin (5-HT) with fear extinction retention deficits and anxiety were analyzed. Note that littermates were used in the gut microbiota analysis to minimize individual differences. Our results demonstrated that autologous FMT significantly ameliorated SPS-induced deficits in fear extinction retention and conditioned anxiety but did not mitigate unconditioned anxiety. These improvements were significantly correlated with the restoration of 5-HT levels in the medial prefrontal cortex (mPFC), dorsal hippocampus (dHPC), and hypothalamus (HT). Autologous FMT also reversed SPS-induced reductions in plasma corticosterone level. Additionally, fecal microbiota analysis revealed significant changes at the genus level, with the relative abundance of the Prevotellaceae Ga6A1 group reduced after SPS, and Intestinimonas increased by FMT, as well as some taxa significantly correlated with fear extinction retention deficits. This study suggests that autologous FMT offers potential as a novel therapeutic strategy for PTSD.},
}

@article {pmid40684867,
year = {2025},
author = {Cao, J and Shi, D and Cui, Y and Zhu, H and Liang, H and Wei, Q and Huang, J},
title = {Genistein maintains intestinal homeostasis in colitis mice via activating GPR30-Nrf2 signaling pathway.},
journal = {The Journal of nutritional biochemistry},
volume = {},
number = {},
pages = {110036},
doi = {10.1016/j.jnutbio.2025.110036},
pmid = {40684867},
issn = {1873-4847},
abstract = {Genistein (GEN) is a natural polyphenolic compound widely present in leguminous plants, which has many biological functions such as anti-inflammatory and antioxidant activities, and has attracted attention in the treatment of inflammatory bowel disease (IBD). However, the molecular mechanism underlying the beneficial effects of GEN in IBD remains unclear. Here, we demonstrated that GEN enhanced the relative abundance of beneficial bacteria (e.g., Akkermansia muciniphila) and increased microbiota-derived short-chain fatty acids (SCFAs) levels in colitis mice. Further, the antibiotic cocktails (ABX) and fecal microbiota transplantation (FMT) treatments confirmed that gut microbiota at least partially mediated the anti-colitis effect of GEN. Interestingly, we found that GEN could also activate G protein-coupled receptor 30 (GPR30) and its downstream transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) in intestinal epithelial cells (IECs). The activation of the GPR30-Nrf2 signaling led to reduced reactive oxygen species (ROS) production, which consequently inhibited NLRP3 inflammasome activation and improved intestinal epithelial barrier dysfunction. In addition, studies using GPR30 knockout mice confirmed that GPR30 is crucial for inhibiting NLRP3 inflammasome activation and alleviating colitis. Collectively, our study unveils that GEN is an effective anti-inflammatory nutrient and suggests that both the gut microbiota and the GPR30-Nrf2 signaling pathway represent potential therapeutic targets for treating IBD.},
}

@article {pmid40684508,
year = {2025},
author = {Wu, B and Tian, XY and Ni, WS and Gao, HX and Wang, YW and Zhang, LH and Li, YB and Lv, YL and Song, YN and Yan, YC and Geng, XZ and Li, YM and Yang, HF and Zhao, J},
title = {Acetamiprid mediates cognitive dysfunction through the gut-brain axis: Synaptic damage and immune-mediated blood-brain barrier dysfunction.},
journal = {Journal of hazardous materials},
volume = {496},
number = {},
pages = {139287},
doi = {10.1016/j.jhazmat.2025.139287},
pmid = {40684508},
issn = {1873-3336},
abstract = {Acetamiprid is a widely used neonicotinoid pesticide that can increase the risk of inducing nervous system diseases. Considering the increased exposure to acetamiprid and its impact on cognitive function, further clarification is needed. Therefore, we used a mouse model of drinking water to evaluate the effects of acetamiprid on cognitive dysfunction and the possible underlying mechanisms. Our study revealed that acetamiprid can cause damage to hippocampal and synaptic structures, which in turn leads to a decline in spatial learning and memory abilities in mice. Importantly, acetamiprid exposure altered the composition and diversity of the intestinal flora and induced a systemic immune response in the gutbrain axis. Specifically, acetamiprid exposure damages the gutbrain axis, including structural disorders of the intestinal flora, related neurotransmitters and systemic immune factors. In addition, fecal microbiota transplantation restored the homeostasis of the gut microbiota and reduced the degree of damage to synaptic and spatial learning and memory. Moreover, intestinal barrier function is restored, effectively preventing the entry of harmful substances into intestinal tissue and thereby reducing damage to the bloodbrain barrier and the immune response in the gutbrain. This study provides new insights into potential new mechanisms of acetamidine exposure related to cognitive function.},
}

@article {pmid40684494,
year = {2025},
author = {Tao, Y and Wang, L and Xiong, S and Ding, Y and Nhamdriel, T and Zhang, Y and Zhang, J and Fan, G},
title = {Milk-processed Polygonatum cyrtonema Hua ameliorates cyclophosphamide-induced immunosuppression in mice by regulating gut microbiota and immune response.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {145},
number = {},
pages = {157076},
doi = {10.1016/j.phymed.2025.157076},
pmid = {40684494},
issn = {1618-095X},
abstract = {BACKGROUND: Immune dysfunction is linked to the progression of various diseases. Milk-processed Polygonatum cyrtonema Hua (MPC) is a traditional medicine with nourishing effects in the Qinghai-Tibet Plateau region of China. However, the immune-enhancing effect of MPC and its underlying mechanism remain unclear.

PURPOSE: This study aims to investigate the therapeutic effect and underlying mechanism of MPC on immunosuppressed mice.

STUDY DESIGN: A cyclophosphamide (CY)-induced immunosuppressive mouse model was established to evaluate the effects of MPC on the gut microbiota, intestinal barrier and immune response.

METHODS: The chemical composition of MPC was identified by UPLC-Q-Exactive Orbitrap MS technology. Immune organ weight, body weight, colon length, biochemical parameters, and histopathology were examined. The levels of three short-chain fatty acids (SCFAs) were quantified via HPLC. 16S rRNA sequencing, fecal microbiota transplantation (FMT), antibiotic intervention, and Western blot were applied to explore the mechanism of MPC.

RESULTS: MPC significantly enhanced the production of some key cytokines (IL-2, IFN-γ, IL-4, IL-10, and TGF-β3), immunoglobulins (IgM and IgG), and transcription factors (T-bet, GATA-3, RORγt, and Foxp3). Additionally, MPC maintained intestinal mucosal integrity by upregulating tight junction proteins ZO-1, Claudin-1, E-cadherin, and Occludin. 16S rRNA sequencing of fecal samples revealed that MPC increased the relative abundance of beneficial SCFA-producing bacteria, specifically Lachnospiraceae_UCG-006, while decreasing the relative abundance of several pathogenic taxa, including Prevotellaceae, Alloprevotella, and Eubacterium_coprostanoligenes_group. Notably, antibiotic intervention and FMT experiments demonstrated that the immune-enhancing effect of MPC was dependent on the gut microbiota. MPC also increased the levels of three SCFAs including acetate, propionate, and butyrate. Besides, MPC was found to activate the SCFAs/GPR43/Blimp-1 pathway, leading to the production of IL-10, which enhanced the immune response.

CONCLUSION: This study demonstrates for the first time that MPC has a significant immune-enhancing effect. The mechanisms include restoring the balance of gut microbiota, promoting the production of SCFAs, repairing intestinal mucosal damage and enhancing immune function. These findings support the potential of MPC as a natural agent for improving gut health and systemic immunity.},
}

@article {pmid40684490,
year = {2025},
author = {Chen, YY and Lu, YT and Wang, YD and Ding, NN and Huang, ZX and Hu, JB and Tong, JX and Zhang, YR and Deng, LJ and Luo, X and Hao, WZ and Chen, JX},
title = {Xiaoyaosan improves depression-like behaviours in mice with post-stroke depression by modulating gut microbiota and microbial metabolism and regulating P2X7R/NLRP3 inflammasome.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {145},
number = {},
pages = {157078},
doi = {10.1016/j.phymed.2025.157078},
pmid = {40684490},
issn = {1618-095X},
abstract = {BACKGROUND: Post-stroke depression (PSD) represents the most prevalent complication of stroke and has been reported to be associated with an imbalance in the gut microbiota. Clinically, Xiaoyaosan (XYS) alleviates depressive symptoms in patients with PSD. However, the existing literature does not provide sufficient evidence to ascertain whether XYS can alleviate these symptoms by modulating gut microbiota.

PURPOSE: This study aims to investigate the potential mechanism of XYS to improve depression-like behavior in mice with PSD by regulating intestinal flora and microbial metabolism.

STUDY DESIGN: The authors assessed the effect of XYS on the behaviour of PSD mice and evaluated the effects of XYS on structure and metabolism of gut microbiota, the protein expression levels of P2X7 and NLRP3, and associated inflammatory factors in PSD mice. In addition, by performing faecal microbiota transplantation (FMT) on PSD mice with faecal bacteria treated with XYS, the authors further clarified the relationship between intestinal flora disorder, the onset of PSD, and the intervention effect of XYS.

METHODS: To investigate the ameliorative effect of XYS on behavioural abnormalities and clarify the important role of intestinal flora regulation in the improvement of PSD by XYS in diseased mice, the authors employed various methodologies, including the PSD model, behavioural tests, haematoxylin and eosin staining, ultrastructural morphology, enzyme-linked immunosorbent assay, western blotting, 16S rRNA sequencing, metabolomic analyses, and FMT.

RESULTS: Oral administration of XYS effectively alleviated depression-like behaviours in PSD mice and repaired the damaged colonic mucosa. XYS inhibited inflammatory factors in serum and hippocampus and regulated the protein expression levels of P2X7 and NLRP3 in the colon and hippocampus of PSD mice. Moreover, XYS restored the gut microbiota and modulated intestinal metabolites in PSD mice. It effectively reduced the abundances of microbes including Ligullacoccus, Streptococcus, and Staphylococcus, while significantly increased the abundances of microbes including Faecalibaculum, Allobaculum, and Monolobus. Furthermore, XYS effectively regulated intestinal metabolites such as methylparaben, valproic acid (Depakene), and disulfiram. More importantly, faecal transplants from the PSD models reproduced depression-like behaviours in normal mice, while XYS-FMT effectively alleviated depression-like behaviours in PSD mice.

CONCLUSION: Our findings indicate that XYS improves depression-like behaviours in mice with PSD by modulating the gut microbiota and microbial metabolism, and regulating the P2X7R/NLRP3 inflammasome.},
}

@article {pmid40683544,
year = {2025},
author = {Ran, C and Xu, Y and Wang, Q and Cao, H and Li, D and Wang, Y and Yan, J and Yang, J and Sun, J and Liu, Y and Xia, Y and Zhang, L and Wang, X and Zhang, F},
title = {Gut microbiota from osteoarthritic patients without obesity aggravates osteoarthritis progression in rats by enriching acetic acid.},
journal = {Microbial pathogenesis},
volume = {207},
number = {},
pages = {107911},
doi = {10.1016/j.micpath.2025.107911},
pmid = {40683544},
issn = {1096-1208},
abstract = {OBJECTIVE: Although obesity is recognized as a mechanical driver of osteoarthritis (OA), emerging evidence suggests gut microbiota independently contributes to OA pathogenesis. OA develops even in individuals without obesity, yet the distinct mechanistic roles of gut microbiota in OA progression among hosts with and without obesity remain uncharacterized. OA can develop in individuals without obesity, yet the distinct roles of gut microbiota in OA progression among those with and without obesity remain unclear. This study directly compares how gut microbiota differentially modulates OA development in these two populations.

METHODS: Twenty-five SD rats underwent anterior cruciate ligament transection (ACLT), gut microbiota depletion and fecal microbiota transplantation (FMT) from four types of donors: healthy controls (C), OA patients without obesity (OA), non-OA patients with obesity (OB), and OA patients with obesity (OAB). Five rats in group SAB underwent sham surgery and received FMT from OA patients with obesity. After 8 weeks, joint histopathology, plasma cytokines, fecal Short-chain fatty acids (SCFAs), and microbiota composition were analyzed.

RESULTS: Rats receiving FMT from OA patients without obesity displayed the most severe cartilage degeneration and synovitis, with elevated levels of IL-6/TNF-α and acetic acid. Bacteroides acidifaciens was the dominant microbe in the OA group and correlated with both OA severity and acetic acid levels. In contrast, rats receiving FMT from patients with/without obesity (OB/OAB) exhibited enrichment of propionic acid producers, Lactobacillus and Oscillibacter, which were inversely associated with inflammation. Mechanical stress primarily drove OA in rats with obesity, whereas OA pathology in individuals without obesity was microbiota dependent.

CONCLUSION: Gut microbiota from OA patients without obesity exacerbates disease via B. acidifaciens mediated acetic acid overproduction, while the presence of obesity enriches beneficial taxa that attenuate inflammation. Mechanical load remains pivotal in OA with obesity. Targeting microbiota dysbiosis may offer novel therapeutic avenues, particularly for OA patients without obesity.},
}

@article {pmid40682107,
year = {2025},
author = {Pianka, ML and Werba, A and Zimmermann, S and Vey, JA and Kalkum, E and Tenckoff, S and Tony-Odigie, A and Michalski, CW and Pianka, F},
title = {The role of the MicroBiome in PANCreatic cancer and its precursors- the study protocol of the MiBiPanc systematic review and meta-analysis.},
journal = {Systematic reviews},
volume = {14},
number = {1},
pages = {150},
pmid = {40682107},
issn = {2046-4053},
support = {01KC2310//Bundesministerium für Bildung und Forschung/ ; },
mesh = {Humans ; *Pancreatic Neoplasms/microbiology ; Systematic Reviews as Topic ; *Microbiota ; Meta-Analysis as Topic ; Pancreas/microbiology ; *Gastrointestinal Microbiome ; Pancreatitis, Chronic/microbiology ; *Precancerous Conditions/microbiology ; },
abstract = {BACKGROUND: Pancreatic cancer is the third leading cause of cancer-related death in Northern America and fourth in Europe. Emerging evidence suggests that the pancreatic microbiome may play a significant role in the development and progression of this disease. Although the human microbiota contributes to health by supporting nutritional and hormonal homeostasis, modulating inflammation, detoxifying harmful compounds, and producing beneficial metabolites, several studies have implicated its crucial modulatory role in numerous diseases, including cancer. The main objective of this review is to investigate the specific relationship between the microbiome and pancreatic carcinogenesis.

METHODS: A comprehensive literature search will identify studies examining the microbiome in human samples of saliva, pancreatic fluid, bile, pancreatic tissue, and feces of patients with chronic pancreatitis, precancerous pancreatic lesions, and pancreatic cancer. Studies differentiating bacteria to at least the genus level will be prioritized. Eligible studies include randomized controlled trials and observational studies analyzing the human microbiome in patients with chronic pancreatitis, pancreatic precursor lesions, or pancreatic cancer compared to healthy controls. Studies analyzing nonhuman samples, single bacterial strains, or lacking comparator groups will be excluded. The following databases will be searched without any restrictions to the publication date up until December 2024: the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE (via PubMed), Embase, and Web of Science. Animal studies, case reports, and studies not reporting analyses of human samples are excluded. Details regarding blinding, risk of bias, and funding sources will be extracted and assessed. The main outcomes include the bacterial diversity in each sample type (stool, saliva, bile, intratumoral, and tissue) itemized for each diagnosis, identifying differentially abundant or depleted taxa, and evaluating the correlation of specific bacteria with disease prevention or progression and clinical outcomes. Data extraction will be performed independently by two reviewers. Risk-of-bias assessment will be performed using Cochrane tools appropriate for each study design. Comparisons will be analyzed by descriptive statistics, and meta-analyses will be performed when applicable. The review will be conducted according to the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) guidelines.

DISCUSSION: In summary, this systematic review aims to synthesize studies analyzing microbiome profiles in patients with chronic pancreatitis, precursor lesions, and pancreatic cancer, focusing on identifying bacterial diversity and specific taxa related to disease progression and development of cancer in comparison to healthy controls and will include a thorough critical appraisal of the available literature. Anticipated limitations include heterogeneity in microbiome sampling methods and potential variability in taxonomic resolution across studies.

PROSPERO CRD42023487995.},
}

Humans
*Pancreatic Neoplasms/microbiology
Systematic Reviews as Topic
*Microbiota
Meta-Analysis as Topic
Pancreas/microbiology
*Gastrointestinal Microbiome
Pancreatitis, Chronic/microbiology
*Precancerous Conditions/microbiology

@article {pmid40680146,
year = {2025},
author = {Li, B and Sakaguchi, T and Tani, H and Ito, T and Murakami, M and Okumura, R and Kobayashi, M and Okuzaki, D and Motooka, D and Ikeuchi, H and Ogino, T and Mizushima, T and Hirota, S and Otake-Kasamoto, Y and Kishikawa, T and Nakamura, S and Kobiyama, K and Ishii, KJ and Hashiguchi, T and Kawai, T and Kuroda, E and Shinzaki, S and Ise, W and Kurosaki, T and Kikuchi, A and Tomofuji, Y and Okada, Y and Takeda, K and Kayama, H},
title = {OTUD3 prevents ulcerative colitis by inhibiting microbiota-mediated STING activation.},
journal = {Science immunology},
volume = {10},
number = {109},
pages = {eadm6843},
doi = {10.1126/sciimmunol.adm6843},
pmid = {40680146},
issn = {2470-9468},
mesh = {Animals ; *Colitis, Ulcerative/immunology/microbiology/prevention & control/genetics/pathology ; Mice ; Humans ; *Membrane Proteins/metabolism/immunology ; *Gastrointestinal Microbiome/immunology ; Mice, Inbred C57BL ; Fibroblasts/metabolism/immunology ; Male ; Female ; Nucleotides, Cyclic/metabolism ; Mice, Knockout ; },
abstract = {Ulcerative colitis (UC) develops through a complicated interaction between the host and microbiota. Intestinal fibroblasts are believed to play crucial roles in the pathogenesis of UC, but the influence of the host-microbiota interaction on the pathophysiology of intestinal fibroblasts remains poorly understood. Here, we demonstrate that OTU deubiquitinase 3 (OTUD3) suppresses pathologic activation of fibroblasts exposed to microbial cyclic GMP-AMP (3'3'-cGAMP) in the colon by deubiquitinating stimulator of interferon genes (STING). Mice harboring a UC risk missense variant in the Otud3 gene showed pathological features of UC in the colon after transplantation of a fecal microbiota with the potential to produce excessive cGAMP from patients with UC. Collectively, these results highlight a mechanism of the interaction between OTUD3 in host fibroblasts and STING-activating microbiota in UC development.},
}

Animals
*Colitis, Ulcerative/immunology/microbiology/prevention & control/genetics/pathology
Mice
Humans
*Membrane Proteins/metabolism/immunology
*Gastrointestinal Microbiome/immunology
Mice, Inbred C57BL
Fibroblasts/metabolism/immunology
Male
Female
Nucleotides, Cyclic/metabolism
Mice, Knockout

@article {pmid40679776,
year = {2025},
author = {Clarke, H and Peer, M and Miles, S and Fitzcharles, MA},
title = {Managing Pain in Fibromyalgia: Current and Future Options.},
journal = {Drugs},
volume = {},
number = {},
pages = {},
pmid = {40679776},
issn = {1179-1950},
abstract = {Pain relief is a key element of fibromyalgia (FM) treatment. Current guidelines recommend antidepressant (i.e. serotonin-norepinephrine reuptake inhibitors) and anticonvulsant medications (gabapentin/pregabalin), drugs that provide only modest relief, with limitations primarily driven by side effects. In contrast, traditional analgesic drugs, although not sufficiently tested in FM, are commonly used by patients. This dearth of effective treatments has led to isolated, mostly small studies of less familiar drug treatments for FM-related pain. Although no single drug has emerged with appreciable effect, some agents such as cannabinoids and naltrexone, amongst others, have shown some pain modulatory effects. In the absence of drugs in the pipeline, non-pharmacological interventions such as behavioural interventions, neuromodulation techniques and faecal transplantation have been studied. This narrative review will focus on drugs and interventions that have been examined in recent years to modulate pain in FM.},
}

@article {pmid40679382,
year = {2025},
author = {},
title = {Correction to: Clostridioides difficile: Treating Sustained Antibiotic Responders With Fecal Microbiota Transplantation Does Not Improve Efficacy.},
journal = {Clinical infectious diseases : an official publication of the Infectious Diseases Society of America},
volume = {},
number = {},
pages = {},
doi = {10.1093/cid/ciaf381},
pmid = {40679382},
issn = {1537-6591},
}

@article {pmid40679068,
year = {2025},
author = {Zhao, X and Cai, Y and Hou, Y and Wu, Y and Wei, T and Li, L and Duan, Z and Lu, X and Meng, J and Zhou, H and Wang, Q and Wang, J and Xu, C and Du, L and Fan, S and Wang, F and Liu, Q and Liu, Y},
title = {Commensal Viruses Promote Intestinal Stem Cell Regeneration Following Radiation Damage by Inhibiting Hyperactivation of RIG-I and Notch Signals.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e05204},
doi = {10.1002/advs.202505204},
pmid = {40679068},
issn = {2198-3844},
support = {82072331//National Natural Science Foundation of China/ ; 2022-I2M-2-003//CAMS Innovation Fund for Medical Sciences/ ; 2021-I2M-1-042//CAMS Innovation Fund for Medical Sciences/ ; 2023-I2M-2-008//CAMS Innovation Fund for Medical Sciences/ ; 23JCZDJC00270//Natural Science Foundation of Tianjin City/ ; },
abstract = {Radiation-induced intestinal injury is a common complication of abdominopelvic cancer radiotherapy, often associated with gut bacteriome dysbiosis. However, the involvement of gut virome in this process remains largely underexplored. Here, it was found that radiation disrupted the gut virome, altered the distribution of phages and their bacterial host. Fecal virome transplantation (FVT) from healthy donors ameliorated radiation-induced intestinal damage and promoted stem cell proliferation by enriching phages targeting Salmonella. Conversely, decreased virome load exacerbated intestinal damage, reduced proliferating stem cells, and impaired secretory lineage differentiation. Mechanistically, exacerbated intestinal injury was associated with hyperactivation of RIG-I and Notch signaling in intestinal stem cells, which was absent in RIG-I-deficient mice. Organoids from RIG-I-deficient mice displayed decreased Notch signals and increased regenerative capacity post radiation. These findings shed light on the intricate interplay between gut virome, intestinal injury, and stem cell responses, highlighting potential therapeutic interventions for targeting the virome to mitigate radiation-induced intestinal damage.},
}

@article {pmid40678181,
year = {2025},
author = {Zhao, M and Zhang, L and Liu, Z},
title = {Gut microbiota-mediated pain sensitization: mechanisms and therapeutic implications.},
journal = {Frontiers in pain research (Lausanne, Switzerland)},
volume = {6},
number = {},
pages = {1626515},
pmid = {40678181},
issn = {2673-561X},
abstract = {Emerging evidence has illuminated the pivotal role of gut microbiota in modulating pain sensitivity through bidirectional gut-brain interactions. Current research demonstrates that gut microbial communities significantly influence pain perception by regulating both central and peripheral sensitization mechanisms across various pain modalities. This review synthesizes current knowledge on the mechanisms underlying gut microbiota-mediated pain sensitization, encompassing: (1) cross-talk within the microbiome-gut-brain axis, (2) regulatory effects of microbial metabolites on central and peripheral sensitization pathways, and (3) bioactive compounds derived from gut microbiota that participate in pain modulation. Furthermore, we systematically evaluate the therapeutic potential of microbiota-targeted interventions including probiotic supplementation, fecal microbiota transplantation, and dietary modifications in pain management. To advance this promising field, future investigations should prioritize three key directions: establishing causal relationships through rigorous verification, accelerating clinical translation of preclinical findings, and developing personalized microbial-based therapeutic strategies.},
}

@article {pmid40676635,
year = {2025},
author = {Shtossel, O and Eshel, A and Fried, S and Geva, M and Danylesko, I and Yerushalmi, R and Shem-Tov, N and Fein, JA and Fabbrini, M and Shimoni, A and Turjeman, S and Louzoun, Y and Nagler, A and Koren, O and Shouval, R},
title = {Microbiome-based prediction of allogeneic hematopoietic stem cell transplantation outcome.},
journal = {Genome medicine},
volume = {17},
number = {1},
pages = {80},
pmid = {40676635},
issn = {1756-994X},
support = {P30 CA008748/CA/NCI NIH HHS/United States ; K08CA282987//NIH-NCI K-award/ ; },
mesh = {Humans ; *Hematopoietic Stem Cell Transplantation/adverse effects ; Graft vs Host Disease/etiology ; Male ; Female ; Adult ; Middle Aged ; Transplantation, Homologous ; Saliva/microbiology ; Feces/microbiology ; Treatment Outcome ; *Gastrointestinal Microbiome ; *Microbiota ; Young Adult ; Aged ; Adolescent ; },
abstract = {BACKGROUND: Allogeneic hematopoietic stem cell transplantation (HSCT) is potentially curative for hematologic malignancies but is frequently complicated by relapse and immune-mediated complications, such as graft-versus-host disease (GVHD). Emerging evidence suggests a role for the intestinal and oral microbiome in modulating HSCT outcomes, yet predictive models incorporating microbiome data remain limited.

METHODS: We applied the RATIO (suRvival Analysis lefT barrIer lOss) model to longitudinal stool and saliva microbiome data from 204 adult HSCT recipients to predict the timing of seven outcomes: overall survival (OS), non-relapse mortality (NRM), relapse, acute GVHD (grades II-IV and III-IV), chronic GVHD, and oral chronic GVHD. A total of 514 stool and 1291 saliva samples were collected over 70 weeks post-HSCT. Model performance was evaluated using the concordance index (CI) and Spearman correlation coefficient (SCC), with SHAP (SHapley Additive exPlanations) analysis used for model interpretability.

RESULTS: Oral and stool microbial dysbiosis peaked within the first 2 weeks post-HSCT, followed by partial recovery. Using the RATIO model, we found that microbiome features from early time points (weeks 1-2) were most predictive of short-term complications such as acute GVHD, while later samples (weeks 36-70) were more informative for long-term outcomes, including overall survival. RATIO outperformed traditional survival models (Cox and Random Survival Forest) across most outcomes (median CI > 0.65), with stool microbiota showing greater predictive power than saliva. SHAP analysis identified specific stool genera, including Collinsella and Eggerthella, associated with shorter time to various complications. External validation using a pediatric GVHD cohort confirmed the model's generalizability and reproducibility. External validation using a pediatric HSCT cohort (n = 90) confirmed the reproducibility and generalizability of these microbiome-based predictions.

CONCLUSIONS: Microbiome profiling of stool and saliva samples offers robust, time-sensitive prediction of post-HSCT complications. The RATIO model enables interpretable, time-to-event prediction across multiple outcomes and may inform microbiome-guided interventions to improve transplant success.},
}

Humans
*Hematopoietic Stem Cell Transplantation/adverse effects
Graft vs Host Disease/etiology
Male
Female
Adult
Middle Aged
Transplantation, Homologous
Saliva/microbiology
Feces/microbiology
Treatment Outcome
*Gastrointestinal Microbiome
*Microbiota
Young Adult
Aged
Adolescent

@article {pmid40676526,
year = {2025},
author = {Nabil, Y and Helal, MM and Qutob, IA and Dawoud, AIA and Allam, S and Haddad, R and Manasrah, GM and AlEdani, EM and Sleibi, W and Faris, A and Hassan, AK and Nandwana, V},
title = {Efficacy and safety of fecal microbiota transplantation in the management of parkinson's disease: a systematic review.},
journal = {BMC neurology},
volume = {25},
number = {1},
pages = {291},
pmid = {40676526},
issn = {1471-2377},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods/adverse effects ; *Parkinson Disease/therapy ; Randomized Controlled Trials as Topic ; Treatment Outcome ; Gastrointestinal Microbiome ; },
abstract = {BACKGROUND: Parkinson's disease (PD) involves progressive neurodegeneration with motor and non-motor symptoms. Gut microbiota alterations are implicated in PD pathogenesis, leading to interest in fecal microbiota transplantation (FMT) as a therapeutic option. This systematic review assesses the efficacy and safety of FMT in managing PD symptoms.

METHODS: We conducted a comprehensive search across PubMed, Scopus, Web of Science, and Cochrane Central Controlled trials databases. Studies were screened based on predetermined inclusion criteria, focusing on randomized controlled trials (RCTs) involving FMT in PD patients. Two reviewers independently performed the data extraction and quality assessment. Key outcomes included improvements in motor and non-motor symptoms, quality of life, and adverse effects.

RESULTS: Five RCTs involving 157 patients met the inclusion criteria. Some studies reported improvements in motor and non-motor symptoms, particularly with colonic FMT, while others found no significant benefit. One trial observed motor function worsening. FMT was generally well-tolerated, with mild and transient gastrointestinal side effects.

CONCLUSION: FMT may relieve PD symptoms, but findings are inconsistent. Larger trials with standardized protocols are needed to determine its long-term efficacy and safety.},
}

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

@article {pmid40675025,
year = {2025},
author = {Cheraghi, M and Nazari, A and Souri, F},
title = {Gut microbiota and cardiac arrhythmogenesis: Unveiling the gut-heart axis.},
journal = {Pathology, research and practice},
volume = {273},
number = {},
pages = {156125},
doi = {10.1016/j.prp.2025.156125},
pmid = {40675025},
issn = {1618-0631},
abstract = {BACKGROUND: Cardiac arrhythmias, a leading cause of morbidity and mortality, have traditionally been linked to structural heart disease and genetic factors. However, growing evidence indicates that the gut microbiota, via its interactions with the cardiovascular system, may also contribute to arrhythmogenesis. The gut-heart axis, involving microbial metabolites, inflammatory signaling, and neural modulation, has emerged as a key regulator of cardiac electrophysiology.

METHODS: This review summarizes recent preclinical and clinical studies investigating the role of gut microbiota in the pathophysiology of cardiac arrhythmias. We examine mechanisms through which microbial products like short-chain fatty acids (SCFAs), trimethylamine N-oxide (TMAO), and bile acids influence arrhythmic risk, with a focus on their effects on ion channels, inflammation, and autonomic regulation.

RESULTS: Evidence from both animal models and human studies indicates that dysbiosis, or imbalance in the gut microbiome, is associated with an increased risk of arrhythmias, including atrial fibrillation and ventricular tachycardia. Microbial metabolites have been shown to influence cardiac electrophysiology through direct and indirect mechanisms, including immune modulation and autonomic nervous system regulation. Furthermore, microbiome-based interventions, such as dietary changes, probiotics, and fecal microbiota transplantation, show promise in reducing arrhythmic burden.

CONCLUSION: The gut microbiota's metabolic, inflammatory, and neural connections with the cardiovascular system increasingly suggest its role in arrhythmia risk. Targeting this gut-heart axis could lead to personalized arrhythmia prevention and treatment strategies.},
}

@article {pmid40673781,
year = {2025},
author = {You, MY and Tang, TWH and Novita, S and Liu, YW and Chang, KC and Wu, YW and Chao, YK and Ruan, SC and Lin, PJ and Chen, HC and Hsieh, PCH},
title = {Young microbiome transplantation enhances recovery after myocardial infarction.},
journal = {Aging},
volume = {17},
number = {},
pages = {},
doi = {10.18632/aging.206279},
pmid = {40673781},
issn = {1945-4589},
abstract = {BACKGROUND: The relationship between aging, gut microbiota, and cardiac repair after myocardial infarction (MI) remains unclear. Understanding this interaction may provide novel strategies for improving cardiovascular outcomes in the elderly.

METHODS: Aged mice were treated with antibiotics followed by fecal microbiota transplantation (FMT) from young or aged donors prior to MI. Cardiac function, gut integrity, immune signaling, and metabolism were evaluated. Gut microbiota and plasma metabolites were also profiled in ST-elevation myocardial infarction (STEMI) patients across age groups.

RESULTS: Young FMT improved post-MI cardiac function and reduced infarct size in aged mice. It preserved intestinal barrier integrity, reduced IL-17A-positive immune cells, and attenuated age-related intestinal shortening. Aging was associated with decreased microbial diversity, loss of beneficial taxa such as Akkermansia, and enrichment of inflammatory pathways. Cardiac metabolomics revealed reduced oxidative metabolism and increased lipid reliance in aged mice. In STEMI patients, aging correlated with lower microbiota diversity, altered taxonomic profiles, and shifts in lipid and amino acid metabolism.

CONCLUSIONS: This study highlights the role of gut microbiota in cardiovascular health and aging. Microbiota transplantation improved cardiac recovery, suggesting its therapeutic potential and offering new insights into the gut-heart axis for future treatments in age-related cardiovascular disease.},
}

@article {pmid40673140,
year = {2025},
author = {Zhao, X and Xue, C and Wang, Y and Liu, X and Li, R and Yi, X},
title = {The potential of olfaction loss to induce cognitive impairment and anxiety behavior in mice via the microbiota-gut-brain axis.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1595742},
pmid = {40673140},
issn = {1664-302X},
abstract = {INTRODUCTION: Olfactory dysfunction and cognition decline are frequently observed; however, very little is known about whether olfactory disorders trigger cognitive impairment.

METHODS: Here, we induced olfactory loss in mice and investigated whether and how olfactory loss induces cognitive impairment and anxiety behavior.

RESULTS: Olfactory loss not only causes a significant decrease in food intake and body weight and an increase in O2 consumption but also induces cognitive impairment and anxiety behavior. Olfactory loss-induced alteration of the gut microbiota is associated with subsequent changes in cecal short-chain fatty acids and serum neurotransmitter levels. Hippocampus proteome and fecal microbial transplantation provide further support for the mechanisms by which olfactory loss triggers cognitive impairment and anxiety behavior via the microbiota-gut-brain axis.

DISCUSSION: Our study is expected to provide some evidence for olfactory dysfunction in triggering cognitive impairment through the microbiota-gut-brain axis.},
}