@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.},
}

@article {pmid40672832,
year = {2025},
author = {Mei, H and Bao, P and Wang, Y and Wei, Z and Yang, Q and Chen, C and Sun, Y and Su, X and Kang, J and Li, W},
title = {Pulmonary cryptococcosis in the setting of immunosuppression by methylprednisolone monotherapy for oral pemphigus: a case report and literature review.},
journal = {Frontiers in medicine},
volume = {12},
number = {},
pages = {1569949},
pmid = {40672832},
issn = {2296-858X},
abstract = {Cryptococcosis is an opportunistic and potentially fatal fungal infectious disease. Pemphigus diseases are characterized by blistering of the cutaneous and mucous membranes. We report a case of pulmonary cryptococcosis (PC) following methylprednisolone treatment for pemphigus vulgaris. Additionally, we analyzed a case series of PC infections recorded in PUBMED from 2013 to 2023. A total of 229 cases of PC were included. The median age was 54 years, with 66.4% of patients being male. Those with previous use of corticosteroids or immunosuppressives accounted for 38.4% of cases. Underlying conditions included solid organ transplantations (25.7%), respiratory diseases (6.6%), malignant tumors (6.1%), rheumatoid arthritis (5.7%), hematological malignancies (4.4%), among others. The main source of infection was exposure to birds, poultry, and their feces (12.7%). Cryptococcus neoformans was most frequently isolated (76.4%). Overall mortality was 14.8%. Previous use of corticosteroids or immunosuppressants was a risk factor for disseminated cryptococcus (p < 0.05). Age, underlying disease, dissemination, and no antifungal therapy were independently associated with increased mortality (p < 0.05). Co-occurrence of pemphigus and PC is rare. Prompt diagnosis and appropriate treatment of PC are essential to prevent fatal consequences. Corticosteroids or immunosuppressive therapy are associated with the development of disseminated cryptococcal infection. Age, underlying disease, and dissemination are related to increased mortality. Timely antifungal therapy can improve prognosis.},
}

@article {pmid40671981,
year = {2025},
author = {Ruiz, NI and Herrera Giron, CG and Arragan Lezama, CA and Frias Redroban, SJ and Ventura Herrera, MO and Sanic Coj, GA},
title = {Timing and Protocols for Microbiome Intervention in Surgical Patients: A Literature Review of Current Evidence.},
journal = {Cureus},
volume = {17},
number = {6},
pages = {e86104},
pmid = {40671981},
issn = {2168-8184},
abstract = {Managing the gut microbiome with a personalized approach can significantly improve surgical outcomes, leading to reduced risk of infections, improved immune function, faster recovery and healing, and decreased risk of postoperative complications. This review explores microbiome-based interventions, such as probiotics, prebiotics, synbiotics, and fecal microbiota transplantation, and their roles in perioperative, preoperative, and postoperative care. Electronic databases, such as PubMed, ScienceDirect, and Google Scholar, were searched using topic-related keywords and MeSH terms. The literature search was limited to English-language peer-reviewed articles within the last 10 years, but the majority of the literature was from the last five years. Microbiome interventions have been associated with reduced postoperative complications and enhanced recovery times. The study found that changing the gut microbiome in specific ways, like using probiotics and synbiotics before and after surgery, can lead to better surgical results. For example, these treatments can lower the risk of infection at the surgery site by 40%-80% compared to standard care, help patients recover their bowel function one to two days faster, and reduce hospital stays by up to 30%. They also decrease levels of important inflammation markers like IL-6 and CRP. Using probiotics and synbiotics before surgery and continuing them for two weeks can lower infection rates and enhance recovery while managing inflammation. The beneficial effects of probiotics, prebiotics, and synbiotics support their use as effective strategies in perioperative care. However, people react differently to probiotics, prebiotics, and synbiotics because of factors like genetics, age, hormonal differences between sexes, and variations in gut microbiota based on race. Future research should focus on developing personalized microbiome-based interventions and establishing standardized protocols tailored to individual patient characteristics to enhance their effectiveness.},
}

@article {pmid40671646,
year = {2025},
author = {Yang, T and Maki, KA and Marques, FZ and Cai, J and Joe, B and Pepine, CJ and Pluznick, JL and Meyer, KA and Kirabo, A and Bennett, BJ and , },
title = {Hypertension and the Gut Microbiome: A Science Advisory From the American Heart Association.},
journal = {Hypertension (Dallas, Tex. : 1979)},
volume = {},
number = {},
pages = {},
doi = {10.1161/HYP.0000000000000247},
pmid = {40671646},
issn = {1524-4563},
abstract = {Although substantial advancements have been made in hypertension research, translation of this research into new pharmacotherapies remains challenging. The need for new therapies is imperative: 15% to 20% of patients with hypertension have treatment-resistant hypertension, which often persists despite aggressive clinical treatments consisting of ≥3 medication classes, including a diuretic. Numerous preclinical studies have demonstrated that alterations in the gut microbiome affect blood pressure, suggesting an important role for this nonconventional cardiovascular risk factor. This innovative association suggests a novel therapeutic opportunity for hypertension: modifying the gut microbiome to control hypertension. In line with this hypothesis, clinical trials have been launched to examine whether hypertension can be managed by targeting the gut microbiome. This American Heart Association Science Advisory aims to outline clinical evidence, raise awareness among the health care community about the importance of the gut microbiome in patients with hypertension, update existing knowledge, identify research gaps, and ultimately facilitate the rapid translation of findings into clinical trials and practice.},
}

@article {pmid40671079,
year = {2025},
author = {Zhong, HJ and Pan, ZY and Wei, YF and Yu, Q and Wu, L and Wei, H and He, XX},
title = {Tongue-coating microbiota as a predictive biomarker of washed microbiota transplantation efficacy in pediatric autism: integration with clinical features.},
journal = {Journal of translational medicine},
volume = {23},
number = {1},
pages = {799},
pmid = {40671079},
issn = {1479-5876},
support = {2022B1111070006//Key-Area Research and Development Program of Guangdong Province/ ; JCYJ20240813140519025//Shenzhen Science and Technology Program/ ; 82201339//National Natural Science Foundation of China Youth Science Fund Project/ ; },
mesh = {Humans ; Animals ; Child ; Biomarkers/metabolism ; Female ; *Fecal Microbiota Transplantation ; *Tongue/microbiology ; Male ; Treatment Outcome ; *Microbiota ; Gastrointestinal Microbiome ; Mice ; Child, Preschool ; *Autistic Disorder/therapy/microbiology ; *Autism Spectrum Disorder/therapy/microbiology ; Feces/microbiology ; },
abstract = {BACKGROUND: Alterations in both oral and gut microbiota have been identified in children with autism spectrum disorder (ASD), but the interaction between these microbiota and their potential to predict outcomes of fecal microbiota transplantation (FMT) remain poorly understood.

METHODS: This study investigated the structure and function of the tongue-coating microbiota in children with ASD and explored its correlation with ASD symptoms and gut microbiota. Germ-free ASD mice, colonized with healthy gut microbiota, and children with ASD treated with washed microbiota transplantation (WMT) were assessed for changes in autism symptoms and microbiota composition. Predictive models were also developed based on pre-treatment tongue-coating microbiota and clinical features to forecast WMT outcomes.

RESULTS: Significant alterations were detected in the tongue-coating microbiota of children with ASD, with several bacterial species showing associations with ASD symptoms and gut microbiota composition. Following WMT, both mice and children exhibited substantial improvements in autism-related behaviors, alongside marked shifts in their gut and tongue-coating microbiota. A significant decrease in Haemophilus in the tongue-coating microbiota, which positively correlated with ASD severity, was observed. Additionally, a reduction in chemoheterotrophic and fermentation functions in the tongue-coating microbiota was identified. Predictive models utilizing pre-treatment tongue-coating microbiota and clinical data demonstrated comparable accuracy to those based on gut microbiota for forecasting WMT outcomes.

CONCLUSIONS: These findings highlight a significant interaction between gut and tongue-coating microbiota in ASD, which may play a pivotal role in treatment outcomes. Predictive models integrating pre-treatment microbiota and clinical features could improve precision treatment strategies for children with ASD undergoing WMT.},
}

Humans
Animals
Child
Biomarkers/metabolism
Female
*Fecal Microbiota Transplantation
*Tongue/microbiology
Male
Treatment Outcome
*Microbiota
Gastrointestinal Microbiome
Mice
Child, Preschool
*Autistic Disorder/therapy/microbiology
*Autism Spectrum Disorder/therapy/microbiology
Feces/microbiology

@article {pmid40671002,
year = {2025},
author = {Liu, H and Wei, Y and Jiang, P and Fan, S and Zhao, Y and Li, Z and Wang, S and Zhang, N and Zhi, J and Wei, Q and Gu, Y and Yang, B and Feng, N and Wu, Y and Liu, F},
title = {Navigating the decision landscape: understanding interstitial cystitis/bladder pain syndrome patients' motivations and medical support needs for fecal microbiota transplantation: a qualitative research.},
journal = {BMC complementary medicine and therapies},
volume = {25},
number = {1},
pages = {268},
pmid = {40671002},
issn = {2662-7671},
support = {No. LY22H160011//Zhejiang Provincial Natural Science Foundation of China/ ; LXR22H160001//Zhejiang Provincial Natural Science Foundation of China/ ; 2021YFA1301100, 2021YFA1301101//the National Key Research and Development Program of China/ ; No. 81874142, 82073041//National Natural Science Foundation of China/ ; },
mesh = {Humans ; Female ; Male ; Middle Aged ; *Cystitis, Interstitial/therapy/psychology ; *Fecal Microbiota Transplantation/psychology ; Qualitative Research ; Adult ; *Decision Making ; Aged ; *Motivation ; },
abstract = {BACKGROUND: Interstitial cystitis/bladder pain syndrome (IC/BPS) patients often confront limited treatment options, leading them to contemplate fecal microbiota transplantation (FMT) as an alternative therapy. Recognizing the factors influencing their decision-making process and their medical support needs is imperative. This study aimed to investigate the determinants of decision-making and the medical support requirements of IC/BPS patients considering FMT as an alternative treatment.

METHODS: Semi-structured interviews were conducted with 18 IC patients to explore their motivations for choosing FMT and their decision-making prerequisites. Data analysis was conducted using a thematic approach.

RESULTS: Two overarching themes and seven subthemes were identified. (1) Reasons for choosing FMT. ① Awareness of the complexity and intractability of the disease: Patients exhibited a profound understanding of IC's intricacy and intractability, which ignited their interest in FMT; ② Current treatment dissatisfaction boosted interest in FMT: Discontent with conventional treatments significantly impelled patients to consider FMT; ③ FMT is perceived as a side-effect-free holistic regulatory therapy; ④ Severe negative emotions drive patients to choose FMT: Strong emotions, such as anxiety and desperation, were motivating factors for patients choosing FMT. (2) Professional assistance required when choosing FMT. ① Access to Information Sources: Patients expressed a strong need for comprehensive information resources to aid their decision-making; ② Patients want to learn about peers' treatment experiences and outcomes: Patients sought insights from individuals who had undergone FMT; ③ Patients want more opportunities for communication with healthcare providers: enhanced communication channels with healthcare professionals were desired.

CONCLUSIONS: These findings emphasize the significance of addressing the intricate informational and emotional needs of IC/BPS patients when considering FMT as a treatment option. Tailored information delivery and peer support can facilitate informed decision-making within the context of FMT for IC/BPS.

TRIAL REGISTRATION: The trial registration number, CHiCTR2100048970, was registered on July 19, 2021.},
}

Humans
Female
Male
Middle Aged
*Cystitis, Interstitial/therapy/psychology
*Fecal Microbiota Transplantation/psychology
Qualitative Research
Adult
*Decision Making
Aged
*Motivation

@article {pmid40670809,
year = {2025},
author = {Talat, A and Zuberi, A and Khan, AU},
title = {Unravelling the Gut-Microbiome-Brain Axis: Implications for Infant Neurodevelopment and Future Therapeutics.},
journal = {Current microbiology},
volume = {82},
number = {9},
pages = {390},
pmid = {40670809},
issn = {1432-0991},
support = {BT/PR40148/BTIS/137/20/2021//Department of Biotechnology, Ministry of Science and Technology, India/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Brain/growth & development/physiology ; Infant ; *Neurodevelopmental Disorders/therapy/microbiology ; Dysbiosis ; Probiotics ; Infant, Newborn ; Animals ; },
abstract = {The microbiome-gut-brain axis signifies the intricate interplay between gut microbiome and brain, facilitated by bidirectional communication channels. The brain modulates gut function through the hypothalamic-pituitary-adrenal axis and the autonomic nervous system, while the gut influences central nervous system (CNS) function through microbial metabolites, neurotransmitters, and gut hormones. Early brain development in infants is shaped by mother to neonate microbiome transmission, mode of birth, gestational length, breastfeeding, maternal and infant antibiotic exposure, and acquired infections. Dysbiosis in the gut microbiome is associated with various neurodevelopmental disorders in children such as attention-deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). In this review, we elucidate the pivotal role of the microbiome-gut brain axis in a child's neural development, exploring factors modulating this intricate interaction. Furthermore, we discuss the potential future therapeutic avenues that can support optimal neurodevelopment, such as probiotics, prebiotics, synbiotics, postbiotics, CRISPR/Cas9, fecal microbiota transplant, and phage therapy.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Brain/growth & development/physiology
Infant
*Neurodevelopmental Disorders/therapy/microbiology
Dysbiosis
Probiotics
Infant, Newborn
Animals

@article {pmid40669701,
year = {2025},
author = {Jeong, SH and Vasavada, SP and Lashner, B and Werneburg, GT},
title = {Reply to Editorial Comment on "Fecal Microbiota Transplant Is Associated With Resolution of Recurrent Urinary Tract Infection".},
journal = {Urology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.urology.2025.07.006},
pmid = {40669701},
issn = {1527-9995},
}

@article {pmid40667879,
year = {2025},
author = {Li, X and Wu, X and Zang, W and Zhou, Z and Cui, W and Chen, Y and Yang, H},
title = {Dietary iron attenuates Clostridioides difficile infection via modulation of intestinal immune response and gut microbiota.},
journal = {Virulence},
volume = {16},
number = {1},
pages = {2529454},
pmid = {40667879},
issn = {2150-5608},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; Mice ; *Clostridioides difficile/drug effects/pathogenicity/immunology ; *Clostridium Infections/immunology/microbiology/prevention & control ; *Iron, Dietary/administration & dosage/pharmacology ; Disease Models, Animal ; Mice, Inbred C57BL ; Fecal Microbiota Transplantation ; RNA, Ribosomal, 16S/genetics ; *Intestines/immunology/microbiology/drug effects ; Escherichia coli ; Male ; },
abstract = {Clostridioides difficile (C. difficile) is one of the majors causes of antibiotic-associated diarrhea globally. Host vulnerability to C. difficile infection (CDI) is largely affected by gut microbiota, which in turn is influenced by diet. However, the mechanism underlying the interplay between diet and the gut microbiota that regulates host susceptibility to CDI remains unclear. This study aimed to investigate how a high-iron diet affects the intestinal immune response, microbiota, and metabolism in mice infected with C. difficile. We explored the specific role of the unique gut microbiota and metabolites on CDI. A mouse model of CDI was constructed with or without high dietary iron treatment. The effect of high iron levels on gut microbiota was analyzed by 16S rRNA gene sequencing, and the role of gut microbiota was confirmed by fecal microbiota transplantation (FMT). High dietary iron (400 mg/kg ferrous sulfate) alleviated CDI by decreasing C. difficile pathogenicity and altering host intestinal neutrophil recruitment. Furthermore, E. coli AVS0501, enriched in the gut microbiota of iron-treated CDI mice, showed prophylactic and therapeutic effects on CDI. Moreover, the production of L-proline and tauroursodeoxycholic acid (TUDCA) in CDI mice treated with high dietary iron influenced C. difficile colonization, toxin production, and in turn, regulates the intestinal neutrophil response. Thus, high dietary iron alleviates C. difficile induced enteritis by regulating gut microbiota maintaining gut homeostasis, suggesting that high dietary iron may be an important determinant of disease control.},
}

Animals
*Gastrointestinal Microbiome/drug effects
Mice
*Clostridioides difficile/drug effects/pathogenicity/immunology
*Clostridium Infections/immunology/microbiology/prevention & control
*Iron, Dietary/administration & dosage/pharmacology
Disease Models, Animal
Mice, Inbred C57BL
Fecal Microbiota Transplantation
RNA, Ribosomal, 16S/genetics
*Intestines/immunology/microbiology/drug effects
Escherichia coli
Male

@article {pmid40666732,
year = {2025},
author = {Cantas, L and Goll, R and Fenton, CG and Paulssen, RH and Sørum, H},
title = {Impact of fecal microbiota transplantation in dogs.},
journal = {Frontiers in veterinary science},
volume = {12},
number = {},
pages = {1505226},
pmid = {40666732},
issn = {2297-1769},
abstract = {BACKGROUND: The digestive tract hosts a variety of microorganisms. These microorganisms "micro-organs" play multiple crucial roles in physiological, immunological, and metabolic processes in the body. The manipulation and transplantation of "micro-organs" have lately gained increasing interest in human medicine with promising clinical outcomes, whereas much less is known in veterinary practice.

OBJECTIVES: The goals of this pilot study were to evaluate the safety and impact of Fecal Microbiota Transplantation (FMT) for dogs suffering from non-infectious digestive disorders.

ANIMALS: Seven client-owned adult dogs with idiopathic persistent diarrhea (>3 weeks) and very poor skin-coat conditions received the intervention (FMT) and were evaluated in a private veterinary clinic.

METHODS: Transplants have been taken from healthy donors and were administered rectally to recipients. Objective clinical examinations with analyses of blood and feces samples on day 0 (pre-FMT) and days 14-28 (post-FMT) were performed. Besides the conventional blood hematology and biochemistry analyses, 16S rRNA sequencing analysis was used in fecal samples.

RESULTS: No FMT-related complications occurred. Five of seven (71%) patients demonstrated improved fecal parameters associated with better overall clinical outcome, whereas four of the five (80%) recovered recipients showed molecular correlation with the donor gut microbiota after rectal FMT. There were insignificant changes shown for the conventionally analyzed blood samples. The serum cobalamin levels showed a tendency to increase in recovered recipients.

CONCLUSION: FMT was easy to apply and displayed certain health benefits in this study. Our findings reveal the important role of a "re-gained" gut microbiome balance in the overall health of dogs. Further research is needed to identify the dynamics and interplay between the different bacterial phyla that may have an impact on the stimuli of host immunologic and metabolic responses.},
}

@article {pmid40664314,
year = {2025},
author = {Li, Y and Zhang, S and Li, C and Shen, J and Cao, P and Sun, Y and Ma, X and An, B},
title = {Prebiotics chronotherapy alleviates depression-like behaviors in FMT mice through enhancing short-chain fatty acids receptors and intestinal barrier.},
journal = {Journal of affective disorders},
volume = {},
number = {},
pages = {119885},
doi = {10.1016/j.jad.2025.119885},
pmid = {40664314},
issn = {1573-2517},
abstract = {BACKGROUND: Prebiotics interventions to restore microbiome homeostasis may have long-lasting benefits for mental health especially in adolescence. However, the anti-depressants of prebiotics, particularly in prebiotics chronotherapy, orchestrated remain unknown. We aimed to elucidate the underlying mechanisms of prebiotics in light of maximum antidepressant effects by appropriate dosing timing.

METHODS: Adolescent depression mouse model was made by fecal microbiota transplantation (FMT) from major depressive disorder (MDD) adolescent patients. Sodium Butyrate (SB), one of SCFAs, was intragastrically administrated to mice at Zeitgeber time 4 (ZT4: the highest short-chain fatty acids (SCFAs) receptor-activated timing) or ZT16 (the lowest SCFA receptor-activated timing) for the last 2 weeks within 4-week-FMT exposure. The success of modeling and antidepressant effects of SB chronotherapy were determined by changes in depression-like behaviors, inflammation, neurotrophy, neuron functions, circadian rhythm, and barrier systems.

RESULTS: SB alleviated depressive symptoms at ZT4 with better efficacy over ZT16. SB decreased inflammation, upregulated neurotrophy, restored functions, and re-established circadian rhythm. Notably, SB increased the expressions of SCFAs receptors to repair the intestinal barrier and blood-brain barrier, thereby alleviating depressive symptoms.

LIMITATION: Only one prebiotic with one disease was involved.

CONCLUSION: SB supplementation could be a promising therapeutic tactic for restoring the integrity of barrier systems by enhancing the intestinal SCFAs receptors. Alignment SB supplementation with circadian clocks might help to obtain better antidepressant efficacy, which may generate novel insights into diseases related to diseases with barrier system impairment and optimize interventions to improve health and human well-being.},
}

@article {pmid40662222,
year = {2025},
author = {Ortiz-Samur, NS and Vijaya, AK and Burokas, A and Mela, V},
title = {Exploring the Role of Microglial Cells in the Gut-Brain Axis Communication: A Systematic Review.},
journal = {Journal of neurochemistry},
volume = {169},
number = {7},
pages = {e70154},
pmid = {40662222},
issn = {1471-4159},
support = {CP22/00033//Instituto de Salud Carlos III/ ; PI24/00347//Instituto de Salud Carlos III/ ; UniversidaddeMálaga/CBUA//Open access charge/ ; },
mesh = {*Microglia/metabolism/physiology ; Animals ; *Gastrointestinal Microbiome/physiology ; Humans ; *Brain/metabolism ; *Brain-Gut Axis/physiology ; Neuroinflammatory Diseases ; },
abstract = {The gut-brain axis (GBA) is a bidirectional communication system between the gastrointestinal tract and the CNS, playing a key role in neurological function, immune response, and metabolism. Microglia, the resident immune cells in the brain, are crucial regulators of neuroinflammation and synaptic plasticity. Recent studies indicate that the gut microbiota modulates microglial activity through metabolic and immune pathways, with implications for neurodegenerative, neurodevelopmental, and psychiatric disorders. However, the mechanisms underlying microbiota-microglia interactions remain unclear. Following a systematic screening of 4481 studies, 20 preclinical studies met the inclusion criteria and were reviewed in depth to assess microbiota-microglia interactions. These studies were found by searching in PubMed, Science Direct, and Google Scholar. The findings synthesize results from 20 carefully selected studies examining the impact of gut microbiota on microglial function. Experimental models, including fecal microbiota transplantation, dietary interventions, and bacterial supplementation, were analyzed. Microglial activity was assessed through immunohistochemistry, gene expression profiling, and functional assays. Most studies suggest that gut dysbiosis promotes microglial overactivation and neuroinflammation through pathways involving microbial-derived short-chain fatty acids (SCFAs), bile acids, and neuroimmune signaling cascades such as TLR4/NF-κB and the NLRP3 inflammasomes, whereas microbiota-targeted interventions reduce inflammation and support cognitive function. Despite these promising findings, inconsistencies in study methodologies and microbiota analyses limit comparability and clinical translation. This review offers a unique synthesis of studies specifically linking gut microbiota alterations to microglial states, neuroinflammatory signatures, and cognitive outcomes across diverse experimental models. It highlights the therapeutic potential of microbiota-based strategies for modulating microglial function and mitigating neuroinflammatory diseases.},
}

*Microglia/metabolism/physiology
Animals
*Gastrointestinal Microbiome/physiology
Humans
*Brain/metabolism
*Brain-Gut Axis/physiology
Neuroinflammatory Diseases

@article {pmid40662074,
year = {2025},
author = {Jia, J and Wu, YB and Liu, SW and Chen, WJ and Li, RL and Bai, YL and Hu, L},
title = {Effectiveness and safety of non-pharmacological therapies for the treatment of inflammatory bowel disease: a network meta-analysis.},
journal = {Frontiers in medicine},
volume = {12},
number = {},
pages = {1593483},
pmid = {40662074},
issn = {2296-858X},
abstract = {BACKGROUND: Inflammatory bowel disease (IBD), encompassing both Crohn's disease (CD) and ulcerative colitis (UC), is a chronic, inflammatory, and immune-mediated disorder of the gastrointestinal tract. If left inadequately treated, IBD can lead to disease progression, resulting in severe long-term complications, including irreversible structural damage to the intestinal tissues. While clinical symptoms are traditionally used to assess treatment efficacy, they do not always align with the underlying mucosal inflammation, particularly in CD. This limitation underscores the importance of exploring alternative treatment strategies. To address this gap, the present study evaluates the effectiveness of non-pharmacological treatments (NPTs) for IBD through a network meta-analysis (NMA), providing a thorough assessment of the available evidence.

METHODS: We systematically reviewed randomized controlled trials (RCTs) from the following databases: PubMed, Embase, Springer, Cochrane Controlled Register of Trials (CENTRAL), and Web of Science, comparing various NPTs for IBD, including Cognitive Behavioral Therapy (CBT), diet interventions (DI), fecal microbiota transplantation (FMT), physical training (PT), and acupuncture and moxibustion (APMX). Outcomes assessed included clinical remission, disease activity, quality of life (QOL), serum biomarkers (fecal calprotectin [FC] and C-reactive protein [CRP]), and adverse effects. The quality assessment was assessed by Cochrane Handbook and GRADEpro software. The risk ratio (RR) was calculated for dichotomous outcomes while standardized mean difference (SMD) was used for continuous variables with 95% credible intervals (CI). Funnel plot was performed to evaluate publication bias. Surface under the cumulative ranking curve (SUCRA) was conducted to rank the included interventions. Data were analyzed with STATA 15.0 and Review Manager 5.3.

RESULTS: A total of 62 eligible RCTs were identified in this NMA. The results showed that standard medical therapy (SMT) exhibited the highest probability in inducing clinical remission, as expected. Among non-pharmacological interventions, APMX, a traditional Chinese medicine involving acupuncture and moxibustion, showed promising results in both animal models and clinical trials, reducing serum TNF-α levels and improving intestinal health. DI was most effective in maintaining clinical remission and reducing serum FC levels. FMT emerged as the most effective treatment for reducing serum CRP levels and ranked second in terms of clinical remission induction.

CONCLUSION: APMX, DI, and FMT represent promising non-pharmacological options for managing IBD. APMX was the most effective for clinical remission and symptom relief, while DI was best for maintaining remission, and FMT showed promise in reducing inflammation. Further high-quality clinical trials are needed to strengthen the evidence and guide clinical practice in IBD management.

https://www.crd.york.ac.uk/PROSPERO/view/CRD42024596233, CRD42024596233.},
}

@article {pmid40661942,
year = {2025},
author = {Yin, J and Kaakoush, NO and Massey, J and Danta, M},
title = {Understanding the microbiome in autologous haemopoietic stem cell transplant for multiple sclerosis.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1590601},
pmid = {40661942},
issn = {1664-3224},
mesh = {Humans ; *Hematopoietic Stem Cell Transplantation/methods ; Adult ; Female ; *Gastrointestinal Microbiome ; Male ; *Multiple Sclerosis/therapy/microbiology ; Middle Aged ; Transplantation, Autologous ; Natalizumab/therapeutic use ; RNA, Ribosomal, 16S/genetics ; Feces/microbiology ; },
abstract = {BACKGROUND: MS is a chronic inflammatory and degenerative disease of the central nervous system (CNS) resulting in neurological deficits associated with physical and/or cognitive disability. The gut microbiome can interact with the CNS and immune system through various molecular pathways and has been previously implicated in MS. Autologous Haematopoietic Stem Cell Transplant (AHSCT) in MS arrests inflammatory disease and has evidence of long-term therapeutic benefit. To date, no study has explored the effect of AHSCT on the gut microbiome in people with MS.

METHOD: The microbiome of people with MS (pwMS) undergoing AHSCT was compared with pwMS on Natalizumab (NTZ). Longitudinal microbiome analysis was also conducted within the AHSCT cohort at two timepoints. Amplicon sequencing of the 16S ribosomal RNA V3-4 region (Illumina MiSeq) was used to evaluate alpha and beta diversity, oral-stool microbiota distances, and relative taxa abundances on both oral and stool microbiota.

RESULTS: The pre-transplant, baseline samples from the AHSCT cohort (n=8) was compared to the Natalizumab group (n=22). The AHSCT cohort had lower oral species richness compared to the NTZ cohort (p=0.026). There was a significant difference in oral beta diversity between the two cohorts (p=0.043). The oral taxa analysis of AHSCT subjects showed increased relative abundances of Porphyromonas and decreased Veillonella.

CONCLUSION: This pilot study identified specific microbiome changes, particularly in the oral alpha diversity and abundance of specific bacteria which may reflect treatment status or disease activity in MS.},
}

Humans
*Hematopoietic Stem Cell Transplantation/methods
Adult
Female
*Gastrointestinal Microbiome
Male
*Multiple Sclerosis/therapy/microbiology
Middle Aged
Transplantation, Autologous
Natalizumab/therapeutic use
RNA, Ribosomal, 16S/genetics
Feces/microbiology

@article {pmid40661744,
year = {2025},
author = {Wang, X and Liu, X and Gong, F and Jiang, Y and Zhang, C and Zhou, W and Zhang, W},
title = {Targeting gut microbiota for diabetic nephropathy treatment: probiotics, dietary interventions, and fecal microbiota transplantation.},
journal = {Frontiers in endocrinology},
volume = {16},
number = {},
pages = {1621968},
pmid = {40661744},
issn = {1664-2392},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; *Probiotics/therapeutic use ; *Gastrointestinal Microbiome/physiology ; *Diabetic Nephropathies/therapy/microbiology ; Animals ; Dysbiosis/therapy ; },
abstract = {Diabetic nephropathy (DN) stands as a prominent microvascular complication of diabetes mellitus and presents a significant global health challenge. Despite advancements in glycemic control and renin-angiotensin system inhibition, current treatments merely delay disease progression without targeting fundamental pathological processes. This review explores gut microbiota modulation as a promising treatment strategy for DN through probiotic supplementation, dietary interventions, and fecal microbiota transplantation(FMT) protocols. The gut microbiota, integral to the "gut-kidney axis," is critically implicated in DN pathogenesis. DN is associated with gut dysbiosis-characterized by reduced microbial diversity, depletion of beneficial short-chain fatty acid (SCFA)-producing bacteria, and proliferation of opportunistic pathogens. This dysbiosis impairs gut barrier integrity, fostering systemic inflammation and the accumulation of uremic toxins like indoxyl sulfate. Furthermore, translocated bacterial lipopolysaccharides activate Toll-like receptors and the NLRP3 inflammasome, exacerbating kidney damage and fibrosis. Interventions targeting the microbiota, including dietary strategies (e.g., enhancing fermentable fibers, low-protein diets) and FMT, show promise in preclinical and early clinical studies, though FMT requires stringent safety and donor screening protocols. Significant challenges persist, such as managing inter-individual microbiota variability for personalized therapies, fully elucidating molecular mechanisms like SCFA-GPR43 signaling, and leveraging multiomics for biomarker discovery. Advancing microbiota-focused interventions for DN towards microbiome-centered precision medicine necessitates addressing standardization, deepening mechanistic understanding, and validating combination therapies, heralding a potential shift from traditional nephroprotective approaches.},
}

Humans
*Fecal Microbiota Transplantation/methods
*Probiotics/therapeutic use
*Gastrointestinal Microbiome/physiology
*Diabetic Nephropathies/therapy/microbiology
Animals
Dysbiosis/therapy

@article {pmid40660288,
year = {2025},
author = {Qin, W and Yin, N and Xu, B and Mei, Q and Fu, Y and Fan, J and Lu, Y and Wang, G and Ai, L and Lu, Z and Zeng, Y and Huang, C},
title = {Faecalibacterium prausnitzii enhances intestinal IgA response by host-microbe derived inecalcitol in colitis.},
journal = {BMC medicine},
volume = {23},
number = {1},
pages = {425},
pmid = {40660288},
issn = {1741-7015},
support = {No. 81970555//National Natural Science Foundation of China/ ; No.CCTR-2022B02//Shanghai General Hospital/ ; 202440170//Shanghai Municipal Health Commission/ ; No.22SJKGGG28//Science and Technology Commission of Songjiang District/ ; No.KY-2023-03-02//Shanghai Jiao Tong University School of Medicine, Digestive Institute/ ; },
mesh = {Animals ; Mice ; *Gastrointestinal Microbiome/immunology ; Humans ; *Faecalibacterium prausnitzii/immunology ; Mice, Knockout ; Mice, Inbred C57BL ; *Colitis, Ulcerative/microbiology/immunology ; Male ; *Immunoglobulin A/metabolism/immunology ; Dextran Sulfate ; Disease Models, Animal ; *Colitis/microbiology/immunology ; *Immunoglobulin A, Secretory ; Female ; Feces/microbiology ; },
abstract = {BACKGROUND: Faecalibacterium prausnitzii plays a crucial role in ulcerative colitis (UC) remission, but its action mechanism is unknown. Here, we aimed to explore the potential mechanisms focusing on the interaction of F. prausnitzii with host immune response and its potential modulation on gut microbiome.

METHODS: RNA-seq analysis together with 16S rRNA sequencing and metabolomics were performed in a dextran sodium sulfate (DSS)-induced colitis mouse model followed by F. prausnitzii gavage. To present evidence of sIgA involved in the anti-inflammatory effects of F. prausnitzii, we further applied immunoglobulin A (IgA) knockout mice and secretory IgA (sIgA) depletion mouse models using polymeric immunoglobulin receptor (pIgR) neutralizing antibody. Colonic immune cells were characterized by flow cytometry. The fecal relative abundance of F. prausnitzii, inecalcitol, and colonic IgA expression were assessed in UC patients.

RESULTS: F. prausnitzii markedly ameliorated colitis by alleviating intestinal inflammation and barrier dysfunction, with significantly decreased abundance of pro-inflammatory taxa (Enterococcus, Desulfovibrio, Escherichia-Shigella, and Enterorhabdus) and increased abundance of Lachnospiraceae NK4A136_group. Functions related to intestinal immune network for IgA production pathway were up-regulated shown by transcriptomics and KEGG pathway analysis. Increased expression of IgA production associated genes including MHCII-related genes, Aicda, and Tnfrsfl3c were verified, accompanied by up-regulated colonic IgA and pIgR. The IgA knockout mice and sIgA depletion model weakened the anti-inflammation and microbiota-modulation effects of F. prausnitzii, which was further proved by fecal microbiota transplantation (FMT). The shift profile of fecal metabolites after F. prausnitzii supplement was characterized by increased production of inecalcitol, which may account for the enhanced IgA response. In a cohort of UC patients, the relative abundance of F. prausnitzii was decreased and positively correlated with colonic IgA expression and negatively correlated with disease severity.

CONCLUSIONS: F. prausnitzii effectively alleviated colonic inflammation and modulated dysbiosis via enhancing colonic IgA response, thus showing promise as a UC treatment.},
}

Animals
Mice
*Gastrointestinal Microbiome/immunology
Humans
*Faecalibacterium prausnitzii/immunology
Mice, Knockout
Mice, Inbred C57BL
*Colitis, Ulcerative/microbiology/immunology
Male
*Immunoglobulin A/metabolism/immunology
Dextran Sulfate
Disease Models, Animal
*Colitis/microbiology/immunology
*Immunoglobulin A, Secretory
Female
Feces/microbiology

@article {pmid40659786,
year = {2025},
author = {Lin, NY and Fukuoka, S and Koyama, S and Motooka, D and Tourlousse, DM and Shigeno, Y and Matsumoto, Y and Yamano, H and Murotomi, K and Tamaki, H and Irie, T and Sugiyama, E and Kumagai, S and Itahashi, K and Tanegashima, T and Fujimaki, K and Ito, S and Shindo, M and Tsuji, T and Wake, H and Watanabe, K and Maeda, Y and Enokida, T and Tahara, M and Yamashita, R and Fujisawa, T and Nomura, M and Kawazoe, A and Goto, K and Doi, T and Shitara, K and Mano, H and Sekiguchi, Y and Nakamura, S and Benno, Y and Nishikawa, H},
title = {Microbiota-driven antitumour immunity mediated by dendritic cell migration.},
journal = {Nature},
volume = {},
number = {},
pages = {},
pmid = {40659786},
issn = {1476-4687},
abstract = {Gut microbiota influence the antitumour efficacy of immune checkpoint blockade[1-6], but the mechanisms of action have not been fully elucidated. Here, we show that a new strain of the bacterial genus Hominenteromicrobium (designated YB328) isolated from the faeces of patients who responded to programmed cell death 1 (PD-1) blockade augmented antitumour responses in mice. YB328 activated tumour-specific CD8[+] T cells through the stimulation of CD103[+]CD11b[-] conventional dendritic cells (cDCs), which, following exposure in the gut, migrated to the tumour microenvironment. Mice showed improved antitumour efficacy of PD-1 blockade when treated with faecal transplants from non-responder patients supplemented with YB238. This result suggests that YB328 could function in a dominant manner. YB328-activated CD103[+]CD11b[-] cDCs showed prolonged engagement with tumour-specific CD8[+] T cells and promoted PD-1 expression in these cells. Moreover, YB238-augmented antitumour efficacy of PD-1 blockade treatment was observed in multiple mouse models of cancer. Patients with elevated YB328 abundance had increased infiltration of CD103[+]CD11b[-] cDCs in tumours and had a favourable response to PD-1 blockade therapy in various cancer types. We propose that gut microbiota enhance antitumour immunity by accelerating the maturation and migration of CD103[+]CD11b[-] cDCs to increase the number of CD8[+] T cells that respond to diverse tumour antigens.},
}

@article {pmid40659623,
year = {2025},
author = {Wang, Z and Wang, S and Liu, S and Wang, Z and Li, F and Bu, Q and An, X},
title = {Polystyrene microplastics induce potential toxicity through the gut-mammary axis.},
journal = {NPJ science of food},
volume = {9},
number = {1},
pages = {139},
pmid = {40659623},
issn = {2396-8370},
support = {2024NC-YBXM-082//Key Research and Development Projects of Shaanxi Province/ ; K4050422535//Experimental Demonstration Base of Dairy Goat in Heshui, Northwest Agriculture and Forestry University, China/ ; },
abstract = {Microplastics (MPs), as an emerging environmental pollutant, pose a grave threat to food safety and public health. However, studies on MP toxicity to organs other than the intestine remain limited, especially its link to the intestinal microbiota. To address this gap, we evaluated the potential toxicity of polystyrene (PS)-MPs to the gut and mammary glands during lactation exposure in mice. PS-MPs (~1 μm) can disrupt the intestinal barrier and cause colonic inflammation and gut microbiota dysbiosis. Moreover, they can accumulate in mammary tissue and cause inflammatory damage. Transcriptome data suggested that PS-MPs cause maternal mammary lipid metabolism disorders and ferroptosis. Fecal microbial transplant (FMT) was then performed, and it reproduced the observed leakage of the blood-milk barrier and inflammation of the mammary gland. This study demonstrated that MPs induced gut and mammary inflammation and exacerbated inflammatory damage through the gut-mammary axis. In addition, MPs caused mammary lipid disorders and ferroptosis. The findings confirmed that PS-MPs may be transported to mammalian organs other than the intestine (e.g., mammary gland) and revealed the critical role of the intestinal microbiota. These findings will provide guidance for further studies on the potential foodborne risks of MPs.},
}

@article {pmid40659561,
year = {2025},
author = {Yang, L and Hua, M and Li, D and Li, F and He, Y and Miao, X and Sun, M and Niu, H and An, F and Wang, J and Yang, M and Lu, J and Xu, H and Wang, J},
title = {Protective Effects of Ginseng Soluble Dietary Fiber and Its Fecal Microbiota Extract on Antibiotic-Induced Gut Dysbiosis Obese Mice.},
journal = {Journal of microbiology and biotechnology},
volume = {35},
number = {},
pages = {e2502013},
doi = {10.4014/jmb.2502.02013},
pmid = {40659561},
issn = {1738-8872},
mesh = {Animals ; *Dysbiosis/chemically induced/drug therapy/prevention & control/microbiology ; *Gastrointestinal Microbiome/drug effects ; Mice ; *Anti-Bacterial Agents/adverse effects ; *Panax/chemistry ; Mice, Obese ; Male ; *Dietary Fiber/pharmacology ; *Obesity/chemically induced ; *Plant Extracts/pharmacology ; Toll-Like Receptor 4/metabolism ; Feces/microbiology ; Mice, Inbred C57BL ; Bacteria/classification/drug effects ; Signal Transduction/drug effects ; Myeloid Differentiation Factor 88/metabolism ; NF-kappa B/metabolism ; Insulin Resistance ; Body Weight/drug effects ; Disease Models, Animal ; Oxidative Stress/drug effects ; },
abstract = {Prolonged or improper antibiotic use may increase the risk of obesity. Ginseng soluble dietary fiber (G-SDF) has been shown to inhibit obesity and promote the growth of intestinal probiotics. However, its role in antibiotic-induced gut dysbiosis obese mice (ADIO) remains unclear, and this study aimed to elucidate this role. The results indicated that G-SDF and its fecal microbiota extract (SDFfbs) significantly reduced body weight, insulin resistance, hepatic fat accumulation, abnormal blood and liver glucose-lipid metabolism, oxidative stress, and immune-inflammatory responses in ADIO mice. G-SDF and SDFfbs also inhibited the LPS/TLR4/MyD88/NF-κB signaling pathway, restored the expression of the gut barrier proteins Occludin and Claudin1, and protected against intestinal damage in ADIO mice. In particular, G-SDF and SDFfbs significantly increased the abundance of Firmicutes and Bacteroidetes and decreased the abundance of harmful Escherichia and Streptococcus. Additionally, they promoted the growth of beneficial bacteria, such as Enterococcus, Lactobacillus, Bifidobacterium, Parabacteroides, and Akkermansia, and these microbial shifts correlated with significant improvements in metabolic indicators in ADIO mice. Notably, SDFfbs can replicate the efficacy of SDF and has even shown stronger effects than the latter. In summary, this study demonstrated that G-SDF and SDFfbs effectively mitigate the double damage caused by obesity and antibiotic exposure by modulating the LPS/TLR4/MyD88/NF-κB pathway, protecting the intestinal barrier, and restoring the gut microbiota balance. These findings provide an important theoretical basis for the use of G-SDF and SDFfbs as fat-reducing and antibiotic-resistant ingredients in health foods.},
}

Animals
*Dysbiosis/chemically induced/drug therapy/prevention & control/microbiology
*Gastrointestinal Microbiome/drug effects
Mice
*Anti-Bacterial Agents/adverse effects
*Panax/chemistry
Mice, Obese
Male
*Dietary Fiber/pharmacology
*Obesity/chemically induced
*Plant Extracts/pharmacology
Toll-Like Receptor 4/metabolism
Feces/microbiology
Mice, Inbred C57BL
Bacteria/classification/drug effects
Signal Transduction/drug effects
Myeloid Differentiation Factor 88/metabolism
NF-kappa B/metabolism
Insulin Resistance
Body Weight/drug effects
Disease Models, Animal
Oxidative Stress/drug effects

@article {pmid40655582,
year = {2025},
author = {Patel, SP and Bhoraniya, SJ and Kalola, SD and Rukadikar, A and Ravi, R and Farooqui, S and Rukadikar, C},
title = {Gut Microbiota and its Impact on Chronic Diseases: A Comprehensive Review.},
journal = {Journal of pharmacy & bioallied sciences},
volume = {17},
number = {Suppl 2},
pages = {S1080-S1082},
pmid = {40655582},
issn = {0976-4879},
abstract = {The intricate community of bacteria that live in the gastrointestinal system, known as the gut microbiota, is essential to preserving human health and equilibrium. The pathophysiology of several chronic illnesses, including as neurological, cardiovascular, immunological, and metabolic disorders, has been progressively associated with its dysbiosis. This thorough analysis looks at the complex relationships that exist between gut microbiota and host physiology, examining processes including metabolic signaling, immunological regulation, and gut-brain axis communication. We discuss current developments in the study of the microbiome, with an emphasis on the role that the variety and makeup of gut microbes play in the development of chronic diseases. In order to restore microbial balance and lessen the severity of the condition, the study also covers new treatment approaches such as dietary changes, probiotics, prebiotics, and fecal microbiota transplantation. The development of novel, microbiome-based diagnostic and therapeutic strategies is made possible by an understanding of the complex link between the gut microbiota and chronic illnesses, highlighting the vital role that personalized medicine plays in enhancing health outcomes.},
}

@article {pmid40654576,
year = {2025},
author = {Xie, H and Yu, S and Tang, M and Xun, Y and Shen, Q and Wu, G},
title = {Gut microbiota dysbiosis in inflammatory bowel disease: interaction with intestinal barriers and microbiota-targeted treatment options.},
journal = {Frontiers in cellular and infection microbiology},
volume = {15},
number = {},
pages = {1608025},
pmid = {40654576},
issn = {2235-2988},
mesh = {Humans ; *Dysbiosis/therapy/microbiology ; *Inflammatory Bowel Diseases/therapy/microbiology ; *Gastrointestinal Microbiome/drug effects ; Probiotics/therapeutic use ; Fecal Microbiota Transplantation ; Anti-Bacterial Agents/therapeutic use ; *Intestinal Mucosa/microbiology ; Animals ; },
abstract = {Recent studies have deepened our understanding on gut microbiota alterations and the interaction with intestinal barrier impairments, which play a crucial role in the etiology and pathophysiology of Inflammatory bowel disease (IBD). The intestinal microbiota dysbiosis in IBD including the altered microbiota composition, decreased beneficial species and increased harmful species. The disturbed gut microbiota results in the aggravation of intestinal barrier dysfunction through regulation of antimicrobial substances in mucus layer, tight junction protein in mechanical layer and inflammatory response in immune layer. The therapeutic options targeted on the microbiota including antibiotics, probiotics and fecal microbiota transplantation (FMT) exhibit efficacies and limitations in the treatment of IBD. Reasonable single or combined use of these treatments can restore intestinal microecological homeostasis, which further contributes to the treatment of IBD. This review analyzes the underlying mechanisms for the interaction between microbiota alterations and gut barrier dysfunction in IBD; meanwhile, it provides new insights into the microbiota-targeted therapeutic options IBD, including the benefits, risks and limitations of antibiotic and probiotic therapies, unresolved clinical application strategies for FMT, and combination administrations of antibiotics and FMT.},
}

Humans
*Dysbiosis/therapy/microbiology
*Inflammatory Bowel Diseases/therapy/microbiology
*Gastrointestinal Microbiome/drug effects
Probiotics/therapeutic use
Fecal Microbiota Transplantation
Anti-Bacterial Agents/therapeutic use
*Intestinal Mucosa/microbiology
Animals

@article {pmid40653357,
year = {2025},
author = {Meena, AS and Singh, P and Shukla, PK},
title = {Cancer and microbiome-targeted therapies.},
journal = {International review of cell and molecular biology},
volume = {395},
number = {},
pages = {99-132},
doi = {10.1016/bs.ircmb.2024.12.006},
pmid = {40653357},
issn = {1937-6448},
mesh = {Humans ; *Neoplasms/therapy/microbiology ; *Microbiota/drug effects ; Animals ; Probiotics/therapeutic use ; Tumor Microenvironment ; Fecal Microbiota Transplantation ; },
abstract = {Emerging research highlights the profound interplay between the microbiome and cancer, offering novel avenues for therapeutic interventions. This review explores the burgeoning field of microbiome-targeted therapies in oncology, focusing on how microbial communities influence cancer development, progression, and response to treatment. The microbiome's role in modulating immune responses, drug metabolism, and tumor microenvironment is examined, revealing its potential to both inhibit and promote tumorigenesis. We discuss current strategies that leverage microbiome modulation, including probiotics, prebiotics, and fecal microbiota transplantation, to enhance the efficacy of conventional cancer therapies and mitigate side effects. Additionally, the review addresses the challenges and future directions in integrating microbiome-based approaches into clinical practice. By elucidating the mechanisms through which the microbiome affects cancer and therapy outcomes, this work aims to pave the way for innovative, personalized treatment strategies that harness the power of microbial communities to improve cancer care.},
}

Humans
*Neoplasms/therapy/microbiology
*Microbiota/drug effects
Animals
Probiotics/therapeutic use
Tumor Microenvironment
Fecal Microbiota Transplantation

@article {pmid40653356,
year = {2025},
author = {Sarath Krishnan, MP and Goyal, B and Nampui, L and Gupta, SC},
title = {The role of microbiome in gastrointestinal cancer.},
journal = {International review of cell and molecular biology},
volume = {395},
number = {},
pages = {67-98},
doi = {10.1016/bs.ircmb.2024.12.009},
pmid = {40653356},
issn = {1937-6448},
mesh = {Humans ; *Gastrointestinal Neoplasms/microbiology/pathology/therapy ; *Gastrointestinal Microbiome ; Animals ; },
abstract = {The human microbiome consists of the diverse microorganisms with their equally diverse functional abilities that have evolved over millions of years with humans. This microbiome creates a mutually beneficial symbiotic relationship with their host. Through their varied functions, the human gut microbiota is crucial for preserving health and homeostasis. Any imbalance in this microbial population can lead to an array of diseased states, including cancer especially of the gastrointestinal system. The focus of this chapter is to discuss the mechanisms through which the gut microbiome creates a conducive environment for initiation and progression of cancer. In addition, the effect of microbial products such as short chain fatty acids, bile acids and Trimethylamine N-oxide on the formation of gastrointestinal cancer is also discussed. The various experimental methods and new molecular techniques that have facilitated the characterization and study of microorganisms is also discussed. The developments in microbiome research have shed light on the potential role of gut microbiota for novel biomarker discovery and therapeutic interventions in gastrointestinal cancer, like fecal microbiota transplantation. The prospects of these areas for further exploration are discussed.},
}

Humans
*Gastrointestinal Neoplasms/microbiology/pathology/therapy
*Gastrointestinal Microbiome
Animals

@article {pmid40653352,
year = {2025},
author = {Singh, K and Bhadauriya, AS},
title = {Effect of microbial dysbiosis on autoimmune associated inflammation.},
journal = {International review of cell and molecular biology},
volume = {395},
number = {},
pages = {1-22},
doi = {10.1016/bs.ircmb.2024.12.016},
pmid = {40653352},
issn = {1937-6448},
mesh = {Humans ; *Dysbiosis/complications/microbiology/immunology ; *Autoimmune Diseases/microbiology/immunology ; *Inflammation/microbiology/immunology/complications ; Animals ; *Gastrointestinal Microbiome/immunology ; },
abstract = {Trillions of microorganisms inhabit the human body, playing crucial roles in the development of the immune system, maintaining balance within the gut's immune system, and overall well-being. When these microbial communities experience imbalance, known as dysbiosis, it can lead to localized inflammatory conditions such as colitis and inflammatory bowel diseases, as well as systemic autoimmune disorders like type 1 diabetes, rheumatoid arthritis, and multiple sclerosis. Gut microbes engage with the immune system through various means, including influencing host microRNAs to regulate gene expression and generating metabolites that interact with cellular receptors such as TLRs and GPCRs. These interactions impact critical immune processes like the differentiation of lymphocytes, the production of interleukins, and the maintenance of gut barrier function. Looking into, how gut microbes contribute to or defend against systemic autoimmune diseases is crucial for developing strategies to manage or prevent these conditions. These approaches may include dietary or lifestyle modifications, microbiome-targeted therapies such as prebiotics or probiotics, the identification of diagnostic biomarkers for predicting disease risk, and monitoring and intervening in shifts in microbial populations during autoimmune flare-ups. Recognizing the microbiome's significance in systemic autoimmune diseases offers promise for transforming these presently challenging-to-treat conditions into more controllable or preventable ones.},
}

Humans
*Dysbiosis/complications/microbiology/immunology
*Autoimmune Diseases/microbiology/immunology
*Inflammation/microbiology/immunology/complications
Animals
*Gastrointestinal Microbiome/immunology

@article {pmid40651297,
year = {2025},
author = {Chen, LJ and Liu, Y and Liu, JL and Chen, ZJ and Zhao, W and Li, JH and Hsu, C and Chen, L and Zeng, JH and Li, XW and Yang, JZ and Li, JH and Xie, XL and Tao, SH and Wang, Q},
title = {Lycopene ameliorates Di-(2-ethylhexyl) phthalate-induced neurotoxicity in mice via the gut-brain axis.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {145},
number = {},
pages = {157057},
doi = {10.1016/j.phymed.2025.157057},
pmid = {40651297},
issn = {1618-095X},
abstract = {BACKGROUND: Di(2-ethylhexyl) phthalate (DEHP), a ubiquitous plasticizer present in numerous consumer products, poses a substantial neurotoxic risk through environmental and dietary exposure. Growing evidence highlights a critical association between DEHP-induced neurotoxicity and gut microbiota dysbiosis. Renowned for its potent antioxidant and anti-inflammatory capabilities, the natural carotenoid lycopene (Lyc) demonstrates therapeutic promise in treating various neurological disorders.

PURPOSE: The potential neuroprotective mechanisms of Lyc against DEHP-induced neurotoxicity in mice were investigated in this study, with a specific focus on its interaction with the gut-brain axis.

METHODS: For 35 consecutive days, mice received daily intragastric administrations of DEHP or Lyc. A comprehensive approach involving integrated transcriptome, microbiome, and molecular biology analyses, in conjunction with bacteriotherapy, was utilized to thoroughly investigate the underlying mechanisms.

RESULTS: Our findings demonstrated that Lyc administration or fecal microbiota transplantation (FMT) from Lyc-treated mice effectively ameliorated DEHP-induced anxiety- and depression-like behaviors. At the molecular level, Lyc mitigated neuroinflammation in the hippocampus, potentially through modulation of the NOD-like receptor signaling pathway. Furthermore, Lyc treatment improved gut microbiota composition by promoting the growth of beneficial bacteria, such as Akkermansiaceae, and enhanced intestinal barrier integrity via increased expression of tight junction proteins. Lyc also regulated the LPS-TLR4/MyD88 signaling pathway in the colon, thereby reducing local inflammation.

CONCLUSION: These results provide compelling evidence that Lyc confers protection against DEHP-induced neurotoxicity through a multifaceted strategy involving modulation of gut-brain axis, suppression of neuroinflammation, and restoration of gut homeostasis. We propose a novel therapeutic strategy to alleviate the risks posed by DEHP to both neurological and intestinal health. This approach involves either supplementation with Lyc or the application of bacteriotherapy.},
}

@article {pmid40650758,
year = {2025},
author = {Kearns, R},
title = {Gut modulation to regulate NF-κB in colorectal and gastric cancer therapy and inflammation.},
journal = {Cancer immunology, immunotherapy : CII},
volume = {74},
number = {8},
pages = {264},
pmid = {40650758},
issn = {1432-0851},
mesh = {Humans ; *NF-kappa B/metabolism ; *Gastrointestinal Microbiome/immunology ; *Stomach Neoplasms/therapy/immunology/metabolism/microbiology/pathology ; *Inflammation/metabolism ; *Colorectal Neoplasms/therapy/immunology/metabolism/microbiology/pathology ; Animals ; Dysbiosis ; Fecal Microbiota Transplantation ; Signal Transduction ; },
abstract = {The nuclear factor-kappa B (NF-κB) pathway plays a pivotal role in cancer progression, immune regulation, and inflammation. Aberrant activation of this pathway, often driven by gut microbiota dysbiosis, contributes to tumorigenesis, therapy resistance, and chronic inflammation. Emerging evidence highlights the bidirectional interaction between gut microbiota and NF-κB signalling, suggesting that microbiota modulation may enhance cancer treatment efficacy and reduce treatment-induced inflammation. This review explores the mechanistic underpinnings of gut microbiota-mediated NF-κB regulation, focusing on microbial metabolites such as short-chain fatty acids (SCFAs) and microbial-associated molecular patterns, including lipopolysaccharides (LPS). It examines how conventional cancer treatments, chemotherapy, radiotherapy, and immune checkpoint inhibitors, exacerbate dysbiosis and NF-κB-driven inflammation, further complicating treatment outcomes. Additionally, this review evaluates the therapeutic potential of gut-targeted interventions, including probiotics, prebiotics, faecal microbiota transplantation (FMT), and dietary modifications, in restoring microbial homeostasis and modulating NF-κB signalling. Despite promising findings, challenges remain regarding the clinical translation of microbiota-based therapies, including the need for standardised microbiota profiling, regulatory frameworks, and long-term safety assessments. Advances in metagenomics and metabolomics are proposed as essential tools to personalise gut-targeted interventions and optimise cancer treatment strategies. Integrating gut modulation into oncology represents a paradigm shift, offering a holistic, patient-centric approach to cancer therapy. However, further research is required to validate these strategies and ensure their efficacy in clinical applications.},
}

Humans
*NF-kappa B/metabolism
*Gastrointestinal Microbiome/immunology
*Stomach Neoplasms/therapy/immunology/metabolism/microbiology/pathology
*Inflammation/metabolism
*Colorectal Neoplasms/therapy/immunology/metabolism/microbiology/pathology
Animals
Dysbiosis
Fecal Microbiota Transplantation
Signal Transduction

@article {pmid40649988,
year = {2025},
author = {Kaltsas, A and Giannakodimos, I and Markou, E and Stavropoulos, M and Deligiannis, D and Kratiras, Z and Chrisofos, M},
title = {The Androbactome and the Gut Microbiota-Testis Axis: A Narrative Review of Emerging Insights into Male Fertility.},
journal = {International journal of molecular sciences},
volume = {26},
number = {13},
pages = {},
doi = {10.3390/ijms26136211},
pmid = {40649988},
issn = {1422-0067},
mesh = {Humans ; Male ; *Gastrointestinal Microbiome/physiology ; *Infertility, Male/microbiology/metabolism ; *Testis/metabolism/microbiology ; Animals ; *Fertility ; Spermatogenesis ; Dysbiosis/microbiology ; },
abstract = {Male infertility is an under-recognized global health burden. Accumulating evidence position the intestinal microbiota as a pivotal regulator of testicular function, underpinning the emerging gut microbiota-testis axis. This narrative review introduces the conceptual term "androbactome", referring to gut microorganisms and microbial genes that are hypothesized to influence androgen biosynthesis, spermatogenesis, and broader reproductive endocrinology. The documented worldwide decline in sperm concentration heightens the urgency of clarifying microbe-mediated influences on male reproductive capacity. The synthesis of preclinical and clinical findings reveals four principal pathways by which dysbiosis compromises fertility: systemic inflammation, oxidative stress, endocrine disruption, and epigenetic alteration. Lipopolysaccharide-driven cytokinaemia, reactive oxygen species generation, hypothalamic-pituitary-gonadal axis suppression, and aberrant germ cell methylation collectively impair sperm quality and hormonal balance. Short-chain fatty acids, secondary bile acids, and indole derivatives emerge as pivotal messengers within this crosstalk. Therapeutic approaches targeting the androbactome, namely dietary optimization, probiotic or prebiotic supplementation, and fecal microbiota transplantation, have demonstrated encouraging improvements in sperm parameters and testosterone levels, yet the causal inference is constrained by predominantly cross-sectional designs and limited long-term safety data. Recognizing the androbactome as a modifiable determinant of male fertility may open new avenues for personalized diagnosis, risk stratification, and adjunctive therapy in regard to idiopathic infertility. The integration of multi-omics platforms to characterize microbial and metabolomic signatures promises to enrich diagnostic algorithms and guide precision interventions, but rigorously controlled longitudinal and interventional studies are required to secure a translational impact.},
}

Humans
Male
*Gastrointestinal Microbiome/physiology
*Infertility, Male/microbiology/metabolism
*Testis/metabolism/microbiology
Animals
*Fertility
Spermatogenesis
Dysbiosis/microbiology

@article {pmid40649705,
year = {2025},
author = {Borbélyová, V and Szabó, J and Sušienková, P and Potvin, J and Belvončíková, P and Groß, T and Jančovičová, A and Bačová, Z and Rašková, B and Szadvári, I and Antal, M and Pirník, Z and Karhánek, M and Šoltys, K and Gardlík, R and Celec, P and Ostatníková, D and Tomova, A},
title = {The Effect of Parental Faecal Microbiome Transplantation from Children with Autism Spectrum Disorder on Behavior and Gastrointestinal Manifestations in the Male Offspring of Shank3 Mice.},
journal = {International journal of molecular sciences},
volume = {26},
number = {13},
pages = {},
doi = {10.3390/ijms26135927},
pmid = {40649705},
issn = {1422-0067},
support = {APVV-20-0114//Slovak Research and Development Agency/ ; VEGA 1/0062/21//Ministry of Education, Science, Research, and Sport of the Slovak Republic/ ; },
mesh = {Animals ; *Autism Spectrum Disorder/therapy/microbiology/genetics ; *Fecal Microbiota Transplantation ; Mice ; Male ; Female ; *Nerve Tissue Proteins/genetics/metabolism ; Humans ; Behavior, Animal ; Pregnancy ; Gastrointestinal Microbiome ; Mice, Knockout ; Disease Models, Animal ; Child ; Prenatal Exposure Delayed Effects ; Microfilament Proteins ; },
abstract = {The increasing incidence of autism spectrum disorder (ASD) increases the urgency of establishing the mechanism of its development for effective prevention and treatment. ASD's etiology includes genetic predisposition and environmental triggers, both of which can play a role in the changed microbiota. Recent research has proved the impact of maternal microbiota on the neurodevelopment of the child. To investigate the co-play of genetic and microbiota factors in ASD development, we performed fecal microbiota transplantation (FMT) from children with ASD to female Shank3b[+/-] mice and studied the autism-like symptoms in the male Shank3b[-/-] and wild-type (WT) offspring. WT animals with prenatal exposure to ASD microbiota had delayed neurodevelopment and impaired food intake behavior, but also elevated plasma leptin concentration and body weight. Shank3b[-/-] mice after FMT ASD exhibited impaired learning and exacerbated anxiety-like behavior in adulthood. Interestingly, FMT ASD improved learning in adolescent Shank3b[-/-] mice. Prenatal exposure to ASD microbiota decreased the activity of hypocretin neurons of the lateral hypothalamic area in both genotypes. The combination of genetic predisposition and FMT ASD led to an increased colon permeability, evaluated by zonula occludens (ZO1, ZO3) and claudin factors. These results suggest the effect of parental FMT exposure on shaping offspring behavior in Shank3b[-/-] mice and the potential of microbiota in the modulation of ASD.},
}

Animals
*Autism Spectrum Disorder/therapy/microbiology/genetics
*Fecal Microbiota Transplantation
Mice
Male
Female
*Nerve Tissue Proteins/genetics/metabolism
Humans
Behavior, Animal
Pregnancy
Gastrointestinal Microbiome
Mice, Knockout
Disease Models, Animal
Child
Prenatal Exposure Delayed Effects
Microfilament Proteins

@article {pmid40647353,
year = {2025},
author = {Liber, A and Więch, M},
title = {The Impact of Fecal Microbiota Transplantation on Gastrointestinal and Behavioral Symptoms in Children and Adolescents with Autism Spectrum Disorder: A Systematic Review.},
journal = {Nutrients},
volume = {17},
number = {13},
pages = {},
doi = {10.3390/nu17132250},
pmid = {40647353},
issn = {2072-6643},
mesh = {Humans ; *Autism Spectrum Disorder/therapy/complications/psychology/microbiology ; *Fecal Microbiota Transplantation/methods ; Child ; Adolescent ; *Gastrointestinal Diseases/therapy/etiology ; Treatment Outcome ; Male ; Female ; Child, Preschool ; Gastrointestinal Microbiome ; *Behavioral Symptoms/therapy ; Dysbiosis/therapy ; },
abstract = {Background: Gastrointestinal (GI) symptoms, often reported by individuals with autism spectrum disorders (ASD), may impair functionality and exacerbate behavioral symptoms. Gut dysbiosis has been identified as a potential environmental factor influencing these symptoms through gut-brain axis dysregulation. Fecal microbiota transplantation (FMT) is a promising therapeutic strategy with potential to alleviate symptoms. This review systematically evaluates the efficacy and safety of FMT in GI and ASD-related symptoms. Methods: This systematic review followed PRISMA 2020 guidelines and was registered in PROSPERO. The review included clinical trials on FMT in children and adolescents with ASD, published up to October 2024. The bias assessments were performed using Cochrane tools. Outcomes focused on changes in GI and ASD-related symptoms using scales selected by the authors. Results: This systematic review included two RCTs and seven before-and-after studies. Improvements in GI and ASD-related outcomes were reported in all before-and-after studies, whereas the results of RCTs were inconsistent. The before-and-after studies showed a high risk of bias, while the RCTs demonstrated a low risk. Conclusions: Although many studies have been conducted, the methodological limitations of some and contradictory findings of others make it difficult to draw clear conclusions about the effectiveness of FMT in children with ASD. Variations in intervention protocols underscore the importance of establishing standardized FMT procedures in future rigorously designed trials.},
}

Humans
*Autism Spectrum Disorder/therapy/complications/psychology/microbiology
*Fecal Microbiota Transplantation/methods
Child
Adolescent
*Gastrointestinal Diseases/therapy/etiology
Treatment Outcome
Male
Female
Child, Preschool
Gastrointestinal Microbiome
*Behavioral Symptoms/therapy
Dysbiosis/therapy

@article {pmid40647217,
year = {2025},
author = {Szczuko, M and Grudniewska, A and Durma, A and Małecki, R and Filipczyńska, I and Franek, E and Kędzierska-Kapuza, K},
title = {Non-Pharmacological Interventions Aimed at Changing the Gut Microbiota for Preventing the Progression of Diabetic Kidney Disease.},
journal = {Nutrients},
volume = {17},
number = {13},
pages = {},
doi = {10.3390/nu17132112},
pmid = {40647217},
issn = {2072-6643},
mesh = {*Gastrointestinal Microbiome ; Humans ; *Diabetic Nephropathies/microbiology/therapy/prevention & control ; *Probiotics/therapeutic use/administration & dosage ; Disease Progression ; Fecal Microbiota Transplantation ; Animals ; Synbiotics/administration & dosage ; Dysbiosis/therapy ; Dietary Supplements ; },
abstract = {BACKGROUND: Diabetic kidney disease (DKD) affects 20-50% of individuals with diabetes. The aim of this review was to identify interventions that positively influence the gut microbiota in DKD.

METHODS: Identification of relevant studies was conducted via a systematic search of databases and registers using the PRISMA guidelines. This review examined the relevant literature published up to 5 January 2025, using a systematic search in PubMed and Scopus. The search was conducted with combinations of keywords including DKD and therapy, supplementation and gut microbiota, and supplementation or probiotics or fecal microbiota transplant. The initial search fielded 132 results from PubMed and 72 from Scopus, which was narrowed to 135 relevant studies. The exclusion criteria included non-English language studies, letters to the editor, and conference abstracts. Eligible studies were independently assessed by a minimum of three authors, with discrepancies resolved through consensus.

RESULTS: Gut microbiota-targeted interventions, including probiotics, synbiotics, and dietary modifications, show promise in modulating the gut microbiota, but evidence specific to DKD remains limited. Some natural food components such as polyphenols and anthocyanins modulate the composition of the gut microbiota translocation of uremic toxins, which slows down the progression of diabetic kidney disease. In animal models, fecal microbiota transplantation (FMT) has shown positive effects in regulating dysbiosis and beneficial effects in chronic kidney disease, but studies involving humans with DKD are insufficient.

CONCLUSIONS: Lactobacillus and Bifidobacterium strains, administered at doses ranging from 0.6 to 90 billion CFU, may help lower urea and creatinine levels, but outcomes vary by disease stage, duration of therapy, and amount used. High-fiber diets (>10.1 g/1000 kcal/day) and supplements such as resistant starch and curcumin (400-1500 mg/day) may reduce uremic toxins through gut microbiota modulation and reduction in oxidative stress. The effect of sodium butyrate requires further human studies.},
}

*Gastrointestinal Microbiome
Humans
*Diabetic Nephropathies/microbiology/therapy/prevention & control
*Probiotics/therapeutic use/administration & dosage
Disease Progression
Fecal Microbiota Transplantation
Animals
Synbiotics/administration & dosage
Dysbiosis/therapy
Dietary Supplements

@article {pmid40645350,
year = {2025},
author = {Fatima, SN and Arif, F and Khalid, R and Khan, M and Naseem, K},
title = {Immunomodulatory role of gut microbiota in autoimmune disorders and the advancement of gut microbiota based therapeutic strategies.},
journal = {Microbial pathogenesis},
volume = {207},
number = {},
pages = {107882},
doi = {10.1016/j.micpath.2025.107882},
pmid = {40645350},
issn = {1096-1208},
abstract = {This review investigates the central hypothesis that gut microbiota dysbiosis contributes to autoimmune pathogenesis via immune dysregulation, increased intestinal permeability, and aberrant metabolite signaling and many other pathways. Mechanisms such as SCFA depletion, Th17/Treg imbalance, molecular mimicry, and disrupted aryl hydrocarbon receptor (AhR) pathways plays central immunomodulatory role in the development as well as management of autoimmune disorders including RA, T1D, MS, and IBD. Emerging interventions like probiotics, prebiotics, SCFA supplementation, and FMT are critically assessed to demonstrating their modulatory effects on cytokine profiles, epithelial integrity, and Treg induction. Clinical and preclinical data support microbial restoration as a viable immunotherapeutic strategy. The review concludes that targeting gut-immune crosstalk through microbiota-directed therapies may offer precise, mechanism-based management for many autoimmune disorders.},
}

@article {pmid40644647,
year = {2025},
author = {Barragan-Carrillo, R and Zengin, ZB and Pal, SK},
title = {Microbiome Modulation for the Treatment of Solid Neoplasms.},
journal = {Journal of clinical oncology : official journal of the American Society of Clinical Oncology},
volume = {},
number = {},
pages = {JCO2500374},
doi = {10.1200/JCO-25-00374},
pmid = {40644647},
issn = {1527-7755},
abstract = {The interplay between the human gut microbiome and the immune system has sparked growing interest in microbiome modulation as a therapeutic strategy in oncology. Preclinical studies have identified specific bacterial species linked to improved responses to immune checkpoint inhibitors (ICIs), leading to clinical investigations in melanoma, renal cell carcinoma (RCC), and non-small cell lung cancer (NSCLC). The stool bacterial abundance of Ruminococcaceae, Akkermansia, and Bifidobacterium correlates with favorable clinical outcomes, whereas the disruption of the gut microbiome through antibiotics before or during ICI initiation is associated with higher rates of primary resistance and shorter survival. Biomarkers such as TOPOSCORE have been developed to better predict ICI benefits and estimate dysbiosis and treatment responses. Several microbiome-modulating strategies have shown potential in patients receiving treatment with ICIs-for instance, high dietary fiber intake may be linked to improved outcomes. As a separate strategy, certain probiotics appear to enhance clinical activity in early trials when incorporated into ICI-based regimens. Finally, fecal microbiota transplantation has shown safety and efficacy in ICI-refractory melanoma and yielded encouraging results in treatment-naïve patients with melanoma, NSCLC, and RCC. Although several compelling signals have been observed to date with microbiome manipulation, the field is lacking large, definitive randomized trials-these are indeed a prerequisite for any of the highlighted strategies to become a standard of care.},
}

@article {pmid40643902,
year = {2025},
author = {Anderer, S},
title = {Fecal Transplant Appears Noninferior to Antibiotics for Treating CDI.},
journal = {JAMA},
volume = {},
number = {},
pages = {},
doi = {10.1001/jama.2025.10327},
pmid = {40643902},
issn = {1538-3598},
}

@article {pmid40643244,
year = {2025},
author = {Seekatz, AM},
title = {Straining to define a healthy microbiome.},
journal = {mSphere},
volume = {},
number = {},
pages = {e0079724},
doi = {10.1128/msphere.00797-24},
pmid = {40643244},
issn = {2379-5042},
abstract = {In 2020, I wrote an mSphere of Influence commentary on two studies that shaped my research perspective on the human gut microbiome (McNulty et al., Sci Transl Med 3:106ra106, 2011, https://doi.org/10.1126/scitranslmed.3002701; Hamilton et al., Gut Microbes 4:125, 2013, https://doi.org/10.4161/gmic.23571). The microbiome field has continued to progress since the publication of these studies over 10 years ago, emerging as a considerable factor in almost all areas focused on disease development. My previous commentary highlighted two areas that piqued my interest early on in my career: (i) that the extant microbial community should be considered when proposing to manipulate the microbiota, such as via probiotics or fecal microbiota transplantation, and (ii) that realized (i.e., transcribed) functional changes of the microbiota may occur independent of changes in its composition. Since writing that commentary, two microbiota-based therapeutics for the treatment of Clostridioides difficile infection have been approved, highlighting the potential success of using the microbiota to treat or prevent disease. Despite these wins and ever-growing evidence of the importance of the microbiome in managing our health, translating mechanistic studies into therapeutic value has been slower. In this minireview, I expand upon two large questions that would increase our ability to translate the microbiome into therapies, highlighting both historical and recent progress.},
}

@article {pmid40642988,
year = {2025},
author = {Wang, F and Wu, Y and Ni, J and Xie, Q and Shen, J and Chen, H and Ma, C and Yao, Y and Wang, J and Xu, L and Xiang, Q and Zhao, Y and Chen, Y and Li, L},
title = {Gut microbiota links to histological damage in chronic HBV infection patients and aggravates fibrosis via fecal microbiota transplantation in mice.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0076425},
doi = {10.1128/spectrum.00764-25},
pmid = {40642988},
issn = {2165-0497},
abstract = {Gut microbiota dysbiosis has been observed in HBV-related cirrhosis, but its role in early-stage disease and its correlation with liver pathology remain unclear. Moreover, whether dysbiosis is a cause or consequence of liver cirrhosis is still debated. We recruited 20 treatment-naïve patients with chronic HBV infection, assessing liver injury via biopsy. Fecal metagenomic sequencing was used to analyze the correlation between gut microbiota and liver histology. To explore the causality, fecal samples from an HBV-related cirrhosis patient were transplanted into mice with CCl4-induced liver fibrosis. Patients with significant histological damage exhibited reduced alpha diversity and greater microbial homogeneity. Species such as Eubacterium_sp_CAG_180, Gemmiger_formicilis, and Oscillibacter_sp_ER4 had decreased abundance, while Parabacteroides_distasonis, Bacteroides_dorei, and Bacteroides_finegoldii were enriched. Mice receiving fecal transplants from the cirrhotic patient showed aggravated liver fibrosis, with increased collagen deposition; elevated ALT, AST, and ALP levels; and heightened hepatic inflammatory gene expression. Additionally, abnormal bile acid profiles with elevated unconjugated bile acids (e.g., GCA and CA) were observed. Gut microbiota dysbiosis is closely associated with liver histological damage in chronic HBV infection and may drive fibrosis progression via microbial-bile acid interactions. These findings suggest potential for gut microbiota-based assessment and treatment strategies in chronic hepatitis B.IMPORTANCEThis study elucidates a significant association between gut microbiota dysbiosis and liver histological damage in patients with chronic hepatitis B (HBV), potentially exacerbating fibrosis progression through bile acid interactions. By analyzing patient gut microbiota and conducting fecal transplant experiments in mice, researchers have identified that gut microbiota dysbiosis contributes to hepatic fibrosis during chronic HBV infection. These findings underscore the importance of the gut-liver axis in HBV disease progression, indicating that monitoring or modulating gut bacteria may facilitate early diagnosis or therapeutic interventions. This research bridges the gap in understanding whether microbial alterations drive disease progression or result from it, providing a foundation for developing therapies targeting the microbiome to mitigate liver damage in chronic HBV infections.},
}

@article {pmid40642664,
year = {2025},
author = {Horwat, P and Mariowska, A and Szymanska, A and Dzieciatkowska, M and Pierudzka, W},
title = {Multimodal Interventions Targeting Gut Microbiota and Microbial Metabolites in Cognitive Impairment.},
journal = {Cureus},
volume = {17},
number = {6},
pages = {e85688},
pmid = {40642664},
issn = {2168-8184},
abstract = {Mild cognitive impairment (MCI) is a transitional stage between normal aging and Alzheimer's disease (AD). Recent studies suggest that alterations in gut microbiota and microbial metabolites are associated with cognitive decline, highlighting the gut-brain axis as a potential therapeutic target. This narrative review explores current evidence on the relationship between gut microbiota, microbial metabolites, and MCI. It summarizes intervention strategies including probiotics, prebiotics, synbiotic, fecal microbiota transplantation, dietary modifications, medicinal herbs, phytochemicals, metformin, and lifestyle factors. Probiotic strains such as Lactobacillus and Bifidobacterium have shown cognitive benefits. Adherence to the Mediterranean and MIND diets, as well as metformin use, is associated with lower MCI risk. Novel strategies, including plant-based compounds and nature exposure, show promise in modulating gut microbiota and improving cognitive outcomes. Gut microbiota modulation represents a promising avenue for early intervention in MCI. Personalized, multifactorial approaches based on individual microbiome profiles may enhance prevention and management strategies. However, more high-quality clinical trials are needed to establish evidence-based guidelines.},
}

@article {pmid40642089,
year = {2025},
author = {Lei, W and Cheng, Y and Liu, X and Gao, J and Zhu, Z and Ding, W and Xu, X and Li, Y and Ling, Z and Jiang, R and Chen, X},
title = {Gut microbiota-driven neuroinflammation in Alzheimer's disease: from mechanisms to therapeutic opportunities.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1582119},
pmid = {40642089},
issn = {1664-3224},
mesh = {Humans ; *Alzheimer Disease/therapy/microbiology/immunology/metabolism/etiology ; *Gastrointestinal Microbiome/immunology ; Animals ; *Neuroinflammatory Diseases/therapy/microbiology ; Dysbiosis/immunology ; Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; Brain/metabolism/immunology ; Brain-Gut Axis ; },
abstract = {Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-beta (Aβ) plaques, tau hyperphosphorylation, and chronic neuroinflammation. While neuroinflammation-mediated by microglial and astrocyte activation-has long been considered a secondary response to Aβ pathology, emerging evidence positions it as a primary driver of cognitive decline. Notably, the gut microbiota, through the microbiota-gut-brain axis (MGBA), is crucial in modulating neuroinflammation. Dysbiosis disrupts gut barrier integrity, promotes systemic inflammation, and exacerbates neuroinflammatory responses, thereby accelerating AD progression. Recent advances reveal that gut microbiota-derived metabolites (e.g., short-chain fatty acids, lipopolysaccharides) directly influence microglial activation and Aβ aggregation. These findings have opened new therapeutic possibilities, with microbiota-targeted approaches such as probiotics, prebiotics, and fecal microbiota transplantation demonstrating promising neuroprotective effects in preclinical studies by reducing neuroinflammation and preserving cognitive function. However, translating these findings into clinical applications requires further validation through randomized controlled trials. This review summarizes the current understanding of gut microbiota-driven neuroinflammation in AD, from molecular mechanisms to potential therapeutic strategies. Targeting the MGBA represents a paradigm shift in AD management, emphasizing the modulation of neuroinflammation and pathological progression through gut microbiota interventions. The discussion also addresses existing research challenges and outlines future directions to advance this promising field.},
}

Humans
*Alzheimer Disease/therapy/microbiology/immunology/metabolism/etiology
*Gastrointestinal Microbiome/immunology
Animals
*Neuroinflammatory Diseases/therapy/microbiology
Dysbiosis/immunology
Fecal Microbiota Transplantation
Probiotics/therapeutic use
Brain/metabolism/immunology
Brain-Gut Axis

@article {pmid40641916,
year = {2025},
author = {Daniluk, U and Świdnicka-Siergiejko, A and Daniluk, J and Rusak, M and Dąbrowska, M and Guzińska-Ustymowicz, K and Pryczynicz, A and Dąbrowski, A},
title = {The development of pancreatic cancer is accompanied by significant changes in the immune response in genetically predisposed mice.},
journal = {Frontiers in oncology},
volume = {15},
number = {},
pages = {1603293},
pmid = {40641916},
issn = {2234-943X},
abstract = {PURPOSE: The pathogenesis of pancreatic cancer (PC) is extremely complex and involves genetic and environmental factors, as well as significant changes in the immune response to tumor cells from the loss of immune surveillance to the development of immunotolerance to cancer. Currently available literature data on this subject is inconsistent. The purpose of our study was to evaluate the status of dendritic cells (DC) and other immune cells in the pancreas and blood of mice genetically predisposed to pancreatic cancer (Kras[G12D] mutation). The second objective was to assess the impact of fecal microbiota transplantation (FMT) from PC mice on pancreatic tumor development and alterations in pancreatic and blood immune cell counts in mice genetically predisposed to PC.

METHODS: We used LSL-K-Ras[G12D] mice, which possess the conditional knock-in mutant K-Ras[G12D] driven by its endogenous promoter and Ela-CreERT mice, which express tamoxifen-regulated CreERT specifically in pancreatic acinar cells under the control of a full-length elastase gene promoter. The immunophenotype of immune cells separated from pancreatic tissue and circulating blood was analyzed with the use of multicolor flow cytometry and immunochemistry staining. Fecal pellets from LSL-K-Ras[G12D] mice, that developed PC after the cerulein (CER) treatment, were collected and transplanted into animals previously treated with the antibiotic.

RESULTS: Using immunohistochemistry and flow cytometry, we found that in mice genetically predisposed to PC, cerulein (CER) administered intraperitoneally induced tumor growth and inflammatory cell infiltration in pancreatic tissue, but without affecting immune cell differentiation in the blood. In contrast, orally administered FMT activated the immune system in the gastrointestinal tract, leading to generalized immune cell activation, as observed in the blood, and local infiltration of cells in the pancreatic tissue of Kras mutant mice that developed pancreatic tumors. Interestingly, immunohistochemical evaluation of pancreatic tissue revealed that the Kras mutation alone causes increased infiltration of CD11b[+], CD20[+], CD3[+], CD4[+], and CD8[+] cells. After FMT, there was a trend toward an increased intensity of infiltration by these immune cells, with the exception of CD11b[+].

CONCLUSIONS: Our data suggest that pancreatic cancer development in genetically predisposed mice is accompanied by profound changes in immune cell composition. Treatment with tumor-inducing agents such as CER or FMT from tumor-bearing mice, accelerated PC progression. The type of immune system response, systemic or local, in mice with pancreatic cancer depends on the route of entry of the inflammatory agent. Oral administration of FMT activated the systemic immune response, in contrast to the intraperitoneal injection of CER.},
}

@article {pmid40641009,
year = {2025},
author = {Siegel, R and Sibert, NT and Breidenbach, C and Gani, C and Neumann, PA and Benz, SR and Post, S and Seufferlein, T and Kolb, V and Behrend, M and Blossey, RD and Bunse, J and Dahlke, M and Diller, R and Emmanouilidis, N and Ettrich, TJ and Fahlke, J and Flemming, S and Freitag, B and Fuchs, M and Haeder, L and Hollerbach, S and Höppner, J and Kim, M and Klink, C and Knuth, J and Koeppen, S and Köninger, J and Kolbe, EW and Kühn, F and Mussa, S and Oehring, R and Petzoldt, S and Piso, P and Prause, C and Prinz, C and Reißfelder, C and Riechmann, M and Ritz, JP and Rolinger, J and Rosenberg, R and Scheuerlein, H and Schilawa, D and Schneider, PM and Schwandner, T and Siech, M and Steinemann, D and Stöltzing, O and von Haeften, E and Weihs, D and Wiegering, A and Zielinski, CB and Kowalski, C},
title = {Impact of preoperative radiotherapy on patient-reported outcomes in rectal cancer.},
journal = {Colorectal disease : the official journal of the Association of Coloproctology of Great Britain and Ireland},
volume = {27},
number = {7},
pages = {e70158},
doi = {10.1111/codi.70158},
pmid = {40641009},
issn = {1463-1318},
support = {//Innovation Fund of the German Federal Joint Committee (Innovationsausschuss beim Gemeinsamen Bundesausschuss, G BA)/ ; },
mesh = {Humans ; *Rectal Neoplasms/surgery/radiotherapy ; *Patient Reported Outcome Measures ; Male ; Female ; Middle Aged ; Prospective Studies ; Quality of Life ; Aged ; *Preoperative Care/methods ; *Neoadjuvant Therapy/methods/adverse effects ; Postoperative Complications/etiology ; Proctectomy ; Radiotherapy, Adjuvant/adverse effects ; Fecal Incontinence/etiology ; Surveys and Questionnaires ; Adult ; Treatment Outcome ; },
abstract = {AIM: To prospectively evaluate the effect of preoperative radiotherapy followed by surgery versus surgery alone on patient-reported outcomes (PROs) 1 year after surgery.

METHOD: Prospective observational cohort study in 127 colorectal cancer centres. Patients with rectal cancer completed European Organization for Research and Treatment of Cancer Quality of Life Questionnaire Core (EORTC-QLQ-C30) and Colorectal module (-CR29) questionnaires (thus providing PROs) before initialization of treatment [baseline (T0)] and at 12 months after surgery [follow up (T1)]. The PRO data together with sociodemographic information were linked to clinical data. Relevant confounders were identified using directed acyclic graphs. The effect of preoperative radiotherapy on selected PROs 12 months after surgery was estimated using adjusted tobit regression models.

RESULTS: Of 1635 patients with rectal cancer for whom both baseline and follow-up PROs were available, 565 (35%) received preoperative radiotherapy. Twelve months after surgery, patients with surgery alone reported better scores for global health status/Quality of Life, urinary incontinence, faecal incontinence (patients without stoma), dyspareunia (female patients) and impotence (male patients) than did patients receiving preoperative radiotherapy. The statistically significant effects ranged between 33.20 (p < 0.001, R[2] = 0.19) for impotence and 39.01 (p = 0.001, R[2] = 0.10) for dyspareunia. For global health status/QoL and urinary incontinence, no statistically significant effect could be found.

CONCLUSION: Radiotherapy in addition to surgery negatively affects selected PROs 1 year after surgery in patients with rectal cancer. Compared with surgery alone, patients report profoundly impaired bowel and sexual function after preoperative radiotherapy. However, global health status/QoL was not affected statistically significantly. These results are an important argument for limiting preoperative radiotherapy to patients with a high risk of recurrence of rectal cancer and may facilitate informed decision-making.

TRIAL REGISTRATION: German Clinical Trial Registry Number DRKS00008724 (https://drks.de/search/de/trial/DRKS00008724).},
}

Humans
*Rectal Neoplasms/surgery/radiotherapy
*Patient Reported Outcome Measures
Male
Female
Middle Aged
Prospective Studies
Quality of Life
Aged
*Preoperative Care/methods
*Neoadjuvant Therapy/methods/adverse effects
Postoperative Complications/etiology
Proctectomy
Radiotherapy, Adjuvant/adverse effects
Fecal Incontinence/etiology
Surveys and Questionnaires
Adult
Treatment Outcome

@article {pmid40640940,
year = {2025},
author = {Wang, N and Sun, C and Yang, Y and Zhang, D and Huang, L and Xu, C and Wang, M and Xu, M and Yan, T and Wu, Y and Xu, L and Ju, Y and Sun, H and Guo, W},
title = {Gut microbiota-derived indoleacetic acid attenuates neuroinflammation and neurodegeneration in glaucoma through ahr/rage pathway.},
journal = {Journal of neuroinflammation},
volume = {22},
number = {1},
pages = {179},
pmid = {40640940},
issn = {1742-2094},
support = {SHSMU-ZDCX20210902//Innovative Research Team of High-level Local University in Shanghai/ ; 82171046//National Natural Science Foundation of China/ ; BYH20220403//Post Graduate Medical Education Program 2022/ ; 20DZ2270800//Research Grant of the Shanghai Science and Technology Committee/ ; },
mesh = {*Gastrointestinal Microbiome/physiology ; Animals ; *Indoleacetic Acids/metabolism/pharmacology/therapeutic use ; Mice ; Humans ; Male ; *Receptors, Aryl Hydrocarbon/metabolism ; *Glaucoma/metabolism/pathology/microbiology ; *Neuroinflammatory Diseases/metabolism ; Signal Transduction/physiology/drug effects ; Mice, Inbred C57BL ; Female ; Fecal Microbiota Transplantation ; Microglia/metabolism/drug effects ; Middle Aged ; Aged ; },
abstract = {BACKGROUND: Gut microbiota has emerged as a promising therapeutic target for neurodegenerative disorders through regulation of neuroinflammatory responses, while its role in optic nerve degeneration remains incompletely characterized. This study elucidates the neuroprotective role of gut microbiota derived tryptophan metabolites in glaucoma through gut-eye communication and inhibition of microglia-mediated neuroinflammation.

METHODS: Gut microbiota profiling (16 S rRNA sequencing) and serum indoleacetic acid (IAA) quantification were performed in glaucoma patients versus controls. Microbiota-metabolite relationships were further validated through fecal microbiota transplantation (FMT). The neuroprotective and anti-neuroinflammatory effect of Bacteroides fragilis (B. fragilis) and IAA was assessed in both microbead-induced ocular hypertension mice model and in vitro BV-2 microglial cell inflammation model via immunofluorescence, qPCR, Western blot and mice behavioral assays. To explore the underlying mechanisms, retinal transcriptomics and microglia-neuron co-cultures were also employed.

RESULT: Glaucoma patients exhibited gut dysbiosis characterized by depleted tryptophan-metabolizing bacteria (B. fragilis, Bacteroides thetaiotaomicron, Anaerostipes hadrus) and reduced serum IAA levels. Mice receiving FMT from glaucoma patients exhibited lower systemic IAA levels. In in vivo and in vitro models, B. fragilis or IAA restored AhR activation, suppressed inflammation by inhibiting microglial activation and the release of pro-inflammatory mediators throughout the retina, reduced retinal ganglion cells (RGCs) loss and preserved visual function. Mechanistically, IAA attenuated RAGE/NF-κB pathway activation via AhR-dependent signaling, conferring neuroprotection.

CONCLUSION: Our study proposes a novel AhR-mediated gut microbiota-eye axis in glaucoma pathogenesis and demonstrates that IAA serves as an effective neuroprotective strategy with clinical potential for managing RGCs neurodegeneration.},
}

*Gastrointestinal Microbiome/physiology
Animals
*Indoleacetic Acids/metabolism/pharmacology/therapeutic use
Mice
Humans
Male
*Receptors, Aryl Hydrocarbon/metabolism
*Glaucoma/metabolism/pathology/microbiology
*Neuroinflammatory Diseases/metabolism
Signal Transduction/physiology/drug effects
Mice, Inbred C57BL
Female
Fecal Microbiota Transplantation
Microglia/metabolism/drug effects
Middle Aged
Aged

@article {pmid40639338,
year = {2025},
author = {Lesmana, I and Qian, C and Hsiao, EY},
title = {Fibromyalgia pain may have a gut solution.},
journal = {Neuron},
volume = {113},
number = {13},
pages = {2029-2031},
doi = {10.1016/j.neuron.2025.06.005},
pmid = {40639338},
issn = {1097-4199},
mesh = {*Fibromyalgia/therapy/microbiology ; Humans ; Animals ; *Fecal Microbiota Transplantation/methods ; *Gastrointestinal Microbiome ; Mice ; *Pain/microbiology ; },
abstract = {In this issue of Neuron, Cai et al.[1] demonstrated that transferring fecal microbiota from fibromyalgia patients to mice confers pain hypersensitivity and depression-like behavior, which is reversed by fecal microbiota transplant from healthy donors. Fibromyalgia patients experience significant symptom relief after fecal microbiota transplantation.},
}

*Fibromyalgia/therapy/microbiology
Humans
Animals
*Fecal Microbiota Transplantation/methods
*Gastrointestinal Microbiome
Mice
*Pain/microbiology

@article {pmid39172632,
year = {2025},
author = {Blount, KF and Papazyan, R and Ferdyan, N and Srinivasan, K and Gonzalez, C and Shannon, WD and Fuchs, BC},
title = {Microbiome and Metabolome Restoration After Administration of Fecal Microbiota, Live-jslm (REBYOTA) for Preventing Recurrent Clostridioides difficile Infection.},
journal = {The Journal of infectious diseases},
volume = {231},
number = {6},
pages = {e1022-e1033},
doi = {10.1093/infdis/jiae418},
pmid = {39172632},
issn = {1537-6613},
support = {//Rebiotix, Inc/ ; },
mesh = {Humans ; *Clostridium Infections/prevention & control/microbiology ; Male ; Female ; Double-Blind Method ; *Metabolome ; *Feces/microbiology ; Clostridioides difficile ; Middle Aged ; *Fecal Microbiota Transplantation/methods ; *Gastrointestinal Microbiome ; Adult ; Bile Acids and Salts/analysis ; Aged ; Dysbiosis/microbiology ; Treatment Outcome ; *Probiotics/administration & dosage ; },
abstract = {BACKGROUND: Microbiota-based treatments are effective in preventing recurrent Clostridioides difficile infection. Fecal microbiota, live-jslm (REBYOTA; RBL, previously RBX2660) was shown to prevent recurrent C difficile infection in a phase 3 clinical trial (PUNCH CD3) based on a randomized, double-blinded, placebo-controlled design.

METHODS: Stool samples from participants in PUNCH CD3 who received a single blinded dose of rectally administered RBL or placebo were sequenced to determine microbial community composition and calculate the Microbiome Health Index for postantibiotic dysbiosis. The composition of bile acids (BAs) in the same samples was quantified by liquid chromatography-mass spectrometry. Relationships between BA composition and microbiota community structure and correlations with treatment outcomes were assessed.

RESULTS: Before administration, Gammaproteobacteria and Bacilli dominated the microbiota community, and primary BAs were more prevalent than secondary BAs. Clinical success after administration correlated with shifts to predominantly Bacteroidia and Clostridia, a significant increase in Microbiome Health Index for postantibiotic dysbiosis, and a shift from primary to secondary BAs. Several microbiota and BA changes were more extensive in RBL-treated responders as compared with placebo-treated responders, and microbiota changes correlated with BA changes.

CONCLUSIONS: Clinical response and RBL administration were associated with significant restoration of microbiota and BA composition.

CLINICAL TRIALS REGISTRATION: NCT03244644 (https://clinicaltrials.gov/ct2/show/NCT03244644).},
}

Humans
*Clostridium Infections/prevention & control/microbiology
Male
Female
Double-Blind Method
*Metabolome
*Feces/microbiology
Clostridioides difficile
Middle Aged
*Fecal Microbiota Transplantation/methods
*Gastrointestinal Microbiome
Adult
Bile Acids and Salts/analysis
Aged
Dysbiosis/microbiology
Treatment Outcome
*Probiotics/administration & dosage

@article {pmid40639240,
year = {2025},
author = {Zhai, L and Zheng, Y and Lo, CW and Xu, S and Jiang, X and Liu, Q and Ching, JY and Ning, Z and Bao, G and Yang, W and Zhang, Q and Cheng, CW and Lam, WC and Chan, KL and Zhang, X and Lam, PY and Wu, XY and Zhong, LLD and Cao, PH and Koh, M and Cheong, PK and Lin, Z and Lin, C and Zhao, L and Wong, XHL and Wu, JC and Bian, Z},
title = {Butyrate-producing commensal bacteria mediates the efficacy of herbal medicine JCM-16021 on abdominal pain in diarrhea-predominant irritable bowel syndrome: a randomized clinical trial.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {145},
number = {},
pages = {157040},
doi = {10.1016/j.phymed.2025.157040},
pmid = {40639240},
issn = {1618-095X},
abstract = {BACKGROUND: Irritable bowel syndrome with diarrhea (IBS-D) presents significant treatment challenges due to limited therapeutic options that effectively target the underlying pathophysiological mechanisms. In this study, we performed a multi-center, double-blind randomized placebo-controlled trial to investigate the efficacy and safety of herbal medicine JCM-16021 on IBS-D with a focus on its effects on gut microbiota.

RESULTS: Our study assessed the clinical efficacy and safety of JCM-16021 in alleviating abdominal pain in IBS-D patients. The results suggested that JCM-16021 is both effective and safe, with its therapeutic effects closely linked to the modulation of short-chain fatty acid (SCFA) producers. Through fecal microbiota transplantation (FMT) experiments in mice, we showed that SCFA producers mediate the alleviation of abdominal pain symptoms by the JCM-16021 treatment. In a TNBS-induced mouse model of IBS, we showed that butyrate producers enriched by JCM-16021 significantly ameliorate abdominal pain. Importantly, baseline gut microbial profiles, such as the presence of Eubacterium rectale in IBS-D patients are predictive of their responses to JCM-16021 treatment.

CONCLUSIONS: Our findings not only affirm the efficacy of JCM-16021 in mitigating abdominal pain in IBS-D patients but also highlight a microbiota-dependent mechanism, underscoring the therapeutic potential of gut microbiota modulation in treating gastrointestinal disorders. By combining clinical trials in humans with biological experiments in mice, this study establishes a translational approach to investigate the role of gut microbiota in the treatment of herbal medicine.

CLINICALTRIALS: gov no: NCT03457324.},
}

@article {pmid40637385,
year = {2025},
author = {Yang, L and Yang, J and Zhang, T and Xie, X and Wu, Q},
title = {Gut microbiota: a novel strategy affecting atherosclerosis.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0048224},
doi = {10.1128/spectrum.00482-24},
pmid = {40637385},
issn = {2165-0497},
abstract = {Atherosclerosis is a common chronic inflammatory cardiovascular disease affecting both coronary and peripheral arteries, which is influenced by multiple factors. It is increasingly evident that gut microbes and their byproducts play a crucial role in the development of atherosclerosis. The most representative feature of microbial dysbiosis in coronary artery disease patients is the reduction of the abundance of the phylum Bacteroidetes and the increase of the abundance of the phylum Firmicutes, which may cause changes in functional genes and metabolites. The gut microbiota and its metabolites influence the early, intermediate, and late stages of atherosclerosis mainly by inhibiting or promoting inflammatory responses. In addition, the reshaping of gut microbiota through probiotics, prebiotics, and fecal microbiota transplantation (FMT) is discussed as an alternative to traditional therapeutic methods. By summarizing how gut microbiota and their metabolites affect the process of atherosclerosis, we can better understand the complex relationship between gut microbiota and atherosclerosis.IMPORTANCEAtherosclerosis is an inflammatory cardiovascular disease, making it crucial to understand its pathogenesis and develop effective treatments. This review thoroughly examines the literature, emphasizing the gut microbiome as a key factor influencing atherosclerosis. It also explores how the gut microbiota and its metabolites impact the primary, intermediate, and advanced stages of atherosclerosis and proposes that remodeling the gut microbiota is a promising strategy for improving atherosclerosis.},
}

@article {pmid40637175,
year = {2025},
author = {Fahim, SM and Huey, SL and Palma Molina, XE and Agarwal, N and Ridwan, P and Ji, N and Kibbee, M and Kuriyan, R and Finkelstein, JL and Mehta, S},
title = {Gut microbiome-based interventions for the management of obesity in children and adolescents aged up to 19 years.},
journal = {The Cochrane database of systematic reviews},
volume = {7},
number = {7},
pages = {CD015875},
pmid = {40637175},
issn = {1469-493X},
mesh = {Humans ; Adolescent ; Child ; Randomized Controlled Trials as Topic ; *Pediatric Obesity/therapy/microbiology ; *Gastrointestinal Microbiome ; Probiotics/therapeutic use ; Child, Preschool ; Young Adult ; Prebiotics/administration & dosage ; Synbiotics/administration & dosage ; Infant ; Fecal Microbiota Transplantation ; Body Mass Index ; Overweight/therapy ; },
abstract = {BACKGROUND: The epidemic of overweight and obesity affects more than 390 million children and adolescents aged 5 to 19 years and 37 million children under five years of age. Overweight and obesity are associated with both short- and long-term consequences, including chronic inflammation, metabolic diseases, as well as alterations in the gut microbiome composition. Gut microbiome-based approaches may impact microbiome-related metrics such as diversity or the abundance of intestinal bacteria, which may be linked to obesity-related outcomes. However, evidence regarding the effect of gut microbiome-based interventions for the management of obesity is limited.

OBJECTIVES: To assess the effects of gut microbiome-based interventions in the management of overweight or obesity in children and adolescents in all their diversity aged 0 to 19 years.

SEARCH METHODS: We searched CENTRAL, MEDLINE, CINAHL, Web of Science Core Collection, BIOSIS Previews, Global Index Medicus (all regions), IBECS, SciELO, PAHO, PAHO IRIS, WHO IRIS, WHOLIS, Bibliomap, TRoPHI as well as ICTRP Search Portal and ClinicalTrials.gov. The date of the last search for all databases was 24 January 2025. We did not apply any language restrictions.

SELECTION CRITERIA: We included randomised controlled trials that evaluated gut microbiome-based interventions [i.e. prebiotics, probiotics, synbiotics, short-chain fatty acids (SCFAs), and faecal microbiota transplantation (FMT)] compared to standard-of-care, placebo, or control interventions in children and adolescents aged 0 to 19 years with overweight or obesity.

DATA COLLECTION AND ANALYSIS: Two review authors independently screened titles and abstracts and full texts, extracted data, and assessed the risk of bias using the Cochrane Risk of Bias 2 tool and certainty of the evidence using Grading of Recommendations Assessment, Development and Evaluation (GRADE), a framework for assessing the certainty of evidence and making recommendations in systematic reviews. Random-effects meta-analyses were performed unless only one study per outcome was available, for which fixed-effect analyses were performed.

MAIN RESULTS: We found 17 studies (838 participants) from various countries, evaluating the effects of prebiotics, probiotics, synbiotics, SCFAs, and FMT on body mass index (BMI), body weight, waist circumference, total body fat percentage (%TBF), systolic and diastolic blood pressure, and adverse events. Of the 17 studies included, five studies were in adolescents aged 10 to 19 years, and 12 studies were in children and adolescents spanning both age groups, 0 to 19 years. Upon contacting authors for data grouped by age of the participants, no studies provided separate outcomes data for children and adolescents. The included studies were funded by either academic funding sources or grants from the public and private sectors. Additionally, 15 studies were classified as currently being conducted ('ongoing'). The certainty of evidence throughout was very low. In adolescents 10 to 19 years of age, probiotics compared to placebo or no intervention may have little to no effect on BMI, body weight, waist circumference, %TBF, blood pressure, and adverse events. Similarly, FMT compared to placebo may have little to no effect on waist circumference, %TBF, blood pressure, and adverse events in this age group. According to one study with 41 participants and in children and adolescents 0 to 19 years of age, intervention with prebiotics compared to placebo may result in a small reduction in BMI (mean difference = -0.70, 95% CI = -1.25 to -0.15) and body weight (mean difference = -1.5, 95% CI = -2.61 to -0.39). Prebiotics compared to placebo may have little to no effect on waist circumference, %TBF, systolic blood pressure, and adverse events. No data were available on the effect of prebiotics on diastolic blood pressure. Probiotics compared to placebo may have little to no effect on BMI, body weight, waist circumference, %TBF, blood pressure, and adverse events in children and adolescents (0 to 19 years). Synbiotics compared to placebo may result in a reduction in systolic blood pressure (mean difference = -40.00, 95% CI = -50.63 to -29.37) in children and adolescents (0 to 19 years); according to one study with 56 participants. The evidence is very uncertain about the effects of synbiotics compared to a placebo on BMI, body weight, waist circumference, blood pressure, and adverse events. No data were available on the effect of synbiotics compared to placebo on %TBF. Synbiotics, compared to probiotics, may have little to no effect on waist circumference, %TBF, and adverse events. No data were available on the effect of synbiotics compared to probiotics on BMI, body weight, and blood pressure. According to one study with 48 participants and very low-certainty of evidence, SCFAs compared to placebo may result in a reduction in waist circumference (mean difference = -5.08, 95% CI = -7.40 to -2.76) and BMI (mean difference = -2.26, 95% CI = -3.24 to -1.28) in children and adolescents (0-19 years). SCFAs compared to placebo may have little to no effect on adverse events. No data were available on the effect of SCFAs on body weight, %TBF, and blood pressure. Adverse events, i.e. abdominal cramps, abdominal discomfort, abdominal pain, diarrhoea, vomiting, and migraine, were reported in the prebiotics group but with very low incidence. Additionally, adverse events such as nausea and headache were reported in the SCFAs group, but with low incidence.

AUTHORS' CONCLUSIONS: In adolescents aged 10 to 19 years, gut microbiome-based interventions may result in little to no difference in obesity-related outcomes. In children and adolescents aged 0 to 19 years, prebiotics may result in a small reduction in BMI and body weight; synbiotics may result in a reduction in systolic blood pressure, and SCFAs may result in a reduction in BMI and waist circumference, albeit the certainty of evidence was very low. The evidence was of very low certainty due to few studies per comparison, small sample sizes, short intervention durations, and insufficient reporting of adverse events. More rigorous research examining different types of gut microbiome-based interventions for the management of obesity is required in children and adolescents, both in clinical and community settings. Future trials should also report methods related to randomisation, blinding, and compliance, as well as include prespecified analysis plans.},
}

Humans
Adolescent
Child
Randomized Controlled Trials as Topic
*Pediatric Obesity/therapy/microbiology
*Gastrointestinal Microbiome
Probiotics/therapeutic use
Child, Preschool
Young Adult
Prebiotics/administration & dosage
Synbiotics/administration & dosage
Infant
Fecal Microbiota Transplantation
Body Mass Index
Overweight/therapy

@article {pmid40635758,
year = {2025},
author = {Pan, J and Lin, S and Qian, Q and Fu, S and Liu, X},
title = {Gut-brain axis in post-traumatic stress disorder: microbial - mediated mechanisms and new therapeutic approaches - A narrative review.},
journal = {Frontiers in pharmacology},
volume = {16},
number = {},
pages = {1621678},
pmid = {40635758},
issn = {1663-9812},
abstract = {Post-traumatic stress disorder (PTSD) is a severe mental disorder that occurs after experiencing or witnessing a traumatic event. Not only does this disorder severely impair the quality of life and emotional wellbeing of patients, but in recent years the global rate of PTSD diagnoses has increased to 1.5-2 times, and the prevalence of PTSD associated with COVID-19 events in particular has surged to 10%-25%, underscoring the urgency of developing effective treatments. The lifetime prevalence of PTSD in the general population is estimated to be approximately 3.9%, while in high-risk populations, such as war veterans, it can be as high as 30%. As a key pathway connecting the central nervous system to peripheral organs, the gut-brain axis has received increasing attention for its role in PTSD. Although the gut-brain axis has been shown to be associated with several psychiatric disorders, especially depression, its specific role in PTSD remains undercharacterized. Existing studies suggest that specific strains of Lactobacillus (e.g., Lactobacillus reuteri) may alleviate inflammatory responses and improve PTSD-like behaviors by down-regulating the expression of pro-inflammatory factors (IL-6 and TNF-α). In this study, we used a narrative review approach to sort out the research progress of gut microbiota alteration in PTSD, and compared the characteristics of changes in specific microbial taxa (e.g., Bacteroides, Lactobacillus, etc.), the index of microbiota diversity (α/β diversity), and the levels of inflammatory markers (e.g., IL-6, TNF-α) between the animal model and the human patients, respectively, in order to We further explored the potential pathogenic mechanisms mediated by microorganisms, such as influencing the vagal pathway, hypothalamic-pituitary-adrenal (HPA) axis function, immune system and other processes involved in the pathology of PTSD, and summarized the intervention strategies targeting gut microecology, such as probiotic supplementation, dietary interventions and fecal bacteria transplantation.},
}

@article {pmid40635387,
year = {2025},
author = {Gragnaniello, V and Cananzi, M and Cavaliere, A and Loro, C and Cazzorla, C and Gueraldi, D and Puma, A and Burlina, AB},
title = {Early Enzyme Replacement Therapy Does Not Prevent the Protein Losing Enteropathy Syndrome in Neurovisceral Gaucher Disease.},
journal = {American journal of medical genetics. Part A},
volume = {},
number = {},
pages = {e64184},
doi = {10.1002/ajmg.a.64184},
pmid = {40635387},
issn = {1552-4833},
abstract = {Gaucher disease (GD) is a rare lysosomal storage disorder characterized by multisystemic involvement. With the advent of enzyme replacement therapy (ERT), patient survival has improved, revealing new long-term complications. We report a case of a 4-year-old male with severe neurovisceral GD who developed protein-losing enteropathy (PLE) secondary to mesenteric lymphadenopathy, despite ERT starting in the neonatal period. Furthermore, we review the literature related to this rare complication. The patient presented with severe recurrent diarrhea, abdominal distension, weight loss, and malnutrition. Abdominal CT revealed multiple enlarged mesenteric lymph nodes with calcification. Laboratory findings showed lymphopenia and increased fecal alpha-1-antitrypsin. Other causes of diarrhea were excluded. Treatment with a specific diet (high-protein, MCT-enriched) and a course of budesonide resulted in persistent clinical improvement and normalization of laboratory parameters. This case highlights the emergence of gastrointestinal complications in patients with neurovisceral GD on long-term ERT, particularly the development of PLE due to mesenteric lymphadenopathy. It underscores the need for vigilance in monitoring GD patients for such complications and demonstrates the potential efficacy of dietary interventions and anti-inflammatory therapy in managing PLE in this context. The case also emphasizes the limitations of current ERT in addressing all aspects of GD, particularly in sequestered sites like lymph nodes, and calls for new therapeutic strategies to address these challenges.},
}

@article {pmid40634307,
year = {2025},
author = {De Sciscio, M and Bryant, RV and Haylock-Jacobs, S and Day, AS and Pitchers, W and Iansek, R and Costello, SP and Kimber, TE},
title = {Faecal microbiota transplant in Parkinson's disease: pilot study to establish safety & tolerability.},
journal = {NPJ Parkinson's disease},
volume = {11},
number = {1},
pages = {203},
pmid = {40634307},
issn = {2373-8057},
support = {2021/23-QA253//Hospital Research Foundation/ ; 2021/23-QA253//Hospital Research Foundation/ ; 2021/23-QA253//Hospital Research Foundation/ ; },
abstract = {Emerging evidence suggests gut microbiota differences in Parkinson's Disease (PD) may impact disease progression and treatment. Faecal Microbiota Transplantation (FMT) offers a potential therapeutic approach. We conducted an open-label pilot study to assess the safety, tolerability, and symptom impact of FMT in 12 patients with mild to moderate PD, administered via enema for 6 months. FMT was safe and well tolerated, causing only mild, transient gastrointestinal symptoms. While no significant motor symptom changes were observed, there was a trend toward reduced daily OFF time at 2 months. Whilst no sustained improvement in non-motor symptoms was found after 6 months, transient improvements in quality of life and non-motor scores were noted at 2 months; these gains regressed by study end. Overall, extended FMT therapy in PD appears safe and tolerable, with reduction in daily motor OFF time and self-reported non-motor symptoms that was not sustained throughout the 6-months of treatment.},
}

@article {pmid40198765,
year = {2025},
author = {Saha, S and Rehman, L and Rehman, A and Darbaniyan, F and Weber, DM and Becnel, M and Gaballa, M and Thomas, SK and Lee, HC and Chang, CC and Arora, R and Menges, M and Corallo, S and Davila, ML and Locke, FL and Tanner, MR and Neelapu, SS and Shpall, EJ and Flowers, CR and Orlowski, RZ and Jenq, RR and Jain, MD and Peterson, C and Hansen, DK and Saini, NY and Patel, KK},
title = {Longitudinal analysis of gut microbiome and metabolome correlates of response and toxicity with idecabtagene vicleucel.},
journal = {Blood advances},
volume = {9},
number = {14},
pages = {3429-3440},
doi = {10.1182/bloodadvances.2024014476},
pmid = {40198765},
issn = {2473-9537},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Metabolome ; *Immunotherapy, Adoptive/adverse effects/methods ; Male ; Female ; Middle Aged ; Aged ; Longitudinal Studies ; Feces/microbiology ; Receptors, Chimeric Antigen ; },
abstract = {Increasing evidence suggests that the gut microbiome may influence the responses and toxicities associated with chimeric antigen receptor T-cell (CAR-T) therapy. We conducted whole-genome shotgun sequencing on stool samples (N = 117) collected at various times from patients with multiple myeloma (n = 33) who underwent idecabtagene vicleucel (ide-cel) anti-B-cell maturation antigen CAR-T therapy. We observed a significant decrease in bacterial diversity after ide-cel infusion, along with significant differences in the bacterial composition linked to therapy response and toxicities. Specifically, we found significant enrichment of Flavonifractor plautii, Bacteroides thetaiotaomicron, Blautia fecis, and Dysosmobacter species in ide-cel responders. A notable finding was the link of major microbiome disruption, defined as the presence of dominant specific taxa (>35% prevalence), and increased facultative pathobionts, like Enterococcus, with ide-cel toxicities, especially cytokine release syndrome (CRS). Patients with genus dominance in baseline samples had a higher incidence of grade 2 or higher CRS at 46.2% than those without genus dominance (11.1%; P = .043). In addition, network analysis and mass spectrometric assessment of stool metabolites revealed important associations and pathways, such as F plautii being linked to increased indole metabolites and pathways in responders. Our findings uncovered novel microbiome associations between ide-cel responses and toxicities that may be useful for developing modalities to improve CAR-T outcomes.},
}

Humans
*Gastrointestinal Microbiome
*Metabolome
*Immunotherapy, Adoptive/adverse effects/methods
Male
Female
Middle Aged
Aged
Longitudinal Studies
Feces/microbiology
Receptors, Chimeric Antigen

@article {pmid40634168,
year = {2025},
author = {Lee, PC and Chang, TE and Wang, YP and Lee, KC and Lin, YT and Yang, UC and Huang, HC and Huang, YH and Luo, JC and Hou, MC},
title = {Response to commentary on 'Alteration of gut microbial composition associated with the therapeutic efficacy of fecal microbiota transplantation in Clostridium difficile infection'.},
journal = {Journal of the Formosan Medical Association = Taiwan yi zhi},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jfma.2025.05.037},
pmid = {40634168},
issn = {0929-6646},
}

@article {pmid40632357,
year = {2025},
author = {Arif, TB and Damianos, JA and Rahman, AU and Hasnain, N},
title = {Fecal Microbiota Transplantation for Disorders of Gut-Brain Interaction: Current Insights, Effectiveness, and Future Perspectives.},
journal = {Current gastroenterology reports},
volume = {27},
number = {1},
pages = {50},
pmid = {40632357},
issn = {1534-312X},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; *Dysbiosis/therapy/complications/microbiology ; *Gastrointestinal Microbiome ; *Brain-Gut Axis ; *Gastrointestinal Diseases/therapy/microbiology ; },
abstract = {PURPOSE OF REVIEW: Dysbiosis can disrupt intestinal barrier integrity and impact the immune and nervous systems, playing a significant role in developing disorders of gut-brain interaction (DGBI). This review aims to provide a comprehensive understanding of dysbiosis and its role in DGBI while examining the latest advancements in fecal microbiota transplantation (FMT). It also highlights key challenges in the field and outlines critical directions for future research to optimize FMT strategies, ultimately improving patient outcomes in this evolving treatment area.

RECENT FINDINGS: In DGBI, dysbiosis triggers immune responses, increases gut permeability, and disrupts nervous system signaling, with contributing factors including diet, antibiotics, stress, and infections. Individuals with DGBI exhibit distinct microbial imbalances, such as an increased Firmicutes-to-Bacteroidetes ratio and reduced beneficial bacteria. FMT has shown mixed results, with factors like patient selection, treatment protocols, and microbiome diversity influencing outcomes. While FMT can improve symptoms in refractory irritable bowel syndrome (IBS), effects may fade over time, requiring repeat treatments. Future FMT approaches should focus on targeted microbial interventions, considering the role of archaea, fungi, and microbial metabolites, while prioritizing optimal donor selection and large-scale trials for long-term efficacy. Despite the promising findings, FMT has not yet been widely endorsed in clinical guidelines due to the variability and heterogeneity of the data available. While much of the research has focused on IBS, studies have also explored the impact of FMT on other conditions such as functional diarrhea, functional constipation, and functional dyspepsia, which all exhibit altered microbial profiles.},
}

Humans
*Fecal Microbiota Transplantation/methods
*Dysbiosis/therapy/complications/microbiology
*Gastrointestinal Microbiome
*Brain-Gut Axis
*Gastrointestinal Diseases/therapy/microbiology

@article {pmid40631858,
year = {2025},
author = {Qu, S and Gu, Y and Hou, X and Wei, M and Wang, M and Su, Y and Miao, Y and Yang, J and Sun, Y and Zeng, Z},
title = {Dual associations of gut and oral microbial networks with kidney transplantation.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0025225},
doi = {10.1128/msystems.00252-25},
pmid = {40631858},
issn = {2379-5077},
abstract = {UNLABELLED: Gut and oral microbiomes play an essential role in the occurrence and development of kidney disease, but their changes after kidney transplantation in patients with end-stage renal disease and their relationships with host health remain unclear. Through shotgun metagenomic sequencing of fecal and saliva samples, we found that for both gut and oral microbiome, the initial loss of species diversity after kidney transplantation led to a reduction in network nodes and interactions, but strengthened the connections among the remaining species, which started to get a recovery approximately 7-14 days later. Different network modules tended to exhibit unique functions and showed different responses to transplantation. These network changes were significantly correlated with clinical indicators, especially with estimated glomerular filtration rate, suggesting that microbial networks contributed to regulating kidney function and host health from dual dimensions. Our study provides novel insights into associating microbiomes with patient recovery after kidney transplantation and offers new diagnostic strategies.

IMPORTANCE: Understanding the dynamics of gut and oral microbiomes after kidney transplantation is crucial for improving post-transplant outcomes and managing potential complications. Through shotgun metagenomic sequencing of fecal and saliva samples from patients following kidney transplantation, our study emphasizes that, in addition to focusing on the various microbial species themselves, the topological properties of gut and oral microbial networks are also critically important for kidney function. We aim to explore the relationship between host health and the oral and gut microbiomes following kidney transplantation from an ecological perspective and extend to other diseases to advance the study of the microbiome and its clinical impact.},
}

@article {pmid40630283,
year = {2025},
author = {Ness, C and Svistounov, D and Solbu, MD and Petrenya, N and Boardman, N and Ytrehus, K and Jenssen, TG and Holmes, A and Simpson, SJ and Zykova, SN},
title = {Gut Microbiome Diversity and Uric Acid in Serum and Urine.},
journal = {Kidney international reports},
volume = {10},
number = {6},
pages = {1683-1693},
pmid = {40630283},
issn = {2468-0249},
abstract = {INTRODUCTION: An increasing body of evidence has shown the importance of the gut microbiota in modulating serum uric acid (SUA) levels. In this study, we aimed to determine the association between gut microbiome diversity, diet, SUA, and fractional excretion of uric acid (FEUA) in the kidney.

METHODS: A cross-sectional study was conducted in 53 adults with normal or elevated SUA and estimated glomerular filtration rate (eGFR) range from 37 to 124 ml/min per 1.73 m[2]. Fecal microbiome composition was analyzed using 16S ribosomal RNA sequencing; and alpha diversity was expressed as reverse Simpson, Shannon, and Richness indices. Dietary data were collected, and dietary patterns were identified using principal component analysis. Unadjusted linear regression and models adjusted for sex, waist-hip ratio (WHR), and eGFR were used to study the association between gut microbial diversity, dietary pattern scores, and SUA/FEUA.

RESULTS: Shannon index was negatively associated with SUA after multiple adjustment (β -36.4, 95% CI [-66.2 to -6.7], P = 0.017; adjusted R[2] = 0.62, P < 0.001). Sex (standardized β = 0.52) and WHR (standardized β = 0.35) had the highest effect on SUA, followed by Shannon diversity index (standardized β = -0.22). We found that Shannon index (standardized β = 0.49, P < 0.001) was positively associated with FEUA after adjustment for sex and "sweet" dietary pattern. This model explained 40% of the variability in FEUA (P < 0.001). None of the dietary patterns were associated with SUA or FEUA.

CONCLUSION: A higher gut microbial diversity was associated with lower SUA and more efficient elimination of uric acid by the kidneys. There is a need for studies assessing efficacy and safety of interventions on the gut microbiome as a treatment of hyperuricemia.},
}

@article {pmid40630180,
year = {2025},
author = {Zhang, Z and Wang, R and Li, M and Lu, M},
title = {Current insights and trends in atopic dermatitis and microbiota interactions: a systematic review and bibliometric analysis.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1613315},
pmid = {40630180},
issn = {1664-302X},
abstract = {BACKGROUND: Atopic dermatitis (AD) is a prevalent chronic inflammatory skin condition influenced by immune dysfunction, genetics, and environmental factors, with emerging evidence highlighting the critical role of skin and gut microbiota in its pathogenesis. This article uniquely integrates a systematic review with bibliometric analysis to map the research landscape of AD and microbiota interactions, offering a comprehensive synthesis of trends and future directions.

METHODS: We conducted a bibliometric analysis using the Web of Science Core Collection, retrieving 1,196 English-language articles and reviews published between 2009 and 2024, employing a detailed search strategy targeting AD and microbiota-related terms. Data were analyzed with tools like CiteSpace, VOSviewer, and Biblioshiny to assess publication trends, geographical contributions, institutional outputs, journal impacts, author networks, reference citations, and keyword evolution.

RESULTS: Research on AD and microbiota has surged since 2016, peaking at 168 publications in 2021, with the USA leading in output (360 papers) and citations (24,655). The University of Copenhagen and the Journal of Allergy and Clinical Immunology emerged as top contributors, while authors like Gallo, Richard L., and Kong, Heidi H. drove influential studies. Key findings underscore the skin and gut microbiomes as research hotspots, with Staphylococcus aureus and the gut-skin axis dominating discussions. Emerging trends from 2020 to 2024 focus on adult AD severity, prebiotics, and personalized interventions like fecal microbiota transplantation (FMT), supported by multi omics data.

CONCLUSION: This study illuminates the dynamic growth and global collaboration in AD and microbiota research, emphasizing microbial dysbiosis and immune modulation as pivotal to AD management. These insights pave the way for precision medicine and dietary interventions, promising enhanced therapeutic strategies and improved patient outcomes through continued multidisciplinary efforts.},
}

@article {pmid40625834,
year = {2025},
author = {Xie, W and Yan, X and Yang, X and Sun, H and Zhang, W},
title = {The regulation of neuroinflammatory response after stroke by intestinal flora microorganisms.},
journal = {Frontiers in cellular and infection microbiology},
volume = {15},
number = {},
pages = {1594834},
pmid = {40625834},
issn = {2235-2988},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; Animals ; Probiotics/therapeutic use ; *Neuroinflammatory Diseases/immunology/therapy/microbiology ; Fecal Microbiota Transplantation ; *Stroke/immunology/microbiology ; Brain-Gut Axis/immunology ; Immunity, Innate ; Brain/immunology ; Prebiotics/administration & dosage ; Adaptive Immunity ; Inflammation ; Blood-Brain Barrier ; Anti-Bacterial Agents/therapeutic use ; },
abstract = {Ischemic stroke (IS) is a severe central nervous system disorder characterized by high incidence, disability, mortality, and recurrence rates, along with numerous complications. The microbiota-gut-brain axis (MGBA) represents a bidirectional communication pathway between the brain and the gut, which can influence the onset and progression of IS through neural, immunoregulatory, and gut metabolite pathways. Recent preclinical and clinical evidence supports the use of fecal microbiota transplantation (FMT), probiotics and prebiotics, dietary interventions, and antibiotics as strategies to suppress neuroinflammation in IS, protect the blood-brain barrier, modulate immune responses, and improve stroke outcomes. In this review, we summarize the manifestations of innate inflammation and adaptive immunity following the onset of IS, highlight the interactions between the MGBA and post-stroke neuroinflammation, and discuss current therapeutic measures, thus providing insights for the development of novel treatment strategies in the future.},
}

Humans
*Gastrointestinal Microbiome/immunology
Animals
Probiotics/therapeutic use
*Neuroinflammatory Diseases/immunology/therapy/microbiology
Fecal Microbiota Transplantation
*Stroke/immunology/microbiology
Brain-Gut Axis/immunology
Immunity, Innate
Brain/immunology
Prebiotics/administration & dosage
Adaptive Immunity
Inflammation
Blood-Brain Barrier
Anti-Bacterial Agents/therapeutic use

@article {pmid40388103,
year = {2025},
author = {Dukaew, N and Noppakun, K and Thongkumkoon, P and Na Takuathung, M and Inpan, R and Kongta, N and Suyayai, N and Manoree, C and Koonrungsesomboon, N},
title = {Associations between the gut microbiota and the metabolism rate of tacrolimus in kidney transplant recipients during the early posttransplant period.},
journal = {Archives of pharmacal research},
volume = {48},
number = {6},
pages = {549-562},
pmid = {40388103},
issn = {1976-3786},
support = {1196/2564//Kidney Foundation of Thailand/ ; 115-2564//Faculty of Medicine, Chiang Mai University/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/physiology/drug effects ; *Tacrolimus/pharmacokinetics/metabolism ; *Kidney Transplantation ; *Immunosuppressive Agents/pharmacokinetics/metabolism/administration & dosage ; Male ; Female ; Middle Aged ; Adult ; Feces/microbiology ; RNA, Ribosomal, 16S/genetics ; },
abstract = {The use of tacrolimus (TAC), a critical immunosuppressant post transplantation, is complicated by its high pharmacokinetic variability. While the gut microbiota has gained attention as a potential contributor, few studies have assessed its role in TAC metabolism variability. This study investigated the associations between the gut microbiota and TAC metabolism rates in kidney transplant recipients during the first month post transplantation-a crucial period for adjusting TAC to achieve therapeutic levels. We recruited 20 kidney transplant recipients and profiled their gut microbiota diversity and composition from stool samples collected before transplantation and at weeks 1 and 4 post transplantation via 16S rRNA sequencing. The TAC pharmacokinetic parameters were also collected. Associations between TAC metabolism status or pharmacokinetic parameters and gut microbiota diversity and composition were evaluated. Recipients with a fast TAC metabolism rate (C0/D ratio < 1.05 ng/mL × 1/mg) presented significantly greater changes in both bacterial alpha and beta diversity metrics at 1 week post transplantation than did those with a slow metabolism rate (C0/D ratio ≥ 1.05 ng/mL × 1/mg). Compared with slow metabolizers, fast metabolizers were associated with a significant increase in the abundance of three bacterial genera (Faecalibacterium, Clostridia vadinBB60, and Ruminococcus) and a significant decrease in the abundance of two bacterial species (Bacteroides plebeius and Parabacteroides goldsteinii). This study revealed links between gut microbiota diversity and composition and TAC metabolism rates in kidney transplant recipients during the early posttransplant period, underscoring the importance of investigating the gut microbiota as a contributor to TAC pharmacokinetic variability. Clarifying this causal relationship could better predict inter- and intraindividual TAC pharmacokinetic variability.},
}

Humans
*Gastrointestinal Microbiome/physiology/drug effects
*Tacrolimus/pharmacokinetics/metabolism
*Kidney Transplantation
*Immunosuppressive Agents/pharmacokinetics/metabolism/administration & dosage
Male
Female
Middle Aged
Adult
Feces/microbiology
RNA, Ribosomal, 16S/genetics

@article {pmid40625618,
year = {2025},
author = {Hu, Y and Zheng, S and Xu, J and Zhao, Y and Wang, J and Fang, Z and Zhou, L},
title = {Gestational diabetes mellitus alters neonatal gut microbiota and increases infection susceptibility.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1600325},
pmid = {40625618},
issn = {1664-302X},
abstract = {INTRODUCTION: Gestational diabetes mellitus (GDM) affects up to 27.6% of pregnancies in certain regions and is associated with a two- to threefold increased risk of neonatal infections. Although maternal gut microbiota undergoes significant remodeling during pregnancy, the specific mechanisms governing GDM-induced microbial reprogramming in offspring and its implications for susceptibility to infections remain unclear. This study aimed to investigate the impact of GDM on the composition of neonatal gut microbiota, metabolomic profiles, and susceptibility to infections using a translational approach.

METHOD: We recruited pregnant women with and without GDM at the JinHua Municipal Central Hospital in China. Meconium and blood samples were collected from newborns within 24 h of birth. The composition of the gut microbiota was analyzed using 16S rDNA amplicon sequencing, and short-chain fatty acids (SCFAs) were quantified using gas chromatography-mass spectrometry. Serum inflammatory markers, including interleukin-6 (IL-6), C-reactive protein (CRP), lipopolysaccharides (LPS), and procalcitonin (PCT), were measured by enzyme-linked immunosorbent assay. To establish causality, fecal microbiota transplantation (FMT) was conducted in antibiotic-treated mice using pooled samples from healthy and GDM-exposed neonates, followed by assessment of inflammatory markers and intestinal barrier integrity.

RESULTS AND DISCUSSION: GDM significantly reduced the diversity of neonatal gut microbiota and altered its composition, characterized by a depletion of beneficial taxa (Bifidobacterium, Blautia, Faecalibacterium) and an enrichment of potential pathogens (Stenotrophomonas, Chryseobacterium). These alterations were accompanied by significant reductions in fecal SCFAs, particularly acetate (49.30%), butyrate (41.00%), and propionate (17.83%). GDM-exposed neonates exhibited elevated serum inflammatory markers, including IL-6, CRP, LPS, and PCT, which correlated negatively with beneficial bacteria and positively with opportunistic pathogens. FMT experiments demonstrated that mice receiving GDM-associated microbiota developed increased systemic inflammation and compromised intestinal barrier function, as evidenced by the downregulation of tight junction proteins (ZO-1, occludin, claudin-1, mucin1). These findings suggest that GDM-induced alterations in neonatal gut microbiota composition and metabolite production may compromise intestinal barrier function and increase susceptibility to infections, highlighting the potential for microbiome-targeted interventions to mitigate infection risk in GDM-exposed neonates.},
}

@article {pmid40625306,
year = {2025},
author = {Wu, J and Xiang, J and Song, P and Bai, Y and Che, Q and Cao, H and Guo, J and Su, Z},
title = {GOS-Modulated Gut Microbiota in Mice Ameliorates Obesity in High-Fat Diet-Fed Mice Through the Gut-Liver Axis and Bile Acid Pathway.},
journal = {Journal of food science},
volume = {90},
number = {7},
pages = {e70361},
doi = {10.1111/1750-3841.70361},
pmid = {40625306},
issn = {1750-3841},
support = {202103000089//the Science and Technology Program of Guangzhou, China/ ; //the Guangdong Demonstration BASe for Joint Cultivation of Postgraduates (2023)/ ; 2020B1515020026//the Science Foundation for Distinguished Young Scholars of Guangdong, China/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Bile Acids and Salts/metabolism ; Diet, High-Fat/adverse effects ; *Obesity/metabolism/microbiology ; Mice ; *Liver/metabolism/drug effects ; Mice, Inbred C57BL ; Male ; Lipid Metabolism/drug effects ; *Oligosaccharides/pharmacology/administration & dosage ; Fibroblast Growth Factors/metabolism ; Signal Transduction/drug effects ; Feces/microbiology ; Mice, Obese ; },
abstract = {This work is meant to study the effect of galacto-oligosaccharide (GOS) intervention in the fecal microbiota of obese mice on lipid metabolism and anti-obesity in mice. A pseudo-germ-free mice model was established by administration of a mixture of antibiotics. The fecal microbiota of GOS-fed obese mice are transplanted into pseudo-germ-free mice. To investigate the effects of GOS intervention on lipid metabolism, lipid quadruple, bile acid metabolism, and intestinal microbiota in obese mice. At the same time, the expression of BAS synthase and the effects of FXR-SHP and FXR-FGF15-FGFR4 signaling pathways on BAS homeostasis were also explored. The fecal microbiota of obese mice intervened by GOS could reshape the structure of intestinal microbiota, regulate the synthesis of bile acids in the enterohepatic circulation and the expression of transport-related factors, and promote metabolic ability to exert anti-obesity effects.},
}

Animals
*Gastrointestinal Microbiome/drug effects
*Bile Acids and Salts/metabolism
Diet, High-Fat/adverse effects
*Obesity/metabolism/microbiology
Mice
*Liver/metabolism/drug effects
Mice, Inbred C57BL
Male
Lipid Metabolism/drug effects
*Oligosaccharides/pharmacology/administration & dosage
Fibroblast Growth Factors/metabolism
Signal Transduction/drug effects
Feces/microbiology
Mice, Obese

@article {pmid40624229,
year = {2025},
author = {Lau, HC and Zhang, X and Yu, J},
title = {Gut microbiome in metabolic dysfunction-associated steatotic liver disease and associated hepatocellular carcinoma.},
journal = {Nature reviews. Gastroenterology & hepatology},
volume = {},
number = {},
pages = {},
pmid = {40624229},
issn = {1759-5053},
abstract = {Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent chronic liver disease worldwide, affecting billions of the global population. It can gradually progress to more severe diseases, including steatohepatitis, cirrhosis and hepatocellular carcinoma. Studies have highlighted the importance of the gut microbiome in the pathogenesis and progression of MASLD. On the other hand, increasing evidence has revealed the clinical potential of targeting the gut microbiome to treat MASLD. In this Review, we summarize gut microbial alterations in MASLD, metabolic dysfunction-associated steatohepatitis and hepatocellular carcinoma. The mechanisms by which a dysregulated gut-liver axis contributes to disease progression are also described, including intestinal barrier dysfunction, chronic inflammation, and altered metabolic pathways (for example, bile acids) and microbial-derived metabolites (for example, short-chain fatty acids, tryptophan derivatives and endogenous ethanol). In addition, we discuss the clinical implications of utilizing the gut microbiome as a diagnostic biomarker and the therapeutic approaches to treat MASLD and related diseases such as faecal microbiota transplantation, probiotics and engineered bacteria, prebiotics and postbiotics, microbial-derived metabolites, antimicrobials and bacteriophages. Finally, we discuss current challenges in basic and translational research on the microbiome in MASLD and propose future directions to drive progress in this field.},
}

@article {pmid40623769,
year = {2025},
author = {Basoya, R and Singh, B and Basi, A and Aggarwal, S},
title = {Role of microbiome in cancer progression.},
journal = {International review of cell and molecular biology},
volume = {394},
number = {},
pages = {79-106},
doi = {10.1016/bs.ircmb.2024.12.013},
pmid = {40623769},
issn = {1937-6448},
mesh = {Humans ; *Neoplasms/microbiology/pathology/therapy ; *Disease Progression ; *Microbiota ; Animals ; },
abstract = {The human microbiome plays a crucial role in maintaining health and preventing disease. Dysbiosis, or imbalance, in the microbiome, has been linked to various diseases, including cancer. This chapter explores the influence of microbiomes on different organs, immune system modulation, and cancer development. Specific microorganisms, such as Helicobacter pylori, Escherichia coli, and human papillomavirus (HPV), contribute to gastric, colorectal, and cervical cancer through mechanisms like immunomodulation and proliferative signaling pathways. Dysbiosis-induced cancer progression involves NF-κB, Wnt/β-catenin, and JAK/STAT signaling. Recent studies highlight the microbiome's potential in cancer diagnosis and immunotherapy. Fecal Microbiota Transplantation (FMT) and predictive biomarkers, such as Porphyromonas gingivalis and Escherichia-Shigella, show promise in treating colorectal cancer. The microbiome influences tumor biology and immune response, affecting immunotherapeutic efficacy. Understanding microbiome-cancer interactions offers new opportunities for improved diagnosis and personalized therapy. This chapter provides comprehensive insights into the role of microbiome in cancer progression, emphasizing the importance of microbiome research in developing effective cancer treatments.},
}

Humans
*Neoplasms/microbiology/pathology/therapy
*Disease Progression
*Microbiota
Animals

@article {pmid40621498,
year = {2025},
author = {Chong, J and Zhou, Y and Li, Z and Li, X and Zhang, J and Cao, H and Ma, J and Ge, L and Zhong, H and Sun, J},
title = {Hyodeoxycholic acid modulates gut microbiota and bile acid metabolism to enhance intestinal barrier function in piglets.},
journal = {Frontiers in veterinary science},
volume = {12},
number = {},
pages = {1610956},
pmid = {40621498},
issn = {2297-1769},
abstract = {Oral bile acids, particularly hyodeoxycholic acid (HDCA), serve as critical drivers for gut microbial community maturation in mice. In the first study, Cy5-labeled HDCA combined with fluorescence imaging revealed rapid gastrointestinal transit of HDCA in piglets, contrasting with its delayed absorption observed in mice. In the second study, the effects of the oral HDCA supplementation on microbiota-host metabolic interactions were investigated using four piglet model groups: OPM-HDCA (naturally born, raised germ-free (GF), and orally administered HDCA), OPM-CON (naturally born, raised GF, and orally administered PBS), SPF-HDCA (naturally born, raised GF, and received fecal microbiota transplantation (FMT) and HDCA), and SPF-CON (naturally born, raised GF with FMT but no HDCA). The results demonstrated that HDCA administration at 0.2 mg/mL suppressed body weight gain in piglets, which was alleviated by FMT. HDCA significantly altered gut microbiota composition in SPF piglets, markedly increasing the Lactobacillus abundance (37.97% vs. 5.28% in SPF-CON) while decreasing the proportion of Streptococcus (28.34% vs. 38.65%) and pathogenic family Erysipelotrichaceae (0.35% vs. 17.15%). Concurrently, HDCA enhanced intestinal barrier integrity by upregulating tight junction proteins (ZO-1, Claudin, Occludin) and suppressing pro-inflammatory cytokines (TNF-α, IL-1β). Additionally, HDCA significantly upregulated ileal gene expression of CYP7A1 (cytochrome P450 family 7 subfamily A member 1) and TGR5 (G protein-coupled bile acid receptor 1) in both SPF-HDCA and OPM-HDCA groups compared to their respective controls (p < 0.05). These findings demonstrate that HDCA exerts microbiota-dependent effects on growth performance, intestinal barrier function, and bile acid metabolism in piglets. Although 0.2 mg/mL HDCA treatment suppressed body weight gain, it potentially enhanced intestinal barrier integrity by activating the TGR5 signaling pathway and increasing the abundance of beneficial bacteria such as Lactobacillus. These results also highlight the critical role of early-life gut microbiota in nutritional interventions, providing a basis for developing precision nutritional strategies targeting intestinal microbial ecology in piglets.},
}

@article {pmid40620607,
year = {2025},
author = {Liu, J and Chen, Y and Wan, Q},
title = {Immune Cell Characteristics in a Gut-Kidney Axis-Induced Mouse Model of IgA Nephropathy: The Upregulated Dendritic Cells and Neutrophils.},
journal = {Journal of inflammation research},
volume = {18},
number = {},
pages = {8579-8592},
pmid = {40620607},
issn = {1178-7031},
abstract = {BACKGROUND: IgA nephropathy (IgAN) is the leading type of primary glomerulonephritis, significantly contributing to chronic kidney disease (CKD) and renal failure. The pathogenesis of IgAN is the multi-hit hypothesis regarding overproduction and accumulation of galactose-deficient (Gd-IgA1). Recent findings have revealed gut microbiota dysbiosis and immune responses are essential in the development of IgAN, attracting increasing attention. This study aimed to map mucosal immune cells in IgAN influenced by gut microbiota, investigating the role of innate immune cells in kidney damage.

METHODS: Fecal samples were acquired from both patients and controls for subsequent animal experiments. Mice received a broad-spectrum antibiotic cocktail to eliminate their intestinal microflora, followed by a gavage with fecal microbiota from clinical individuals. Murine intestinal and kidney tissues were collected for flow cytometry. Intestine and kidney histopathology, immunofluorescence, and inflammatory cytokine expression were assessed in the murine models. The mucosal epithelium's structure and function, along with the innate immune cell response, were analyzed.

RESULTS: Mice exhibited the IgAN phenotype following colonization with gut microbiota from IgAN patients. These mice (IgAN-FMT mice) showed renal dysfunction and increased pathology of tissue injury in both intestine and kidneys. IgAN-FMT mice showed heightened pro-inflammatory cytokine (IL-6 and TNF-α) activity, greater antibody (IgA and complement C3) deposition and decreased expression of mucosal barrier protein (ZO-1, Occludin) compared to the control group. Furthermore, CD11c[+]dendritic cells were more abundant in the murine intestine and kidneys compared to the control group.

CONCLUSION: The gut-kidney axis, including microbiota homeostasis and innate immune cell response, contributes to the pathogenesis of IgAN. Gut dysbiosis and hyperactivated immune cells like CD11c[+]dendritic cells can affect the mucosal barrier and exacerbate the renal damage, being novel insights into immunotherapeutic strategies for IgAN.},
}

@article {pmid40620312,
year = {2025},
author = {Sopel, A and Szczuciński, W and Gosiewski, T and Salamon, D},
title = {The role of fecal microbiota transplantation in selected neurodegenerative diseases and neurodevelopmental disorders.},
journal = {Przeglad gastroenterologiczny},
volume = {20},
number = {2},
pages = {127-141},
pmid = {40620312},
issn = {1895-5770},
abstract = {Fecal microbiota transplantation (FMT) is a medical procedure that allows to establish a stable and healthy intestinal microbiota in various diseases believed to be related to a gut dysbiosis. Currently, FMT is successfully used to treat recurrent Clostridioides difficile infection. However, in recent years there has been evidence that changes in composition of gut microbiota may also be relevant in the pathogenesis of several neuropsychiatric and neurodevelopmental conditions including Alzheimer's disease, multiple sclerosis, Parkinson's disease, autism spectrum disorders and schizophrenia. This review focuses on exploring the complex connection between gut microbiota and pathogenesis of these neurological conditions. It also presents current research on a possible use of FMT as a therapeutic intervention targeting the gut-brain axis.},
}

@article {pmid40619214,
year = {2025},
author = {Bai, X and Ihara, E and Tanaka, Y and Minoda, Y and Wada, M and Hata, Y and Esaki, M and Ogino, H and Chinen, T and Ogawa, Y},
title = {The interplay of gut microbiota and intestinal motility in gastrointestinal function.},
journal = {Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi},
volume = {61},
number = {},
pages = {51-58},
doi = {10.1540/jsmr.61.51},
pmid = {40619214},
issn = {1884-8796},
mesh = {Humans ; *Gastrointestinal Motility/physiology ; *Gastrointestinal Microbiome/physiology ; Bile Acids and Salts/metabolism ; Animals ; Irritable Bowel Syndrome/microbiology/physiopathology/therapy ; Probiotics/therapeutic use ; *Gastrointestinal Tract/microbiology/physiology ; Interstitial Cells of Cajal/physiology ; Fecal Microbiota Transplantation ; Prebiotics ; Constipation/microbiology ; Gastrointestinal Diseases/microbiology/therapy ; Fatty Acids, Volatile/metabolism ; },
abstract = {The relationship between gut microbiota and intestinal motility is crucial for maintaining gastrointestinal health. Intestinal motility refers to the coordinated movements of the digestive tract, essential for effective digestion, nutrient absorption, and timely waste elimination. Recent studies have demonstrated that microbiota play a crucial role not only in the maturation of intestinal motility but also in the ongoing maintenance of established motility patterns. Disruptions in motility can lead to various disorders, such as chronic constipation, irritable bowel syndrome, and chronic idiopathic pseudo-obstruction. Gut microbiota significantly influence intestinal motility through mechanisms like bile acid metabolism and the production of short-chain fatty acids. In patients with diarrhea-predominant irritable bowel syndrome, elevated primary-to-secondary bile acid ratios suggest a complex interaction between gut bacteria and bile acids that can enhance motility via receptors like TGR5. Additionally, the role of interstitial cells of Cajal in facilitating non-neuronal contractions has revolutionized our understanding of motility regulation, highlighting both neural and non-neural factors. Various therapeutic approaches, including prebiotics, probiotics, and fecal microbiota transplantation, have been explored to improve intestinal motility, although their effectiveness has been limited. Advancements in gene-related research and innovative diagnostic methods are vital for a deeper understanding of how the gut microbiome regulates motility. This review synthesizes current knowledge on the interplay between gut microbiota and intestinal motility, emphasizing the need for interdisciplinary research to develop effective treatments targeting gut microbiota for gastrointestinal disorders. By unraveling these complex interactions, we can pave the way for novel therapeutic strategies that enhance intestinal health and improve the quality of life for those affected by motility-related disorders.},
}

Humans
*Gastrointestinal Motility/physiology
*Gastrointestinal Microbiome/physiology
Bile Acids and Salts/metabolism
Animals
Irritable Bowel Syndrome/microbiology/physiopathology/therapy
Probiotics/therapeutic use
*Gastrointestinal Tract/microbiology/physiology
Interstitial Cells of Cajal/physiology
Fecal Microbiota Transplantation
Prebiotics
Constipation/microbiology
Gastrointestinal Diseases/microbiology/therapy
Fatty Acids, Volatile/metabolism

@article {pmid40618491,
year = {2025},
author = {Tian, Y and Meng, J and Zhang, D and Zhai, B and Cheng, J and Zou, J and Shi, Y and Guo, D},
title = {Wendan Decoction exerts therapeutic effects on insomnia by regulating gut microbiota and tryptophan metabolism.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {145},
number = {},
pages = {157028},
doi = {10.1016/j.phymed.2025.157028},
pmid = {40618491},
issn = {1618-095X},
abstract = {BACKGROUND: Insomnia has been a public problem threatening human health. Wendan Decoction (WDD) has good therapeutic effects on insomnia. However, its mechanism to improve sleep remains unclear.

PURPOSE: To investigate the potential mechanism of WDD in treating insomnia from the perspective of gut microbiota and metabolism.

METHODS: The chemical composition of WDD was analyzed by UHPLCOrbitrap Exploris/MS. The efficacy of WDD on PCPA-induced insomnia rats was evaluated through behavioral tests, ELISA, histopathological examination, immunofluorescence and western blotting. 16S rRNA sequencing, untargeted metabolomics, and network pharmacology were integrated to explore the mechanism of WDD in treating insomnia. The role of gut microbiota in WDD treatment was validated by antibiotic treatment and fecal microbiota transplantation (FMT). Targeted metabolomics was used to detect changes in fecal tryptophan metabolites after FMT. Additionally, RT-qPCR and western blotting were used to investigate the potential mechanisms.

RESULTS: WDD effectively shortened sleep latency, prolonged sleep duration, alleviated anxiety-like behaviors, attenuated neuronal damage, and modulated neurotransmitter levels in rats with insomnia. Moreover, WDD alleviated intestinal damage, reduced the number of Iba-1 positive cells, increased IL-10 levels and decreased IL-6, IL-1β, TNF-α and LPS levels in the colon, serum and hippocampus. It also increased the expression of Occludin, Claudin-1, and ZO-1 in both the colon and brain. 16S rRNA sequencing suggested that WDD improved gut microbiota disorders. Untargeted metabolomics and network pharmacology jointly suggested that WDD could regulate tryptophan metabolism. Antibiotic treatment and FMT confirmed the involvement of gut microbiota in the therapeutic effects of WDD in alleviating insomnia. Changes of tryptophan metabolites in feces, serum, and hippocampus confirmed the regulatory effect of WDD on tryptophan metabolism. Further mechanistic analysis suggested that WDD may correct the abnormal kynurenine pathway of tryptophan metabolism through inhibition of the expression of indoleamine 2,3-dioxygenase 1 and kynurenine-3-monooxygenase.

CONCLUSION: WDD can modulate the neurotransmitter disorders, reduce inflammatory cytokine levels, and strengthen the intestinal barrier and blood-brain barrier by regulating gut microbiota and tryptophan metabolism, thereby improving sleep. This study provides evidence for the potential therapeutic effect of WDD on insomnia via the microbiota-gut-brain axis.},
}

@article {pmid40618377,
year = {2025},
author = {Le, TT and Hoang, TN and Do, DH and Nguyen, XH and Huynh, C and Viet, HD and Dat, VQ and Zengler, K and Gilbert, JA and Avedissian, SN and Tran, TM and Le, J},
title = {Current state of microbiota clinical applications in neonatal and pediatric bacterial infections.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2529400},
doi = {10.1080/19490976.2025.2529400},
pmid = {40618377},
issn = {1949-0984},
mesh = {Humans ; Infant, Newborn ; Child ; *Bacterial Infections/microbiology/therapy ; Dysbiosis/microbiology/therapy ; *Gastrointestinal Microbiome ; Anti-Bacterial Agents/therapeutic use ; Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; Infant ; Bacteria/classification/isolation & purification/genetics ; Child, Preschool ; },
abstract = {The microbiota plays a crucial role in pediatric health by shaping immune development and influencing infection susceptibility. In infants and children, an immature microbiota may compromise immune defense, increasing the risk of bacterial infections. This review evaluates clinical trials on the microbiota's role in neonatal and pediatric bacterial infections, including sepsis, infections in pediatric cancer patients, and Clostridioides difficile-associated dysbiosis. We summarized original research articles published from 2000 to May 2024 on the microbiota and bacterial infections in neonates and children. A balanced microbiota is essential for infection prevention, particularly in premature infants and immunocompromised children. Studies of microbiome signatures in the gut, oral cavity, and nasopharynx have highlighted how microbiota composition influences infection risk, treatment response, and adverse effects from antibiotics and chemotherapy. Disruptions from antibiotic exposure, chemotherapy, and hematopoietic stem cell transplantation frequently lead to dysbiosis, characterized by depletion of commensal bacteria and overgrowth of pathobionts, including antibiotic-resistant strains such as C. difficile. Conversely, microbiota-restorative interventions, such as probiotics and fecal microbiota transplantation, show promise in reducing bacterial infections by enhancing microbial resilience. The microbiota plays a critical role in predicting and potentially treating bacterial infections in children. While antibiotics remain essential, their widespread use has significant consequences for microbiota health. Striking a balance between effective infection control and microbiota preservation is crucial, particularly in vulnerable pediatric populations. Implementing judicious antibiotic use and exploring microbiota-based therapies may mitigate long-term microbiota disruptions, ultimately improving infection outcomes and overall pediatric health.},
}

Humans
Infant, Newborn
Child
*Bacterial Infections/microbiology/therapy
Dysbiosis/microbiology/therapy
*Gastrointestinal Microbiome
Anti-Bacterial Agents/therapeutic use
Fecal Microbiota Transplantation
Probiotics/therapeutic use
Infant
Bacteria/classification/isolation & purification/genetics
Child, Preschool

@article {pmid40618373,
year = {2025},
author = {Li, L and Yang, Z and Yi, Y and Song, Y and Zhang, W},
title = {Gut microbiota and radiation-induced injury: mechanistic insights and microbial therapies.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2528429},
doi = {10.1080/19490976.2025.2528429},
pmid = {40618373},
issn = {1949-0984},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology/radiation effects ; *Radiation Injuries/therapy/microbiology ; Animals ; Fecal Microbiota Transplantation ; Probiotics ; Signal Transduction ; Oxidative Stress ; Neoplasms/radiotherapy ; Radiotherapy/adverse effects ; Prebiotics ; },
abstract = {Radiotherapy represents a crucial therapeutic modality in cancer treatment, yet its efficacy is frequently limited by radiation-induced toxicity. Growing evidence indicates that gut microbiota and their metabolites serve as key regulators of both radioprotective and radiosensitizing effects. This review systematically examines three fundamental regulatory mechanisms through which gut microbiota and its metabolites mitigate radiation-induced injury: (1) modulation of intestinal epithelial cell regeneration and tumor cell apoptosis via Wnt/β-catenin and PI3K/AKT/mTOR pathways; (2) immunomodulation via Toll-like receptor activation and NF-κB signaling; (3) oxidative stress management via Nrf2 signaling. We also evaluate various microbiota-targeted interventions, ranging from probiotics and prebiotics to fecal microbiota transplantation and emerging engineered microbial therapies, highlighting their potential in clinical radiotherapy. Finally, we emphasize current limitations and future research directions, underscoring the need to overcome existing challenges in microbiome analysis and therapeutic durability to fully realize the potential of precision radio-microbiome medicine, which may provide valuable references for developing personalized radiotherapy strategies based on gut microbiota and their metabolites.},
}

Humans
*Gastrointestinal Microbiome/physiology/radiation effects
*Radiation Injuries/therapy/microbiology
Animals
Fecal Microbiota Transplantation
Probiotics
Signal Transduction
Oxidative Stress
Neoplasms/radiotherapy
Radiotherapy/adverse effects
Prebiotics

@article {pmid40617533,
year = {2025},
author = {Chen, L and Li, B and Zu, M and Reis, RL and Kundu, SC and Xiao, B},
title = {Advances and mechanisms of gut microbiota modulation in enhancing immune checkpoint inhibitor efficacy.},
journal = {Seminars in cancer biology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.semcancer.2025.06.012},
pmid = {40617533},
issn = {1096-3650},
abstract = {The gut microbiota is crucial for maintaining human health by regulating immune homeostasis and metabolic function. Immune checkpoint inhibitors (ICIs) have emerged as a cornerstone of cancer immunotherapy, yet their effectiveness is often hampered by treatment resistance and immune-related adverse events (irAEs). Increasing evidence highlights gut microbiota as a critical determinant of ICI efficacy. Here, we summarize the advances from preclinical mouse models and clinical trials to systematically illustrate how gut microbiota modulation strategies, such as fecal microbiota transplantation, specific microorganism supplementation, dietary and lifestyle interventions, and prebiotic/postbiotic supplementation, can enhance ICI therapeutic outcomes and mitigate irAEs. Mechanistically, the gut microbiota shape host immune responses, influencing innate, adaptive, and mucosal immunity, as well as immune checkpoint expression, through microbial translocation, microbiota-derived metabolites, and extracellular vesicles. This review elucidates the intricate interplay between gut microbiota and ICI treatment responses, laying a theoretical groundwork for developing personalized microbiota-based strategies to optimize cancer immunotherapy.},
}

@article {pmid40617323,
year = {2025},
author = {Lu, Y and Zhang, Z and Chen, L and Xue, P and Zhang, Y and Li, Y and Guo, H},
title = {Prospect of interdisciplinary research on gut microbiota and colorectal cancer immunotherapy.},
journal = {Critical reviews in oncology/hematology},
volume = {},
number = {},
pages = {104832},
doi = {10.1016/j.critrevonc.2025.104832},
pmid = {40617323},
issn = {1879-0461},
abstract = {Immune checkpoint blockade (ICB) is considered as a promising therapy in a variety of cancers, while colorectal cancer (CRC) is mostly resistant to it. The ICB efficacy is proved to be associated with gut microbiota. However, the research on improving ICB outcomes of CRC by microbes or their metabolites is obstructed compared to other types of cancers. Through summarizing the main progress and limitations in previous work, we provide our proposal for further study on CRC. For preclinical basic investigation, microbial tryptophan metabolism regulates ICB therapy outcomes particularly in CRC and requires specific focus. For clinical trials, sources of recruited cohorts and donators of fecal microbiota transplantation can be diversified. For future application, interdisciplinary methods and models coupled with advanced technologies are suggested for designing precise intervention strategies based on prebiotics.},
}

@article {pmid40617308,
year = {2025},
author = {Dan, W and Xiong, C and Zhou, G and Chen, J and Pan, F},
title = {Gut microbiota as a mediator of cancer development and management: From colitis to colitis-associated dysplasia and carcinoma.},
journal = {Biochimica et biophysica acta. Reviews on cancer},
volume = {},
number = {},
pages = {189381},
doi = {10.1016/j.bbcan.2025.189381},
pmid = {40617308},
issn = {1879-2561},
abstract = {Colitis-associated colorectal cancer (CAC) develops as a result of prolonged colitis in patients with inflammatory bowel disease. In recent years, the role of the gut microbiota in colitis-associated colorectal carcinogenesis has begun to be recognized. Specific microbes, such as enterotoxigenic Bacteroides fragilis, Fusobacterium nucleatum, and pks[+]Escherichia coli, promote carcinogenesis by regulating oncogenic signaling, epithelial-mesenchymal transition, autophagy induction, and the immune microenvironment. Conversely, commensal fungi and probiotics exert tumor-suppressive effects by inhibiting inflammatory pathways and immune cell recruitment. Emerging microbiota-targeted strategies, including precision probiotics and fecal microbiota transplantation, can restore ecological homeostasis, attenuate inflammation, and enhance the efficacy of conventional therapies. This review summarizes the current understanding of the mechanisms underlying microbiota-driven CAC pathogenesis and assesses the potential applications of gut microbiota in the development of diagnostic tools and therapeutic interventions.},
}

@article {pmid40615821,
year = {2025},
author = {Upadhyay, P and Kumar, S and Tyagi, A and Tyagi, AR and Barbhuyan, T and Gupta, S},
title = {Gut Microbiome rewiring via fecal transplants: Uncovering therapeutic avenues in Alzheimer's disease models.},
journal = {BMC neuroscience},
volume = {26},
number = {1},
pages = {39},
pmid = {40615821},
issn = {1471-2202},
support = {File no.R.12014/20/2018//Department of Health Research, India/ ; DBT Core grant//National Institute of Immunology New Delhi India/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; *Fecal Microbiota Transplantation/methods ; *Alzheimer Disease/therapy/microbiology/psychology ; Mice ; Disease Models, Animal ; Mice, Inbred C57BL ; Male ; Mice, Transgenic ; Oxidative Stress ; },
abstract = {BACKGROUND: Emerging evidence implicates the gut microbiome in Alzheimer's disease (AD) pathogenesis, yet the underlying mechanisms remain elusive. This study elucidates the bidirectional relationship between gut microbiota and AD using fecal microbiota transplantation (FMT) in a mouse model.

RESULT: Through meticulous experimentation, we conducted reciprocal FMT between AD (5xFAD) and healthy (C57BL/6) mice to unravel the impact of gut microbiome alterations on cognitive function and neuroinflammation. FMT from 5xFAD to C57BL/6 mice induced profound memory impairment and cognitive deficits, accompanied by elevated inflammatory cytokine levels, oxidative stress markers, and systemic inflammation, as evidenced by increased plasma cytokines. Conversely, transplanting healthy microbiota into 5xFAD mice yielded remarkable behavioral improvements, including enhanced spatial memory performance in the Morris water maze, directly correlating with cognitive recovery. Our findings underscore the pivotal role of the gut microbiome in AD pathogenesis and offer a promising therapeutic avenue.

CONCLUSION: Targeted modulation of the gut microbiome through strategies like FMT may offer potential benefits in Alzheimer's disease by influencing neuroinflammation, oxidative stress, and cognitive function. This comprehensive study provides novel insights into the gut-brain axis dynamics and paves the way for innovative microbiome-based interventions in AD management.},
}

Animals
*Gastrointestinal Microbiome/physiology
*Fecal Microbiota Transplantation/methods
*Alzheimer Disease/therapy/microbiology/psychology
Mice
Disease Models, Animal
Mice, Inbred C57BL
Male
Mice, Transgenic
Oxidative Stress

@article {pmid40615512,
year = {2025},
author = {Ruan, S and Liu, J and Yuan, X and Ye, X and Zhang, Q},
title = {Aerobic exercise alleviates cognitive impairment in T2DM mice through gut microbiota.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {23917},
pmid = {40615512},
issn = {2045-2322},
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; *Cognitive Dysfunction/therapy/etiology/microbiology ; *Physical Conditioning, Animal ; *Diabetes Mellitus, Type 2/complications/microbiology ; Male ; Mice ; Mice, Inbred C57BL ; *Diabetes Mellitus, Experimental/complications/microbiology ; Fecal Microbiota Transplantation ; },
abstract = {The risk of cognitive impairment is markedly elevated in patients with type 2 diabetes mellitus (T2DM). While exercise has been shown to mitigate cognitive deficits associated with diabetes, the underlying mechanisms remain poorly understood. Recent studies suggest that exercise can modulate the composition of the gut microbiota, which, in turn, may influence the central nervous system via the microbiota-gut-brain axis. However, the specific role of gut microbiota in mediating exercise-induced improvements in cognitive function in T2DM remains unclear. In this study, we aimed to investigate whether exercise can alleviate cognitive impairment in T2DM mice by modulating the intestinal microbiota, and to elucidate the mechanisms underlying this effect. This study was conducted using male C57BL/6J mice. Mice fed a normal diet were assigned to the non-diabetic control group (NC), while those fed a high-fat diet were intraperitoneally injected with streptozotocin (STZ) and subsequently divided into the diabetic control group (DM), an exercise group (DM-EXE), and a fecal microbiota transplantation group (DM-FMT). The DM-EXE group underwent treadmill exercise for 8 weeks. During this period, the DM-FMT group received fecal microbiota transplants from the DM-EXE group for 2 consecutive days per week. Following the 8-week intervention, stool samples were collected for 16S rDNA high-throughput sequencing. The fear conditioning test was performed to assess cognitive function. Intestinal mucosa samples were collected to evaluate the expression of intestinal tight junction proteins. Additionally, the expression levels of synaptic proteins, glucose transporters, neurotrophic factors, and inflammatory markers were measured in the hippocampus. Our findings demonstrate that T2DM mice exhibit impaired cognitive function and significant alterations in their gut microbiota compared to non-diabetic controls. Exercise partially reversed these changes in the intestinal microbiota and alleviated cognitive impairment in T2DM mice. Additionally, transplantation of intestinal microbiota from exercised mice improved cognitive function in T2DM mice. Aerobic exercise may mitigate cognitive impairment in T2DM mice by modulating the gut microbiota. The underlying mechanisms appear to involve enhanced neural synaptic plasticity, reduced neuroinflammation, and improved neuronal glucose metabolism.},
}

Animals
*Gastrointestinal Microbiome/physiology
*Cognitive Dysfunction/therapy/etiology/microbiology
*Physical Conditioning, Animal
*Diabetes Mellitus, Type 2/complications/microbiology
Male
Mice
Mice, Inbred C57BL
*Diabetes Mellitus, Experimental/complications/microbiology
Fecal Microbiota Transplantation

@article {pmid40615289,
year = {2025},
author = {Chen, H},
title = {Mapping the clinical trial landscape of gut microbiota modulation in neurodegenerative diseases.},
journal = {European journal of internal medicine},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ejim.2025.06.032},
pmid = {40615289},
issn = {1879-0828},
}

@article {pmid40614920,
year = {2025},
author = {Yadav, S and Raj, RG},
title = {Parkinson's disease and the gut microbiota connection: unveiling dysbiosis and exploring therapeutic horizons.},
journal = {Neuroscience},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.neuroscience.2025.07.003},
pmid = {40614920},
issn = {1873-7544},
abstract = {Parkinson's disease (PD) is a progressive neurodegenerative disorder marked by dopaminergic neuronal loss, α-synuclein aggregation, and sustained neuroinflammation. Emerging evidence supports the gut-brain-microbiota axis as a pivotal player in the disease's pathogenesis. Dysbiosis, disruptions in the gut microbial composition, has been consistently observed in individuals with PD, with notable reductions in beneficial, short-chain fatty acid-producing bacteria and elevations in pro-inflammatory microbial species. These alterations contribute to increased intestinal permeability, systemic inflammation, and heightened neuroinflammatory responses that may drive α-synuclein misfolding and dopaminergic degeneration. In addition, microbial metabolites, including lipopolysaccharides and amyloid proteins such as curli, may promote neurodegeneration via immune and molecular mimicry pathways. Recent advances highlight the bidirectional influence of the microbiota-gut-brain axis on PD symptoms, ranging from motor deficits to non-motor features like constipation, depression, and cognitive decline. Several microbiota-modulating interventions, including probiotics, prebiotics, dietary strategies, antibiotics, and fecal microbiota transplantation, have demonstrated neuroprotective potential in both preclinical and clinical contexts. However, inter-individual variability, methodological heterogeneity, and the absence of longitudinal, multi-omics-integrated studies limit current understanding. The gut microbiome also holds promise as a non-invasive biomarker for early PD detection and prognosis, though standardization remains a challenge. Future research must clarify causal mechanisms, optimize therapeutic delivery, and integrate genetic, metabolic, and environmental data to advance precision medicine approaches. This review consolidates current knowledge on gut microbiota's role in PD pathophysiology and therapeutic innovation, providing a roadmap for future research directions.},
}

@article {pmid40614649,
year = {2025},
author = {Wang, Y and Ma, S and Wu, L and Zhao, R},
title = {Betaine promotes chicken growth through modulating gut microbiota and FXR-mediated activation of IGF genes.},
journal = {Poultry science},
volume = {104},
number = {9},
pages = {105455},
doi = {10.1016/j.psj.2025.105455},
pmid = {40614649},
issn = {1525-3171},
abstract = {Betaine is a growth-promoting additive used in both the animal production and microbial fermentation industries. The primary mechanisms by which betaine promotes animal growth are well known through its direct action on the host cells. However, it remains unclear whether betaine exerts its growth-promoting effects in chickens dependent on the gut microbiota. Here, we found that betaine promotes the growth of broiler chickens while enhancing the richness and diversity of the cecal microbiota and increasing beneficial bacteria, such as Lactobacillus, Limosilactobacillus, and Prevotella (P < 0.05). However, the growth-promoting effects of betaine were abolished in broilers treated with an antibiotic cocktail. Furthermore, fecal microbiota transplantation from betaine-supplemented chickens could recapitulate the promoting effect of betaine on body weight, breast muscle weight, and hepatic insulin-like growth factors (IGFs) synthesis (P < 0.05), indicating that the gut microbiota plays an indispensable role in betaine's growth-promoting action. Mechanistically, betaine promotes (P < 0.05) the synthesis of bile acids, and microbial function predictions suggest that betaine upregulates the biosynthetic pathways of primary and secondary bile acids. Notably, the expression of the bile acid receptor farnesoid X receptor (FXR) was upregulated (P < 0.05) in the liver, promoting FXR binding to the IGFs genes promoter regions and activating the transcription of IGFs gene. Taken together, our findings suggest that betaine promotes broiler growth via microbiota-dependent mechanisms, accompanied by FXR-mediated upregulation of IGFs gene expression in the liver, providing new perspectives and theoretical support for understanding the complexity of animal growth regulation.},
}

@article {pmid40613778,
year = {2025},
author = {Wang, W and He, X and Liang, C and Wang, Y and Yu, Y and Zhang, F},
title = {Washed microbiota transplantation alleviates tyrosine kinase inhibitors associated gastrointestinal adverse effects.},
journal = {International journal of cancer},
volume = {},
number = {},
pages = {},
doi = {10.1002/ijc.70034},
pmid = {40613778},
issn = {1097-0215},
support = {2021YFA0717004//the National Key R&D Program of China/ ; 2023-3HIM//Nanjing Medical University Fan Daiming Research Funds for Holistic Integrative Medicine/ ; },
abstract = {Gut microbiota dysbiosis is implicated in tyrosine kinase inhibitor (TKI)-induced gastrointestinal adverse effects (GAEs), often necessitating medication adjustments or discontinuation in severe or persistent cases. This study aimed to evaluate the efficacy and safety of washed microbiota transplantation (WMT) in managing TKI-induced GAEs. This prospective study involved cancer patients presenting TKI-induced GAEs. The primary outcome was the clinical remission rate at Week 8 post-WMT, which was assessed by the common terminology criteria for adverse events grade. The secondary outcomes included the clinical asymptomatic rate, the onset time of clinical remission, and the variation of C-reactive protein (CRP) levels. Twenty-four patients undergoing 66 WMTs were analyzed. The overall clinical remission and asymptomatic rates were 75.00% (18/24) and 29.17% (7/24), respectively. GAEs, including diarrhea, abdominal pain, and abdominal distention, showed significant improvement post-WMT (all p < .05), while hematochezia exhibited a decreasing trend in severity. Median time to remission was 14.5 days (inter-quartile range, 7-24). Within 8 weeks post-WMT, three initially responsive patients experienced relapse. CRP levels significantly decreased (p < .05), and no severe adverse events were reported. This study proposes WMT as a potential treatment for TKI-induced GAEs, particularly for patients who do not respond adequately to conventional treatments.},
}

@article {pmid40613520,
year = {2025},
author = {Ramos Martínez, A and Gutiérrez-Villanueva, A and González-Haba Ruiz, M and Diego-Yagüe, I and Nieto-Fernández, A and Muñez, E and Fernández Cruz, A and Calderón Parra, J},
title = {Fecal microbiota transplantation for prevention of recurrent acute cholangitis. Review of four published cases.},
journal = {Revista espanola de enfermedades digestivas},
volume = {},
number = {},
pages = {},
doi = {10.17235/reed.2025.11404/2025},
pmid = {40613520},
issn = {1130-0108},
abstract = {INTRODUCTION: Recurrent acute cholangitis (RAC) constitutes a relevant clinical problem that may condition the prognosis of the patient. Chronic suppressive antibiotic therapy can be used for preventive purposes, but it is associated with adverse effects and can select resistant bacterial strains. Fecal microbiota transfer (FMT) has been shown to be effective in preventing recurrent Clostridioides difficile infection and could be a useful strategy in patients with RAC.

OBJECTIVE: To review the experience of the use of FMT in the prevention of episodes of RAC by reviewing published cases.

RESULT: Four cases were identified in which FMT significantly reduced RAC episodes. The patients were characterized by lack of efficacy of conventional treatments, had different predisposing factors for RAC and frequent colonization and infection by multidrug-resistant bacteria.

CONCLUSIONS: The four cases presented provide limited but encouraging evidence of the preventive effect of FMT on successive episodes in patients without biliary tract obstruction. Larger and more adequately designed studies will be necessary to deepen the knowledge of this possible preventive strategy.},
}

@article {pmid40613134,
year = {2025},
author = {Yao, Y and Ye, Y and Zheng, C},
title = {The Impact of Microbiota-Mediated Immune Regulation on Recurrent Pregnancy Loss and Intervention Strategies.},
journal = {American journal of reproductive immunology (New York, N.Y. : 1989)},
volume = {94},
number = {1},
pages = {e70121},
doi = {10.1111/aji.70121},
pmid = {40613134},
issn = {1600-0897},
support = {LHDMZ23H190002//Huadong Medicine Joint Funds of the Zhejiang Provincial Natural Science Foundation of China/ ; },
mesh = {Humans ; Female ; *Abortion, Habitual/immunology/microbiology/therapy ; Pregnancy ; *Gastrointestinal Microbiome/immunology ; *Dysbiosis/immunology ; *Microbiota/immunology ; *Endometrium/microbiology/immunology ; Probiotics/therapeutic use ; Fecal Microbiota Transplantation ; Animals ; Immune Tolerance ; },
abstract = {Recurrent pregnancy loss (RPL) significantly affects reproductive health in couples of childbearing age. Its pathogenesis is complex, with nearly 50% of cases remaining unexplained, and immune regulation plays a key role in its development. This review focuses on the relationship between human microbiota (gut, reproductive tract, and endometrial microbiota), immune regulation, and RPL, systematically summarizing related research progress. RPL patients exhibit characteristic changes in the gut, reproductive tract, and endometrial microbiota, such as reduced gut microbial diversity, decreased beneficial bacteria, increased harmful bacteria in the reproductive tract, and an imbalanced endometrial microbiota structure. Dysbiosis can lead to immune regulation abnormalities, increasing the risk of RPL by disrupting immune tolerance, triggering inflammatory responses, and interfering with metabolism. Although microbiota-based interventions, such as probiotics, prebiotics, and fecal microbiota transplantation, show potential, they face challenges related to strain selection, donor screening, and unclear mechanisms. Current research also faces limitations in detection technology and sample size, and the understanding of the microbiota-immune-RPL relationship requires further deepening. Future studies should clarify causal relationships using advanced technologies, develop more effective detection and intervention methods, and create personalized treatment plans based on individual patient characteristics to improve clinical diagnosis and treatment of RPL and safeguard women's reproductive health.},
}

Humans
Female
*Abortion, Habitual/immunology/microbiology/therapy
Pregnancy
*Gastrointestinal Microbiome/immunology
*Dysbiosis/immunology
*Microbiota/immunology
*Endometrium/microbiology/immunology
Probiotics/therapeutic use
Fecal Microbiota Transplantation
Animals
Immune Tolerance