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Cholesterol gallstones (CGS) still lack effective noninvasive treatment. The etiology of experimentally proven cholesterol stones remains underexplored. This cross‐sectional study aims to comprehensively evaluate potential biomarkers in patients with gallstones and assess the effects of microbiome‐targeted interventions in mice. Microbiome taxonomic profiling was conducted on 191 samples via V3−V4 16S rRNA sequencing. Next, 60 samples (30 age‐ and sex‐matched CGS patients and 30 controls) were selected for metagenomic sequencing and fecal metabolite profiling via liquid chromatography‐mass spectrometry. Microbiome and metabolite characterizations were performed to identify potential biomarkers for CGS. Eight‐week‐old male C57BL/6J mice were given a lithogenic diet for 8 weeks to promote gallstone development. The causal relationship was examined through monocolonization in antibiotics‐treated mice. The effects of short‐chain fatty acids such as sodium butyrate, sodium acetate (NaA), sodium propionate, and fructooligosaccharides (FOS) on lithogenic diet‐induced gallstones were investigated in mice. Gut microbiota and metabolites exhibited distinct characteristics, and selected biomarkers demonstrated good diagnostic performance in distinguishing CGS patients from healthy controls. Multi‐omics data indicated associations between CGS and pathways involving butanoate and propanoate metabolism, fatty acid biosynthesis and degradation pathways, taurine and hypotaurine metabolism, and glyoxylate and dicarboxylate metabolism. The incidence of gallstones was significantly higher in the Clostridium glycyrrhizinilyticum group compared to the control group in mice. The grade of experimental gallstones in control mice was significantly higher than in mice treated with NaA and FOS. FOS could completely inhibit the formation of gallstones in mice. This study characterized gut microbiome and metabolome alterations in CGS. C. glycyrrhizinilyticum contributed to gallstone formation in mice. Supplementing with FOS could serve as a potential approach for managing CGS by altering the composition and functionality of gut microbiota. Alterations in gut microbial composition and fecal metabolome have been reported in patients with gallstones. The gut microbiota plays a crucial role in shaping the host's fecal metabolic profile. Specifically, metabolites of amino acids, fatty acids, and nicotinic acid may affect the synthesis, transport, or metabolism of cholesterol, thereby impacting gallstone formation. Oral administration of C. glycyrrhizinilyticum can promote histological liver damage and affect liver lipid metabolism, contributing to cholesterol gallstone formation. Fructooligosaccharides can be a new, cost‐effective, and relatively simple microbiota‐targeted therapeutic approach for cholesterol gallstones. Microbiome‐targeted therapies, involving the modulation of gut microbiota, should be explored as potential treatments for gallstones. Highlights Metabolites of amino acids, fatty acids, and nicotinic acid may affect the synthesis, transport, or metabolism of cholesterol, thereby impacting gallstone formation. Oral administration of C. glycyrrhizinilyticum can contribute to cholesterol gallstone formation. Fructooligosaccharides could serve as an inexpensive microbiota‐targeted therapeutic option for cholesterol gallstones.

Hepatic encephalopathy (HE) is a serious complication of cirrhosis that causes neuropsychiatric problems, such as cognitive dysfunction and movement disorders. The link between the microbiota and the host plays a key role in the pathogenesis of HE. The link between the gut microbiome and disease can be positively utilized not only in the diagnosis area of HE but also in the treatment area. Probiotics and prebiotics aim to resolve gut dysbiosis and increase beneficial microbial taxa, while fecal microbiota transplantation aims to address gut dysbiosis through transplantation (FMT) of the gut microbiome from healthy donors. Antibiotics, such as rifaximin, aim to improve cognitive function and hyperammonemia by targeting harmful taxa. Current treatment regimens for HE have achieved some success in treatment by targeting the gut microbiota, however, are still accompanied by limitations and problems. A focused approach should be placed on the establishment of personalized trial designs and therapies for the improvement of future care. This narrative review identifies factors negatively influencing the gut–hepatic–brain axis leading to HE in cirrhosis and explores their relationship with the gut microbiome. We also focused on the evaluation of reported clinical studies on the management and improvement of HE patients with a particular focus on microbiome-targeted therapy.

Acne vulgaris is a widespread dermatological condition that significantly affects the quality of life of adolescents and adults. Traditionally, acne pathogenesis has been linked to factors such as excess sebum production, follicular hyperkeratinization, and the presence of Cutibacterium acnes (C. acnes). However, recent studies have highlighted the role of the skin microbiome, shifting focus from individual pathogens to microbial community dynamics. This review critically evaluates existing research on the skin microbiome and its relationship to acne, focusing on microbial diversity, C. acnes strain variability, and emerging therapies targeting the microbiome. While certain studies associate C. acnes with acne severity, others show this bacterium’s presence in healthy skin, suggesting that strain-specific differences and overall microbial balance play crucial roles. Emerging therapeutic approaches, such as probiotics and bacteriophage therapy, aim to restore microbial equilibrium or selectively target pathogenic strains without disturbing the broader microbiome. However, the lack of standardized methodologies, limited longitudinal studies, and the narrow focus on bacterial communities are major limitations in current research. Future research should explore the broader skin microbiome, including fungi and viruses, use consistent methodologies, and focus on longitudinal studies to better understand microbial fluctuations over time. Addressing these gaps will enable the development of more effective microbiome-based treatments for acne. In conclusion, while microbiome-targeted therapies hold promise, further investigation is needed to validate their efficacy and safety, paving the way for innovative, personalized acne management strategies.

The aetiologies and origins of neurodegenerative diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS) and Huntington’s disease (HD), are complex and multifaceted. A growing body of evidence suggests that the gut microbiome plays crucial roles in the development and progression of neurodegenerative diseases. Clinicians have come to realize that therapeutics targeting the gut microbiome have the potential to halt the progression of neurodegenerative diseases. This narrative review examines the alterations in the gut microbiome in AD, PD, ALS and HD, highlighting the close relationship between the gut microbiome and the brain in neurodegenerative diseases. Processes that mediate the gut microbiome–brain communication in neurodegenerative diseases, including the immunological, vagus nerve and circulatory pathways, are evaluated. Furthermore, we summarize potential therapeutics for neurodegenerative diseases that modify the gut microbiome and its metabolites, including diets, probiotics and prebiotics, microbial metabolites, antibacterials and faecal microbiome transplantation. Finally, current challenges and future directions are discussed.

Background The study aimed to comprehensively analyze and establish a framework for evaluating the efficacy of microbiome–targeted treatment (MTT) for depression. Methods We searched PubMed, Embase, Cochrane Library, Web of Science, and the Chinese National Knowledge Infrastructure database for randomized controlled trials (RCTs) on MTT in treating depression until October 19, 2023. A meta-analysis was conducted to evaluate the efficacy and safety of MTT. Comprehensive subgroup analyses were undertaken to explore factors influencing MTT’s efficacy in treating depression. This study was registered with PROSPERO (CRD42023483649). Results The study selection process identified 51,570 studies, of which 34 met the inclusion criteria. The overall pooled estimates showed that MTT significantly improved depression symptoms (SMD −0.26, 95% CI [−0.32, −0.19], I 2  = 54%) with acceptable safety. Subgroup analyses by geography showed that effectiveness was demonstrated in Asia (SMD −0.46, 95% CI [−0.56, −0.36], I 2  = 36%), while no evidence of effectiveness was found in Europe (SMD −0.07, 95% CI [−0.19, 0.05], I 2  = 55%), America (SMD −0.33, 95% CI [−0.67, 0.02], I 2  = 60%), and Oceania (SMD 0.00, 95% CI [−0.18, 0.18], I 2  = 0%). Besides, the efficacy was shown in depressed patients without comorbidities (SMD −0.31, 95% CI [−0.40, −0.22], I 2  = 0%), whereas effectiveness was poor in those with digestive disorders, such as irritable bowel syndrome (SMD −0.37, 95% CI [−0.89, 0.16], I 2  = 74%), chronic diarrhea (SMD −0.34, 95% CI [−0.73, 0.05]), and chronic constipation (SMD −0.23, 95% CI [−0.57, 0.11], I 2  = 0%). In perinatal depressed patients, MTT was not effective (SMD 0.16, 95% CI [0.01, 0.31], I 2  = 0%). It was found that < 8 weeks (SMD −0.33, 95% CI [−0.45, −0.22], I 2  = 0%) and 8–12 weeks (SMD −0.34, 95% CI [−0.44, −0.23], I 2  = 57%) MTT were effective, while > 12 weeks (SMD 0.02, 95% CI [−0.12, 0.17], I 2  = 68%) MTT was ineffective. Conclusions Despite the overall effectiveness of MTT in treating depression and its acceptable safety profile, caution is warranted in drawing this conclusion due to limitations posed by the small sample size of included studies and heterogeneity. The efficacy of MTT for depression exhibits variation influenced by geography, patient comorbidities, and duration of administration.

Cancers are causing millions of deaths and leaving a huge clinical and economic burden. High costs of cancer drugs are limiting their access to the growing number of cancer cases. The development of more affordable alternative therapy could reach more patients. As gut microbiota plays a significant role in the development and treatment of cancer, microbiome-targeted therapy has gained more attention in recent years. Dietary and natural compounds can modulate gut microbiota composition while providing broader and more accessible access to medicine. Tea compounds have been shown to have anti-cancer properties as well as modulate the gut microbiota and their related metabolites. However, there is no comprehensive review that focuses on the gut modulatory effects of tea compounds and their impact on reshaping the metabolic profiles, particularly in cancer models. In this review, the effects of different tea compounds on gut microbiota in cancer settings are discussed. Furthermore, the relationship between these modulated bacteria and their related metabolites, along with the mechanisms of how these changes led to cancer intervention are summarized.

Dysbiosis of the gut microbiome plays a critical role in diabetic kidney disease (DKD) development and progression. We stratified 46 type 2 DKD patients from Ruijin Hospital into early or advanced DKD groups in this cross-sectional study. Fecal samples underwent 16S rRNA sequencing. Statistical analyses (t-tests, Chi-square, GLMs) and MR were performed using SPSS and R. We found that advanced DKD patients exhibited distinct gut microbiota profiles, with LEfSe analysis showing higher , , and and lower compared to early DKD, while DKD-susceptible individuals had elevated and reduced and . GLMs linked , , to DKD susceptibility (  < 0.05), and and to early/resistant DKD. MR analysis demonstrated causality: (OR: 2.382), (OR: 1.278), (OR: 2.518), and (OR: 1.622) worsened DKD, whereas and protected against eGFR decline (  < 0.05). Reverse MR revealed the bidirectional effects-severe DKD increased 2 but suppressed and (  < 0.05), underscoring microbiota-DKD interplay. Sensitivity analyses (MR-Egger, weighted median, leave-one-out) confirmed the robustness and directionality of these causal effects. In conclusion, 10 key bacterial genera were causally linked to DKD progression and susceptibility, including harmful ( , , , , , , 2) and protective taxa ( , , ). These genera serve as novel biomarkers for early detection and risk stratification, and as potential therapeutic targets for microbiota-modulating interventions to mitigate DKD progression. The bidirectional microbiota-DKD interplay further underscores the promise of targeting gut dysbiosis in DKD precision management.

Infectious diseases have long posed a significant threat to global health and require constant innovation in treatment approaches. However, recent groundbreaking research has shed light on a previously overlooked player in the pathogenesis of disease—the human microbiome. This review article addresses the intricate relationship between the microbiome and infectious diseases and unravels its role as a crucial mediator of host–pathogen interactions. We explore the remarkable potential of harnessing this dynamic ecosystem to develop innovative treatment strategies that could revolutionize the management of infectious diseases. By exploring the latest advances and emerging trends, this review aims to provide a new perspective on combating infectious diseases by targeting the microbiome.

The microbiome has emerged as a critical, context-dependent regulator of tumorigenesis and anticancer immunity, capable of either promoting cancer progression or protecting against malignancy. This dual role is mediated by multiple interconnected mechanisms—including chronic inflammation, modulation of immune responses, and alterations in host metabolic signaling. These microbiome-cancer interactions vary across organs, influencing malignancies in the colon, breast, lung, and beyond. Clinically, the microbiome significantly affects patient responses to cancer therapies, particularly immunotherapies such as immune checkpoint blockade (ICB) and chimeric antigen receptor (CAR)-T cell therapy. Although emerging therapeutic strategies aimed at modulating the microbiome have shown promising early results, challenges remain, including individual microbiome variability and the dynamic interplay between the immune system and microbial communities. Nevertheless, harnessing the microbiome holds significant potential to transform precision oncology, offering personalized cancer prevention and treatment strategies tailored to each patient’s unique microbial ecosystem.

The gut microbiota plays a critical role in maintaining gastrointestinal homeostasis, immune regulation, and metabolic processes. Recent evidence has highlighted its significant influence on gastric carcinogenesis. Helicobacter pylori, a well-established class I carcinogen, remains the most prominent microbial risk factor for gastric cancer. However, emerging studies indicate that alterations in the broader gastric and intestinal microbial communities, referred to as dysbiosis, may also contribute to tumor initiation, progression, and immune evasion. These microbial shifts can lead to chronic inflammation, genotoxic metabolite production, and modulation of signaling pathways such as NF-κB and Wnt/β-catenin. This review explores the current understanding of the gut microbiome’s contribution to gastric cancer pathogenesis, including microbial signatures associated with precancerous lesions and the tumor microenvironment. Furthermore, the potential of microbiota-based biomarkers and therapeutic interventions, including probiotics, prebiotics, and fecal microbiota transplantation, is discussed as part of emerging precision medicine strategies.