Increased fructose intake is a triggering factor in a series of inflammatory diseases. However, the pathogenic role of fructose overconsumption in acute graft-versus-host disease (aGVHD) has not yet been clarified. In this study, we found that a high-fructose diet (HFR) aggravated the severity and mortality of aGVHD in mice and enhanced gut dysbiosis and bacterial translocation with impairment of the intestinal epithelial barrier. Fecal microbiota transplantation experiments further demonstrated that the microbiota derived from HFR-fed aGVHD mice was sufficient to reproduce intestinal barrier disruption and bacterial translocation in aGVHD recipients. HFR exacerbated the severity of aGVHD after depletion of the gut microbiota by antibiotics. Given the results that in vitro cultivated T-cells do not respond to fructose stimulation, we further investigated whether fructose overexposure affects macrophage activation. In fructose-treated bone marrow-derived macrophages (BMDMs), HIF-1α was stabilized by mitochondrial reactive oxygen species production, resulting in increased glycolysis and subsequently augmented expression of the inflammatory cytokines IL-6, IL-12, TNF-α, and IL-1β. Interestingly, we found that macrophages derived from HFR-fed aGVHD mice were able to enhance T-cell proliferation and Th1/Th17 differentiation. In parallel, correlation analysis integrating 16S rRNA and metabolomics sequencing data revealed that the abundances of Akkermansiaceae and Erysipelotrichaceae were positively correlated with the levels of indole-5,6-quinone and 6,7-dimethyl-8-(D-ribityl)lumazine. After depletion of macrophages and the gut microbiota in host mice, GVHD severity was significantly reversed even after HFR treatment. Taken together, our data reveal that high fructose intake exacerbated aGVHD by inducing a gut microbiota imbalance and promoting inflammatory macrophage activation. This provides a potential therapeutic strategy to alleviate aGVHD via precise adjustment of the fructose dietary.
{"title":"Overconsumption of fructose aggravates acute GVHD by inducing gut dysbiosis and promoting macrophage-mediated inflammatory response.","authors":"Kunpeng Wu,Huihui Yu,Kankan Cao,Bo Dai,Yan Yuan,Xiaohan Qian,Haoshu Zhong,Ying Qu,Hua Jiang,Tong Chen","doi":"10.1080/19490976.2026.2642459","DOIUrl":"https://doi.org/10.1080/19490976.2026.2642459","url":null,"abstract":"Increased fructose intake is a triggering factor in a series of inflammatory diseases. However, the pathogenic role of fructose overconsumption in acute graft-versus-host disease (aGVHD) has not yet been clarified. In this study, we found that a high-fructose diet (HFR) aggravated the severity and mortality of aGVHD in mice and enhanced gut dysbiosis and bacterial translocation with impairment of the intestinal epithelial barrier. Fecal microbiota transplantation experiments further demonstrated that the microbiota derived from HFR-fed aGVHD mice was sufficient to reproduce intestinal barrier disruption and bacterial translocation in aGVHD recipients. HFR exacerbated the severity of aGVHD after depletion of the gut microbiota by antibiotics. Given the results that in vitro cultivated T-cells do not respond to fructose stimulation, we further investigated whether fructose overexposure affects macrophage activation. In fructose-treated bone marrow-derived macrophages (BMDMs), HIF-1α was stabilized by mitochondrial reactive oxygen species production, resulting in increased glycolysis and subsequently augmented expression of the inflammatory cytokines IL-6, IL-12, TNF-α, and IL-1β. Interestingly, we found that macrophages derived from HFR-fed aGVHD mice were able to enhance T-cell proliferation and Th1/Th17 differentiation. In parallel, correlation analysis integrating 16S rRNA and metabolomics sequencing data revealed that the abundances of Akkermansiaceae and Erysipelotrichaceae were positively correlated with the levels of indole-5,6-quinone and 6,7-dimethyl-8-(D-ribityl)lumazine. After depletion of macrophages and the gut microbiota in host mice, GVHD severity was significantly reversed even after HFR treatment. Taken together, our data reveal that high fructose intake exacerbated aGVHD by inducing a gut microbiota imbalance and promoting inflammatory macrophage activation. This provides a potential therapeutic strategy to alleviate aGVHD via precise adjustment of the fructose dietary.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"3 1","pages":"2642459"},"PeriodicalIF":12.2,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147446957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Radiation proctitis (RP) is a frequent complication of pelvic radiotherapy that compromises treatment delivery and patient quality of life, yet the factors shaping injury severity remain incompletely defined. We prospectively profiled pretreatment fecal microbiomes and metabolomes from 55 patients and stratified them by outcome into mild versus severe RP. Baseline microbial composition showed Bacteroidales enriched in severe RP and Firmicutes enriched in mild cases. Multi-omics integration highlighted nicotinate/nicotinamide pathways; severe RP was characterized by concomitant reductions in both fecal and tissue NAD⁺ levels, along with an enrichment of microbial nicotinate/nicotinamide metabolism genes, primarily contributed by Bacteroides ovatus, B. xylanisolvens, and B. fragilis. In mice, fecal microbiota transplantation from severe-RP donors exacerbated radiation-induced colorectal injury and decreased colorectal NAD⁺, supporting a causal role for the microbiota. Gavage with Bacteroides similarly worsened pathology and lowered NAD⁺, whereas nicotinamide mononucleotide (NMN) supplementation attenuated the injury. Mechanistically, Bacteroides gavage reduced mitochondrial membrane potential, decreased the Lgr5⁺ stem-cell proportion and proliferative indices, associated with Wnt pathway modulation. NMN reversed these effects in parallel with NAD⁺ restoration. Together, these results identify a microbiota‒metabolite association wherein Bacteroidales enrichment is associated with NAD⁺ depletion, reduced mucosal proliferative capacity, and exacerbated radiation-induced colorectal injury. The work deepens insight into RP pathogenesis and suggests a potential basis for microbiome- and metabolite-targeted approaches to attenuate severe RP.
{"title":"Bacteroides-associated NAD⁺ depletion correlates with exacerbated radiation-induced colorectal injury and impaired mucosal proliferative capacity.","authors":"Jiayuan Huang,Qiyuan Qin,Xiangyu Li,Keming Jiang,Jun Xu,Yudan Mao,Wanying Kang,Rongsui Gao,Yikan Cheng,Wenjing Zhao,Jia Ke,Xiangyu Mou","doi":"10.1080/19490976.2026.2641260","DOIUrl":"https://doi.org/10.1080/19490976.2026.2641260","url":null,"abstract":"Radiation proctitis (RP) is a frequent complication of pelvic radiotherapy that compromises treatment delivery and patient quality of life, yet the factors shaping injury severity remain incompletely defined. We prospectively profiled pretreatment fecal microbiomes and metabolomes from 55 patients and stratified them by outcome into mild versus severe RP. Baseline microbial composition showed Bacteroidales enriched in severe RP and Firmicutes enriched in mild cases. Multi-omics integration highlighted nicotinate/nicotinamide pathways; severe RP was characterized by concomitant reductions in both fecal and tissue NAD⁺ levels, along with an enrichment of microbial nicotinate/nicotinamide metabolism genes, primarily contributed by Bacteroides ovatus, B. xylanisolvens, and B. fragilis. In mice, fecal microbiota transplantation from severe-RP donors exacerbated radiation-induced colorectal injury and decreased colorectal NAD⁺, supporting a causal role for the microbiota. Gavage with Bacteroides similarly worsened pathology and lowered NAD⁺, whereas nicotinamide mononucleotide (NMN) supplementation attenuated the injury. Mechanistically, Bacteroides gavage reduced mitochondrial membrane potential, decreased the Lgr5⁺ stem-cell proportion and proliferative indices, associated with Wnt pathway modulation. NMN reversed these effects in parallel with NAD⁺ restoration. Together, these results identify a microbiota‒metabolite association wherein Bacteroidales enrichment is associated with NAD⁺ depletion, reduced mucosal proliferative capacity, and exacerbated radiation-induced colorectal injury. The work deepens insight into RP pathogenesis and suggests a potential basis for microbiome- and metabolite-targeted approaches to attenuate severe RP.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"77 1","pages":"2641260"},"PeriodicalIF":12.2,"publicationDate":"2026-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147383284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
PD-1 blockade therapy is widely used in clinical practice. Intestinal ischemia reperfusion (IR) injury is a serious clinical complication that leads to remote organ damage through disruption of the gut barrier. However, the effects of PD-1 blockade on gut homeostasis and intestinal IR injury remain unclear. Here, we demonstrate that, in contrast to PD-1 deficiency, PD-1 blockade activates intestinal immunoglobulin A (IgA) responses in mice via a MyD88-dependent pathway. The increased production and bacteria-binding capacity of IgA induced by PD-1 blockade significantly reshape the gut microbial composition and metabolite profile. Furthermore, PD-1 blockade promotes intestinal mucosal CD4+ T cell IL-10 production. Notably, microbiota depletion by antibiotics attenuates intestinal IL-10 production, whereas transplantation of PD-1 blockade-altered microbiota facilitates IL-10 upregulation. These IL-10 enhancements appears to be driven by an increase in Lachnospiraceae_NK4A136_group, a recognized butyrate-producing bacterium, and elevated levels of microbiota-derived butyrate, which were increased after PD-1 blockade and significantly correlated with enhanced IL-10 production in the intestinal mucosa. The upregulation of intestinal IL-10 following PD-1 blockade suppresses inflammatory activation, thereby ameliorating the gut barrier impairment and remote organ injury induced by intestinal IR. In addition, we show that, in vivo and in vitro, butyrate supplementation enhances IL-10 expression in CD4+ T cells through PI3Kγ/phospho-mTOR signaling. Collectively, these findings indicate that PD-1 blockade promotes intestinal mucosal CD4+ T cell IL-10 production by modulating immune‒microbiota interactions and subsequently mitigates intestinal IR-induced gut barrier dysfunction and organ damage.
{"title":"PD-1 blockade promotes mucosal CD4+ T cell IL-10 production through altering microbiota to reduce intestinal ischemia reperfusion injury.","authors":"Shi-Hong Wen,Yi-Nan Zhang,Jian-Tong Shen,Yi Guo,Ze-Nan Chang,Hu-Fei Zhang,Zi-Meng Liu,Xu-Yu Zhang","doi":"10.1080/19490976.2026.2638008","DOIUrl":"https://doi.org/10.1080/19490976.2026.2638008","url":null,"abstract":"PD-1 blockade therapy is widely used in clinical practice. Intestinal ischemia reperfusion (IR) injury is a serious clinical complication that leads to remote organ damage through disruption of the gut barrier. However, the effects of PD-1 blockade on gut homeostasis and intestinal IR injury remain unclear. Here, we demonstrate that, in contrast to PD-1 deficiency, PD-1 blockade activates intestinal immunoglobulin A (IgA) responses in mice via a MyD88-dependent pathway. The increased production and bacteria-binding capacity of IgA induced by PD-1 blockade significantly reshape the gut microbial composition and metabolite profile. Furthermore, PD-1 blockade promotes intestinal mucosal CD4+ T cell IL-10 production. Notably, microbiota depletion by antibiotics attenuates intestinal IL-10 production, whereas transplantation of PD-1 blockade-altered microbiota facilitates IL-10 upregulation. These IL-10 enhancements appears to be driven by an increase in Lachnospiraceae_NK4A136_group, a recognized butyrate-producing bacterium, and elevated levels of microbiota-derived butyrate, which were increased after PD-1 blockade and significantly correlated with enhanced IL-10 production in the intestinal mucosa. The upregulation of intestinal IL-10 following PD-1 blockade suppresses inflammatory activation, thereby ameliorating the gut barrier impairment and remote organ injury induced by intestinal IR. In addition, we show that, in vivo and in vitro, butyrate supplementation enhances IL-10 expression in CD4+ T cells through PI3Kγ/phospho-mTOR signaling. Collectively, these findings indicate that PD-1 blockade promotes intestinal mucosal CD4+ T cell IL-10 production by modulating immune‒microbiota interactions and subsequently mitigates intestinal IR-induced gut barrier dysfunction and organ damage.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"15 1","pages":"2638008"},"PeriodicalIF":12.2,"publicationDate":"2026-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147368390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The role of gut microbiota‒derived metabolites in regulating the intestinal mucosal barrier remains poorly defined. Here, we identified 4-guanidinobutanoic acid (4-GBA), produced by Bacteroides stercorirosoris, as a critical regulator of intestinal homeostasis. Using untargeted metabolomics, organoid co-cultures, mouse models, and single-cell RNA sequencing, we demonstrated that 4-GBA enhances intestinal stem cells (ISCs) function and goblet cell differentiation. This promotes Akkermansia muciniphila enrichment through mucus-dependent niche expansion, establishing a microbiota‒host feedback loop. Mechanistically, 4-GBA upregulates the proton-coupled amino acid transporter SLC36A1 and activates the Hedgehog signaling pathway to drive epithelial reprogramming. Clinically, SLC36A1 expression inversely correlates with ulcerative colitis (UC) severity in human samples. Furthermore, the SLC36A1 agonist sarcosine enhances barrier homeostasis and attenuates colitis in mice, highlighting the diagnostic and therapeutic potential of this axis in UC. Our findings reveal a novel microbiome-host axis through which a microbial metabolite modulates epithelial function and microbial ecology, offering a potential therapeutic strategy targeting microbiota-epithelial crosstalk for UC management.
{"title":"A 4-guanidinobutanoic acid-SLC36A1 axis drives a microbiota‒host feedback loop to regulate intestinal homeostasis.","authors":"Jianming Yang,Yawen Xiao,Jifang Cui,Ruofan Song,Wanxia Ma,Jiangpeng Liu,Chunhui Miao,Xinyu Sun,Xueting Kong,Zhi-Song Zhang,Lu Zhou,Zhi Yao,Quan Wang","doi":"10.1080/19490976.2026.2639216","DOIUrl":"https://doi.org/10.1080/19490976.2026.2639216","url":null,"abstract":"The role of gut microbiota‒derived metabolites in regulating the intestinal mucosal barrier remains poorly defined. Here, we identified 4-guanidinobutanoic acid (4-GBA), produced by Bacteroides stercorirosoris, as a critical regulator of intestinal homeostasis. Using untargeted metabolomics, organoid co-cultures, mouse models, and single-cell RNA sequencing, we demonstrated that 4-GBA enhances intestinal stem cells (ISCs) function and goblet cell differentiation. This promotes Akkermansia muciniphila enrichment through mucus-dependent niche expansion, establishing a microbiota‒host feedback loop. Mechanistically, 4-GBA upregulates the proton-coupled amino acid transporter SLC36A1 and activates the Hedgehog signaling pathway to drive epithelial reprogramming. Clinically, SLC36A1 expression inversely correlates with ulcerative colitis (UC) severity in human samples. Furthermore, the SLC36A1 agonist sarcosine enhances barrier homeostasis and attenuates colitis in mice, highlighting the diagnostic and therapeutic potential of this axis in UC. Our findings reveal a novel microbiome-host axis through which a microbial metabolite modulates epithelial function and microbial ecology, offering a potential therapeutic strategy targeting microbiota-epithelial crosstalk for UC management.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"3 1","pages":"2639216"},"PeriodicalIF":12.2,"publicationDate":"2026-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147350664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-04DOI: 10.1080/19490976.2026.2638004
Edson Mambuque,Ana Del Amo-de Palacios,Samuel G Huete,Charissa C Marsh,Grant Theron,Alberto L García-Basteiro,Sergio Serrano-Villar
Tuberculosis (TB) remains a leading infectious killer, with growing evidence that the human microbiome-particularly in the gut and lungs-shapes susceptibility, progression, and treatment outcomes. Over the past decade, studies have reported that TB-associated dysbiosis, which is more common in the gut than in the lung, is often marked by the loss of short-chain fatty acid-producing taxa and the expansion of opportunistic microbes. However, findings are frequently confounded by diet, antibiotic exposure, comorbidities, geography, and methodological variability. Most research has relied on compositional profiling, offering limited insight into functional mechanisms. This narrative review synthesizes recent evidence, emphasizing the need to integrate multiomics approaches-metagenomics, metatranscriptomics, and metabolomics-and experimental validation to uncover causal links between microbiome alterations and TB pathogenesis or therapy response. We discuss potential clinical applications, including microbiome-based diagnostics (such as stool-based microbial or metabolite signatures for TB risk stratification), prognostic indicators (such as gut microbiome recovery predicting immune normalization during therapy), and adjunctive interventions (including microbiome-derived products to reduce drug-induced liver injury or fecal microbiota transplantation, which has been shown to be safe in people with HIV on stable ART) to mitigate drug toxicity or enhance immune recovery. Key priorities include methodological standardization, confounder control, mechanistic studies, and the inclusion of high-burden settings. By moving beyond descriptive surveys toward functional, translational research, integrating insights from different microbiome methods into TB prevention, diagnosis, and treatment could redefine the clinical research agenda and open new avenues for precision medicine in this global disease.
{"title":"Beyond bacilli: integrating the microbiome into the TB research agenda.","authors":"Edson Mambuque,Ana Del Amo-de Palacios,Samuel G Huete,Charissa C Marsh,Grant Theron,Alberto L García-Basteiro,Sergio Serrano-Villar","doi":"10.1080/19490976.2026.2638004","DOIUrl":"https://doi.org/10.1080/19490976.2026.2638004","url":null,"abstract":"Tuberculosis (TB) remains a leading infectious killer, with growing evidence that the human microbiome-particularly in the gut and lungs-shapes susceptibility, progression, and treatment outcomes. Over the past decade, studies have reported that TB-associated dysbiosis, which is more common in the gut than in the lung, is often marked by the loss of short-chain fatty acid-producing taxa and the expansion of opportunistic microbes. However, findings are frequently confounded by diet, antibiotic exposure, comorbidities, geography, and methodological variability. Most research has relied on compositional profiling, offering limited insight into functional mechanisms. This narrative review synthesizes recent evidence, emphasizing the need to integrate multiomics approaches-metagenomics, metatranscriptomics, and metabolomics-and experimental validation to uncover causal links between microbiome alterations and TB pathogenesis or therapy response. We discuss potential clinical applications, including microbiome-based diagnostics (such as stool-based microbial or metabolite signatures for TB risk stratification), prognostic indicators (such as gut microbiome recovery predicting immune normalization during therapy), and adjunctive interventions (including microbiome-derived products to reduce drug-induced liver injury or fecal microbiota transplantation, which has been shown to be safe in people with HIV on stable ART) to mitigate drug toxicity or enhance immune recovery. Key priorities include methodological standardization, confounder control, mechanistic studies, and the inclusion of high-burden settings. By moving beyond descriptive surveys toward functional, translational research, integrating insights from different microbiome methods into TB prevention, diagnosis, and treatment could redefine the clinical research agenda and open new avenues for precision medicine in this global disease.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"61 1","pages":"2638004"},"PeriodicalIF":12.2,"publicationDate":"2026-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147350665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-02DOI: 10.1080/19490976.2026.2638001
Shuang Wang,Tao Zhou,Xiuqi Wang,Jiangchao Zhao,Xiaofan Wang
Prevotella and Segatella are important, keystone genera in the gut microbiota, renowned for their exceptional fiber-degrading capacity. These genera critically modulate gut microbial composition, influence host metabolic pathways and gut barrier function, and exhibit formidable ecological niche competitiveness, underscoring their pivotal role in gut ecosystem dynamics. While they dominate healthy gut microbiomes, their probiotic potential on epithelial barrier function has been disproportionately overlooked. This review comprehensively elucidates their microbial eco-profiling and the underlying molecular mechanisms in sustaining intestinal barrier function, considering physical, chemical, biological, and microbiological dimensions, thereby providing insights relevant to the prevention and treatment of intestinal diseases such as inflammatory bowel disease, irritable bowel syndrome, and metabolic disorders. Most importantly, we have summarized 23 current commercial and research-based isolation and cultivation approaches for Prevotella/Segatella, integrating the emerging high-throughput methodologies to expand the available strain repertoire. We also emphasize the critical need for subsequent research to characterize strain-specific functional profiles through multi-omics approaches, which will be essential for developing targeted and personalized microbial therapeutics.
{"title":"Bridging the gap: Prevotella/Segatella's impact on gut barrier function and advanced cultivation strategies to realize the uses in gut health.","authors":"Shuang Wang,Tao Zhou,Xiuqi Wang,Jiangchao Zhao,Xiaofan Wang","doi":"10.1080/19490976.2026.2638001","DOIUrl":"https://doi.org/10.1080/19490976.2026.2638001","url":null,"abstract":"Prevotella and Segatella are important, keystone genera in the gut microbiota, renowned for their exceptional fiber-degrading capacity. These genera critically modulate gut microbial composition, influence host metabolic pathways and gut barrier function, and exhibit formidable ecological niche competitiveness, underscoring their pivotal role in gut ecosystem dynamics. While they dominate healthy gut microbiomes, their probiotic potential on epithelial barrier function has been disproportionately overlooked. This review comprehensively elucidates their microbial eco-profiling and the underlying molecular mechanisms in sustaining intestinal barrier function, considering physical, chemical, biological, and microbiological dimensions, thereby providing insights relevant to the prevention and treatment of intestinal diseases such as inflammatory bowel disease, irritable bowel syndrome, and metabolic disorders. Most importantly, we have summarized 23 current commercial and research-based isolation and cultivation approaches for Prevotella/Segatella, integrating the emerging high-throughput methodologies to expand the available strain repertoire. We also emphasize the critical need for subsequent research to characterize strain-specific functional profiles through multi-omics approaches, which will be essential for developing targeted and personalized microbial therapeutics.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"45 1","pages":"2638001"},"PeriodicalIF":12.2,"publicationDate":"2026-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147329321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-22DOI: 10.1080/19490976.2026.2632979
Manish Kumar, Rachel Son, Sarah M. Preston, Robert W. P. Glowacki, Kelley M. Carr, Jiyeon Kim, Jin Z. Ma, Philip P. Ahern, Jan Claesen, Naseer Sangwan, Florian Rieder, Ina Nemet
{"title":"The role of gut microbes in production of aromatic carboxaldehydes","authors":"Manish Kumar, Rachel Son, Sarah M. Preston, Robert W. P. Glowacki, Kelley M. Carr, Jiyeon Kim, Jin Z. Ma, Philip P. Ahern, Jan Claesen, Naseer Sangwan, Florian Rieder, Ina Nemet","doi":"10.1080/19490976.2026.2632979","DOIUrl":"https://doi.org/10.1080/19490976.2026.2632979","url":null,"abstract":"","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"9 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146260718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-22DOI: 10.1080/19490976.2026.2631834
Raquel Benedé-Ubieto, Olga Estévez-Vázquez, Rana Acar, Hector Leal-Lassalle, Alejandro H. Gutierrez, Ana Redondo-Urzainqui, Salvador Iborra, Vera E. Odintsova, Alexander Tyakht, José María Herranz, Zehra Firat, Merve Basol, Busra Korkmaz, Carlos Sanz-García, Oriol Juanola, Esther Caparrós, Rubén Francés, Andreea Ciudin, Juan M. Pericàs, Beatriz Gómez-Santos, Patricia Aspichueta, Nicole Treichel, Thomas Clavel, Johanna Reißing, Tony Bruns, Matthias Bartneck, Marina S. Mazariegos, Justina Clarinda Wolters, Gonzalo Jorquera, Christian Liedtke, Javier Vaquero, Rafael Bañares, Gulcin Cakan-Akdogan, Matías A. Ávila, Ozlen Konu, Francisco Javier Cubero, Yulia A. Nevzorova
{"title":"Alcohol consumption in metabolic dysfunction-associated steatotic liver disease (MASLD): understanding the gut–liver crosstalk for clinical translation","authors":"Raquel Benedé-Ubieto, Olga Estévez-Vázquez, Rana Acar, Hector Leal-Lassalle, Alejandro H. Gutierrez, Ana Redondo-Urzainqui, Salvador Iborra, Vera E. Odintsova, Alexander Tyakht, José María Herranz, Zehra Firat, Merve Basol, Busra Korkmaz, Carlos Sanz-García, Oriol Juanola, Esther Caparrós, Rubén Francés, Andreea Ciudin, Juan M. Pericàs, Beatriz Gómez-Santos, Patricia Aspichueta, Nicole Treichel, Thomas Clavel, Johanna Reißing, Tony Bruns, Matthias Bartneck, Marina S. Mazariegos, Justina Clarinda Wolters, Gonzalo Jorquera, Christian Liedtke, Javier Vaquero, Rafael Bañares, Gulcin Cakan-Akdogan, Matías A. Ávila, Ozlen Konu, Francisco Javier Cubero, Yulia A. Nevzorova","doi":"10.1080/19490976.2026.2631834","DOIUrl":"https://doi.org/10.1080/19490976.2026.2631834","url":null,"abstract":"","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"128 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146260742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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