Pub Date : 2024-08-27DOI: 10.1016/j.chom.2024.07.026
Christopher J. Anderson, Laura Boeckaerts, Pricilla Chin, Javier Burgoa Cardas, Wei Xie, Amanda Gonçalves, Gillian Blancke, Sam Benson, Sebastian Rogatti, Mariska S. Simpson, Anna Davey, Sze Men Choi, Sandrien Desmet, Summer D. Bushman, Geert Goeminne, Peter Vandenabeele, Mahesh S. Desai, Lars Vereecke, Kodi S. Ravichandran
Cytotoxic chemotherapies have devastating side effects, particularly within the gastrointestinal tract. Gastrointestinal toxicity includes the death and damage of the epithelium and an imbalance in the intestinal microbiota, otherwise known as dysbiosis. Whether dysbiosis is a direct contributor to tissue toxicity is a key area of focus. Here, from both mammalian and bacterial perspectives, we uncover an intestinal epithelial cell death-Enterobacteriaceae signaling axis that fuels dysbiosis. Specifically, our data demonstrate that chemotherapy-induced epithelial cell apoptosis and the purine-containing metabolites released from dying cells drive the inter-kingdom transcriptional re-wiring of the Enterobacteriaceae, including fundamental shifts in bacterial respiration and promotion of purine utilization-dependent expansion, which in turn delays the recovery of the intestinal tract. Inhibition of epithelial cell death or restriction of the Enterobacteriaceae to homeostatic levels reverses dysbiosis and improves intestinal recovery. These findings suggest that supportive therapies that maintain homeostatic levels of Enterobacteriaceae may be useful in resolving intestinal disease.
{"title":"Metabolite-based inter-kingdom communication controls intestinal tissue recovery following chemotherapeutic injury","authors":"Christopher J. Anderson, Laura Boeckaerts, Pricilla Chin, Javier Burgoa Cardas, Wei Xie, Amanda Gonçalves, Gillian Blancke, Sam Benson, Sebastian Rogatti, Mariska S. Simpson, Anna Davey, Sze Men Choi, Sandrien Desmet, Summer D. Bushman, Geert Goeminne, Peter Vandenabeele, Mahesh S. Desai, Lars Vereecke, Kodi S. Ravichandran","doi":"10.1016/j.chom.2024.07.026","DOIUrl":"https://doi.org/10.1016/j.chom.2024.07.026","url":null,"abstract":"<p>Cytotoxic chemotherapies have devastating side effects, particularly within the gastrointestinal tract. Gastrointestinal toxicity includes the death and damage of the epithelium and an imbalance in the intestinal microbiota, otherwise known as dysbiosis. Whether dysbiosis is a direct contributor to tissue toxicity is a key area of focus. Here, from both mammalian and bacterial perspectives, we uncover an intestinal epithelial cell death-Enterobacteriaceae signaling axis that fuels dysbiosis. Specifically, our data demonstrate that chemotherapy-induced epithelial cell apoptosis and the purine-containing metabolites released from dying cells drive the inter-kingdom transcriptional re-wiring of the Enterobacteriaceae, including fundamental shifts in bacterial respiration and promotion of purine utilization-dependent expansion, which in turn delays the recovery of the intestinal tract. Inhibition of epithelial cell death or restriction of the Enterobacteriaceae to homeostatic levels reverses dysbiosis and improves intestinal recovery. These findings suggest that supportive therapies that maintain homeostatic levels of Enterobacteriaceae may be useful in resolving intestinal disease.</p>","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":null,"pages":null},"PeriodicalIF":30.3,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142084854","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 : 2024-08-27DOI: 10.1016/j.chom.2024.07.027
Robert Thänert, Drew J. Schwartz, Eric C. Keen, Carla Hall-Moore, Bin Wang, Nurmohammad Shaikh, Jie Ning, L. Colleen Rouggly-Nickless, Anna Thänert, Aura Ferreiro, Skye R.S. Fishbein, Janice E. Sullivan, Paula Radmacher, Marilyn Escobedo, Barbara B. Warner, Phillip I. Tarr, Gautam Dantas
Aberrant preterm infant gut microbiota assembly predisposes to early-life disorders and persistent health problems. Here, we characterize gut microbiome dynamics over the first 3 months of life in 236 preterm infants hospitalized in three neonatal intensive care units using shotgun metagenomics of 2,512 stools and metatranscriptomics of 1,381 stools. Strain tracking, taxonomic and functional profiling, and comprehensive clinical metadata identify Enterobacteriaceae, enterococci, and staphylococci as primarily exploiting available niches to populate the gut microbiome. Clostridioides difficile lineages persist between individuals in single centers, and Staphylococcus epidermidis lineages persist within and, unexpectedly, between centers. Collectively, antibiotic and non-antibiotic medications influence gut microbiome composition to greater extents than maternal or baseline variables. Finally, we identify a persistent low-diversity gut microbiome in neonates who develop necrotizing enterocolitis after day of life 40. Overall, we comprehensively describe gut microbiome dynamics in response to medical interventions in preterm, hospitalized neonates.
{"title":"Clinical sequelae of gut microbiome development and disruption in hospitalized preterm infants","authors":"Robert Thänert, Drew J. Schwartz, Eric C. Keen, Carla Hall-Moore, Bin Wang, Nurmohammad Shaikh, Jie Ning, L. Colleen Rouggly-Nickless, Anna Thänert, Aura Ferreiro, Skye R.S. Fishbein, Janice E. Sullivan, Paula Radmacher, Marilyn Escobedo, Barbara B. Warner, Phillip I. Tarr, Gautam Dantas","doi":"10.1016/j.chom.2024.07.027","DOIUrl":"https://doi.org/10.1016/j.chom.2024.07.027","url":null,"abstract":"<p>Aberrant preterm infant gut microbiota assembly predisposes to early-life disorders and persistent health problems. Here, we characterize gut microbiome dynamics over the first 3 months of life in 236 preterm infants hospitalized in three neonatal intensive care units using shotgun metagenomics of 2,512 stools and metatranscriptomics of 1,381 stools. Strain tracking, taxonomic and functional profiling, and comprehensive clinical metadata identify <em>Enterobacteriaceae</em>, enterococci, and staphylococci as primarily exploiting available niches to populate the gut microbiome. <em>Clostridioides difficile</em> lineages persist between individuals in single centers, and <em>Staphylococcus epidermidis</em> lineages persist within and, unexpectedly, between centers. Collectively, antibiotic and non-antibiotic medications influence gut microbiome composition to greater extents than maternal or baseline variables. Finally, we identify a persistent low-diversity gut microbiome in neonates who develop necrotizing enterocolitis after day of life 40. Overall, we comprehensively describe gut microbiome dynamics in response to medical interventions in preterm, hospitalized neonates.</p>","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":null,"pages":null},"PeriodicalIF":30.3,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142084853","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 : 2024-08-23DOI: 10.1016/j.chom.2024.07.024
Elena Mitsi, Elissavet Nikolaou, Andre Goncalves, Annie Blizard, Helen Hill, Madlen Farrar, Angela Hyder-Wright, Oluwasefunmi Akeju, Josh Hamilton, Ashleigh Howard, Filora Elterish, Carla Solorzano, Ryan Robinson, Jesus Reiné, Andrea M. Collins, Stephen B. Gordon, Richard E. Moxon, Jeffrey N. Weiser, Debby Bogaert, Daniela M. Ferreira
Epidemiological studies report the impact of co-infection with pneumococcus and respiratory viruses upon disease rates and outcomes, but their effect on pneumococcal carriage acquisition and bacterial load is scarcely described. Here, we assess this by combining natural viral infection with controlled human pneumococcal infection in 581 healthy adults screened for upper respiratory tract viral infection before intranasal pneumococcal challenge. Across all adults, respiratory syncytial virus (RSV) and rhinovirus asymptomatic infection confer a substantial increase in secondary infection with pneumococcus. RSV also has a major impact on pneumococcal density up to 9 days post challenge. We also study rates and kinetics of bacterial shedding through the nose and oral route in a subset. High levels of pneumococcal colonization density and nasal inflammation are strongly correlated with increased odds of nasal shedding as opposed to cough shedding. Protection against respiratory viral infections and control of pneumococcal density may contribute to preventing pneumococcal disease and reducing bacterial spread.
{"title":"RSV and rhinovirus increase pneumococcal carriage acquisition and density, whereas nasal inflammation is associated with bacterial shedding","authors":"Elena Mitsi, Elissavet Nikolaou, Andre Goncalves, Annie Blizard, Helen Hill, Madlen Farrar, Angela Hyder-Wright, Oluwasefunmi Akeju, Josh Hamilton, Ashleigh Howard, Filora Elterish, Carla Solorzano, Ryan Robinson, Jesus Reiné, Andrea M. Collins, Stephen B. Gordon, Richard E. Moxon, Jeffrey N. Weiser, Debby Bogaert, Daniela M. Ferreira","doi":"10.1016/j.chom.2024.07.024","DOIUrl":"https://doi.org/10.1016/j.chom.2024.07.024","url":null,"abstract":"<p>Epidemiological studies report the impact of co-infection with pneumococcus and respiratory viruses upon disease rates and outcomes, but their effect on pneumococcal carriage acquisition and bacterial load is scarcely described. Here, we assess this by combining natural viral infection with controlled human pneumococcal infection in 581 healthy adults screened for upper respiratory tract viral infection before intranasal pneumococcal challenge. Across all adults, respiratory syncytial virus (RSV) and rhinovirus asymptomatic infection confer a substantial increase in secondary infection with pneumococcus. RSV also has a major impact on pneumococcal density up to 9 days post challenge. We also study rates and kinetics of bacterial shedding through the nose and oral route in a subset. High levels of pneumococcal colonization density and nasal inflammation are strongly correlated with increased odds of nasal shedding as opposed to cough shedding. Protection against respiratory viral infections and control of pneumococcal density may contribute to preventing pneumococcal disease and reducing bacterial spread.</p>","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":null,"pages":null},"PeriodicalIF":30.3,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142043070","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 : 2024-08-23DOI: 10.1016/j.chom.2024.07.025
Andrew W.L. Rogers, Lauren C. Radlinski, Henry Nguyen, Connor R. Tiffany, Thaynara Parente Carvalho, Hugo L.P. Masson, Michael L. Goodson, Lalita Bechtold, Kohei Yamazaki, Megan J. Liou, Brittany M. Miller, Scott P. Mahan, Briana M. Young, Aurore M. Demars, Sophie R. Gretler, Anaïs B. Larabi, Jee-Yon Lee, Derek J. Bays, Renee M. Tsolis, Andreas J. Bäumler
The gut microbiota prevents harmful microbes from entering the body, a function known as colonization resistance. The enteric pathogen Salmonella enterica serovar (S.) Typhimurium uses its virulence factors to break colonization resistance through unknown mechanisms. Using metabolite profiling and genetic analysis, we show that the initial rise in luminal pathogen abundance was powered by a combination of aerobic respiration and mixed acid fermentation of simple sugars, such as glucose, which resulted in their depletion from the metabolome. The initial rise in the abundance of the pathogen in the feces coincided with a reduction in the cecal concentrations of acetate and butyrate and an increase in epithelial oxygenation. Notably, these changes in the host environment preceded changes in the microbiota composition. We conclude that changes in the host environment can weaken colonization resistance even in the absence of overt compositional changes in the gut microbiota.
{"title":"Salmonella re-engineers the intestinal environment to break colonization resistance in the presence of a compositionally intact microbiota","authors":"Andrew W.L. Rogers, Lauren C. Radlinski, Henry Nguyen, Connor R. Tiffany, Thaynara Parente Carvalho, Hugo L.P. Masson, Michael L. Goodson, Lalita Bechtold, Kohei Yamazaki, Megan J. Liou, Brittany M. Miller, Scott P. Mahan, Briana M. Young, Aurore M. Demars, Sophie R. Gretler, Anaïs B. Larabi, Jee-Yon Lee, Derek J. Bays, Renee M. Tsolis, Andreas J. Bäumler","doi":"10.1016/j.chom.2024.07.025","DOIUrl":"https://doi.org/10.1016/j.chom.2024.07.025","url":null,"abstract":"<p>The gut microbiota prevents harmful microbes from entering the body, a function known as colonization resistance. The enteric pathogen <em>Salmonella enterica</em> serovar (<em>S</em>.) Typhimurium uses its virulence factors to break colonization resistance through unknown mechanisms. Using metabolite profiling and genetic analysis, we show that the initial rise in luminal pathogen abundance was powered by a combination of aerobic respiration and mixed acid fermentation of simple sugars, such as glucose, which resulted in their depletion from the metabolome. The initial rise in the abundance of the pathogen in the feces coincided with a reduction in the cecal concentrations of acetate and butyrate and an increase in epithelial oxygenation. Notably, these changes in the host environment preceded changes in the microbiota composition. We conclude that changes in the host environment can weaken colonization resistance even in the absence of overt compositional changes in the gut microbiota.</p>","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":null,"pages":null},"PeriodicalIF":30.3,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142043071","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 : 2024-08-14DOI: 10.1016/j.chom.2024.07.019
This perspective explores the current understanding of the gut microbiota’s impact on cognitive function in apparently healthy humans and in individuals with metabolic disease. We discuss how alterations in gut microbiota can influence cognitive processes, focusing not only on bacterial composition but also on often overlooked components of the gut microbiota, such as bacteriophages and eukaryotes, as well as microbial functionality. We examine the mechanisms through which gut microbes might communicate with the central nervous system, highlighting the complexity of these interactions. We provide a comprehensive overview of the emerging field of microbiota-gut-brain interactions and its significance for cognitive health. Additionally, we summarize novel therapeutic strategies designed to promote cognitive resilience and reduce the risk of cognitive disorders, focusing on interventions that target the gut microbiota. An in-depth understanding of the microbiome-brain axis is imperative for developing innovative treatments aimed at improving cognitive health.
{"title":"Unlocking the mind-gut connection: Impact of human microbiome on cognition","authors":"","doi":"10.1016/j.chom.2024.07.019","DOIUrl":"https://doi.org/10.1016/j.chom.2024.07.019","url":null,"abstract":"<p>This perspective explores the current understanding of the gut microbiota’s impact on cognitive function in apparently healthy humans and in individuals with metabolic disease. We discuss how alterations in gut microbiota can influence cognitive processes, focusing not only on bacterial composition but also on often overlooked components of the gut microbiota, such as bacteriophages and eukaryotes, as well as microbial functionality. We examine the mechanisms through which gut microbes might communicate with the central nervous system, highlighting the complexity of these interactions. We provide a comprehensive overview of the emerging field of microbiota-gut-brain interactions and its significance for cognitive health. Additionally, we summarize novel therapeutic strategies designed to promote cognitive resilience and reduce the risk of cognitive disorders, focusing on interventions that target the gut microbiota. An in-depth understanding of the microbiome-brain axis is imperative for developing innovative treatments aimed at improving cognitive health.</p>","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":null,"pages":null},"PeriodicalIF":30.3,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141981001","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 : 2024-08-14DOI: 10.1016/j.chom.2024.07.010
Pregnant women undergoing a cesarean section (CS) typically receive antibiotics prior to skin incision to prevent infections. To investigate if the timing of antibiotics influences the infant gut microbiome, we conducted a randomized controlled trial (NCT06030713) in women delivering via a scheduled CS who received antibiotics either before skin incision or after umbilical cord clamping. We performed a longitudinal analysis on 172 samples from 28 infants at 8 post-birth time points and a cross-sectional analysis at 1 month in 79 infants from 3 cohorts. Although no significant associations with bacterial composition, metabolic pathways, short-chain fatty acids, and bile acids were found, we observed subtle differences between the groups at the bacterial strain level and in the load of antibiotic resistance genes. Rather, feeding mode was a predominant and defining factor impacting infant microbial composition. In conclusion, antibiotic administration during CS has only limited effects on the early-life gut microbiome.
{"title":"Maternal antibiotic prophylaxis during cesarean section has a limited impact on the infant gut microbiome","authors":"","doi":"10.1016/j.chom.2024.07.010","DOIUrl":"https://doi.org/10.1016/j.chom.2024.07.010","url":null,"abstract":"<p>Pregnant women undergoing a cesarean section (CS) typically receive antibiotics prior to skin incision to prevent infections. To investigate if the timing of antibiotics influences the infant gut microbiome, we conducted a randomized controlled trial (NCT06030713) in women delivering via a scheduled CS who received antibiotics either before skin incision or after umbilical cord clamping. We performed a longitudinal analysis on 172 samples from 28 infants at 8 post-birth time points and a cross-sectional analysis at 1 month in 79 infants from 3 cohorts. Although no significant associations with bacterial composition, metabolic pathways, short-chain fatty acids, and bile acids were found, we observed subtle differences between the groups at the bacterial strain level and in the load of antibiotic resistance genes. Rather, feeding mode was a predominant and defining factor impacting infant microbial composition. In conclusion, antibiotic administration during CS has only limited effects on the early-life gut microbiome.</p>","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":null,"pages":null},"PeriodicalIF":30.3,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141981003","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 : 2024-08-14DOI: 10.1016/j.chom.2024.07.008
The gut microbiota has been recognized as an important determinant in the initiation and progression of colorectal cancer (CRC), with recent studies shining light on the molecular mechanisms that may contribute to the interactions between microbes and the CRC microenvironment. Despite the increasing wealth of associations being established in the field, proving causality remains challenging. Obstacles include the high variability of the microbiome and its context, both across individuals and across time. Additionally, there is a lack of large and representative cohort studies with long-term follow-up and/or appropriate sampling methods for studying the mucosal microbiome. Finally, most studies focus on CRC, whereas interactions between host and bacteria in early events in carcinogenesis remain elusive, reinforced by the heterogeneity of CRC development. Here, we discuss these current most prominent obstacles, the recent developments, and research needs.
{"title":"Navigating beyond associations: Opportunities to establish causal relationships between the gut microbiome and colorectal carcinogenesis","authors":"","doi":"10.1016/j.chom.2024.07.008","DOIUrl":"https://doi.org/10.1016/j.chom.2024.07.008","url":null,"abstract":"<p>The gut microbiota has been recognized as an important determinant in the initiation and progression of colorectal cancer (CRC), with recent studies shining light on the molecular mechanisms that may contribute to the interactions between microbes and the CRC microenvironment. Despite the increasing wealth of associations being established in the field, proving causality remains challenging. Obstacles include the high variability of the microbiome and its context, both across individuals and across time. Additionally, there is a lack of large and representative cohort studies with long-term follow-up and/or appropriate sampling methods for studying the mucosal microbiome. Finally, most studies focus on CRC, whereas interactions between host and bacteria in early events in carcinogenesis remain elusive, reinforced by the heterogeneity of CRC development. Here, we discuss these current most prominent obstacles, the recent developments, and research needs.</p>","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":null,"pages":null},"PeriodicalIF":30.3,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141981036","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 : 2024-08-14DOI: 10.1016/j.chom.2024.07.018
In this issue of Cell Host & Microbe, Sinha et al. describe their randomized trial assessing whether antibiotics given for maternal benefit prior to Cesarean disrupted the infants’ microbiomes. Despite pre-incision antibiotics reaching the neonate, there was no meaningful alteration to the infant microbiome—especially when compared with breastmilk feeding.
{"title":"Lost in translation: Cesarean antibiotics and the infant microbiome","authors":"","doi":"10.1016/j.chom.2024.07.018","DOIUrl":"https://doi.org/10.1016/j.chom.2024.07.018","url":null,"abstract":"<p>In this issue of <em>Cell Host & Microbe</em>, Sinha et al. describe their randomized trial assessing whether antibiotics given for maternal benefit prior to Cesarean disrupted the infants’ microbiomes. Despite pre-incision antibiotics reaching the neonate, there was no meaningful alteration to the infant microbiome—especially when compared with breastmilk feeding.</p>","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":null,"pages":null},"PeriodicalIF":30.3,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141981008","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 : 2024-08-14DOI: 10.1016/j.chom.2024.07.011
Alcohol-associated liver disease is a leading cause of chronic liver conditions, yet there are limited effective therapies. In this issue of Cell Host & Microbe, Shen et al. demonstrate that soluble dietary fiber enhances intestinal Bacteroides acidifaciens, which ameliorates alcohol-associated liver injury in mice by activating hepatic ornithine aminotransferase.
{"title":"Bacteroides acidifaciens drives a liver detox program","authors":"","doi":"10.1016/j.chom.2024.07.011","DOIUrl":"https://doi.org/10.1016/j.chom.2024.07.011","url":null,"abstract":"<p>Alcohol-associated liver disease is a leading cause of chronic liver conditions, yet there are limited effective therapies. In this issue of <em>Cell Host & Microbe</em>, Shen et al. demonstrate that soluble dietary fiber enhances intestinal <em>Bacteroides acidifaciens,</em> which ameliorates alcohol-associated liver injury in mice by activating hepatic ornithine aminotransferase.</p>","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":null,"pages":null},"PeriodicalIF":30.3,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141980992","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}