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AI in microbiome research: Where have we been, where are we going? 微生物组研究中的人工智能：我们去了哪里？
IF 30.3 1区 医学
Cell host & microbe Pub Date : 2024-08-14 DOI: 10.1016/j.chom.2024.07.021
{"title":"AI in microbiome research: Where have we been, where are we going?","authors":"","doi":"10.1016/j.chom.2024.07.021","DOIUrl":"https://doi.org/10.1016/j.chom.2024.07.021","url":null,"abstract":"<p>Artificial intelligence (AI), a subdiscipline of computer science that develops machines or software that mimic characteristically human cognitive functions, is currently undergoing a revolution. In this commentary article, I will give my perspective on the evolution of the field and my thoughts on how AI may impact microbiome research in the next decade.</p>","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"145 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141980996","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}
引用次数: 0
Fishing for obesity-related gut microbiome enterotype 寻找与肥胖有关的肠道微生物群肠型
IF 30.3 1区 医学
Cell host & microbe Pub Date : 2024-08-14 DOI: 10.1016/j.chom.2024.07.002
{"title":"Fishing for obesity-related gut microbiome enterotype","authors":"","doi":"10.1016/j.chom.2024.07.002","DOIUrl":"https://doi.org/10.1016/j.chom.2024.07.002","url":null,"abstract":"<p>Despite debate, the concept of enterotype-like clusters remains valuable for exploring the human gut microbiome and associated environmental factors. In this issue of <em>Cell Host &amp; Microbe</em>, Wu et al. robustly identified an obesity-related enterotype-like cluster, <em>Megamonas</em>, and demonstrated its clinical relevance through cohort studies, mice, and cell experiments.</p>","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"30 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141980995","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}
引用次数: 0
Intestinal gases as a non-invasive measurement of microbial fermentation and host health 肠道气体作为微生物发酵和宿主健康的无创测量方法
IF 30.3 1区 医学
Cell host & microbe Pub Date : 2024-08-14 DOI: 10.1016/j.chom.2024.07.004
{"title":"Intestinal gases as a non-invasive measurement of microbial fermentation and host health","authors":"","doi":"10.1016/j.chom.2024.07.004","DOIUrl":"https://doi.org/10.1016/j.chom.2024.07.004","url":null,"abstract":"<p>Microbial fermentation and associated products provide insights into the gut microbiota-host relationship. Here, we propose using improved technologies that allow non-invasive, real-time measurements of intestinal gases as a metric for microbial fermentation. This approach has the potential to provide a basis for personalized interventions that improve host metabolic health.</p>","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"25 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141980997","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}
引用次数: 0
Microbiome modification for personalized treatment of dysbiotic diseases 改变微生物组，个性化治疗菌群失调疾病
IF 30.3 1区 医学
Cell host & microbe Pub Date : 2024-08-14 DOI: 10.1016/j.chom.2024.07.023
{"title":"Microbiome modification for personalized treatment of dysbiotic diseases","authors":"","doi":"10.1016/j.chom.2024.07.023","DOIUrl":"https://doi.org/10.1016/j.chom.2024.07.023","url":null,"abstract":"<p>Fecal microbial transplantation (FMT) for inflammatory diseases or refractory immune checkpoint inhibitor therapy is less effective than for preventing recurrent <em>Clostridioides difficile</em> infection. This commentary outlines strategies to use biomarkers of successful FMT to guide newer approaches to restore microbial homeostasis in individuals with dysbiosis-mediated inflammation.</p>","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"93 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141980994","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}
引用次数: 0
Fighting the invisible foe in cancer therapy 对抗癌症治疗中的隐形敌人
IF 30.3 1区 医学
Cell host & microbe Pub Date : 2024-08-14 DOI: 10.1016/j.chom.2024.07.016
{"title":"Fighting the invisible foe in cancer therapy","authors":"","doi":"10.1016/j.chom.2024.07.016","DOIUrl":"https://doi.org/10.1016/j.chom.2024.07.016","url":null,"abstract":"In this issue of Cell Host & Microbe, Huang et al. determine that an oncogenic bacterium contributes to colorectal cancer progression and resistance t…","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"11 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141980993","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}
引用次数: 0
Alleviating protein-condensation-associated damage at the endoplasmic reticulum enhances plant disease tolerance 减轻内质网蛋白质缩聚相关损伤可提高植物的抗病能力
IF 30.3 1区 医学
Cell host & microbe Pub Date : 2024-08-06 DOI: 10.1016/j.chom.2024.07.013
{"title":"Alleviating protein-condensation-associated damage at the endoplasmic reticulum enhances plant disease tolerance","authors":"","doi":"10.1016/j.chom.2024.07.013","DOIUrl":"https://doi.org/10.1016/j.chom.2024.07.013","url":null,"abstract":"<p>Disease tolerance is an essential defense strategy against pathogens, alleviating tissue damage regardless of pathogen multiplication. However, its genetic and molecular basis remains largely unknown. Here, we discovered that protein condensation at the endoplasmic reticulum (ER) regulates disease tolerance in <em>Arabidopsis</em> against <em>Pseudomonas syringae</em>. During infection, Hematopoietic protein-1 (HEM1) and Bax-inhibitor 1 (BI-1) coalesce into ER-associated condensates facilitated by their phase-separation behaviors. While BI-1 aids in clearing these condensates via autophagy, it also sequesters lipid-metabolic enzymes within condensates, likely disturbing lipid homeostasis. Consequently, mutations in <em>hem1</em>, which hinder condensate formation, or in <em>bi-1</em>, which prevent enzyme entrapment, enhance tissue-damage resilience, and preserve overall plant health during infection. These findings suggest that the ER is a crucial hub for maintaining cellular homeostasis and establishing disease tolerance. They also highlight the potential of engineering disease tolerance as a defense strategy to complement established resistance mechanisms in combating plant diseases.</p>","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"82 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141895788","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}
引用次数: 0
BCAA-producing Clostridium symbiosum promotes colorectal tumorigenesis through the modulation of host cholesterol metabolism 产生 BCAA 的共生梭菌通过调节宿主胆固醇代谢促进结直肠肿瘤发生
IF 30.3 1区 医学
Cell host & microbe Pub Date : 2024-08-05 DOI: 10.1016/j.chom.2024.07.012
{"title":"BCAA-producing Clostridium symbiosum promotes colorectal tumorigenesis through the modulation of host cholesterol metabolism","authors":"","doi":"10.1016/j.chom.2024.07.012","DOIUrl":"https://doi.org/10.1016/j.chom.2024.07.012","url":null,"abstract":"<p>Identification of potential bacterial players in colorectal tumorigenesis has been a focus of intense research. Herein, we find that <em>Clostridium symbiosum</em> (<em>C. symbiosum</em>) is selectively enriched in tumor tissues of patients with colorectal cancer (CRC) and associated with higher colorectal adenoma recurrence after endoscopic polypectomy. The tumorigenic effect of <em>C. symbiosum</em> is observed in multiple murine models. Single-cell transcriptome profiling along with functional assays demonstrates that <em>C. symbiosum</em> promotes the proliferation of colonic stem cells and enhances cancer stemness. Mechanistically, <em>C. symbiosum</em> intensifies cellular cholesterol synthesis by producing branched-chain amino acids (BCAAs), which sequentially activates Sonic hedgehog signaling. Low dietary BCAA intake or blockade of cholesterol synthesis by statins could partially abrogate the <em>C. symbiosum</em>-induced cell proliferation <em>in vivo</em> and <em>in vitro</em>. Collectively, we reveal <em>C. symbiosum</em> as a bacterial driver of colorectal tumorigenesis, thus identifying a potential target in CRC prediction, prevention, and treatment.</p>","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"29 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141892154","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}
引用次数: 0
Protein arginine methyltransferase 6 mediates antiviral immunity in plants 精氨酸甲基转移酶 6 在植物抗病毒免疫中起介导作用
IF 30.3 1区 医学
Cell host & microbe Pub Date : 2024-08-05 DOI: 10.1016/j.chom.2024.07.014
{"title":"Protein arginine methyltransferase 6 mediates antiviral immunity in plants","authors":"","doi":"10.1016/j.chom.2024.07.014","DOIUrl":"https://doi.org/10.1016/j.chom.2024.07.014","url":null,"abstract":"<p>Viral suppressor RNA silencing (VSR) is essential for successful infection. Nucleotide-binding and leucine-rich repeat (NLR)-based and autophagy-mediated immune responses have been reported to target VSR as counter-defense strategies. Here, we report a protein arginine methyltransferase 6 (PRMT6)-mediated defense mechanism targeting VSR. The knockout and overexpression of <em>PRMT6</em> in tomato plants lead to enhanced and reduced disease symptoms, respectively, during tomato bush stunt virus (TBSV) infection. PRMT6 interacts with and inhibits the VSR function of TBSV P19 by methylating its key arginine residues R43 and R115, thereby reducing its dimerization and small RNA-binding activities. Analysis of the natural tomato population reveals that two major alleles associated with high and low levels of <em>PRMT6</em> expression are significantly associated with high and low levels of viral resistance, respectively. Our study establishes PRMT6-mediated arginine methylation of VSR as a mechanism of plant immunity against viruses.</p>","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"52 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141892156","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}
引用次数: 0
Bacterial homologs of innate eukaryotic antiviral defenses with anti-phage activity highlight shared evolutionary roots of viral defenses 具有抗噬菌体活性的先天真核生物抗病毒防御系统的细菌同源物凸显了病毒防御系统的共同进化根源
IF 30.3 1区 医学
Cell host & microbe Pub Date : 2024-08-01 DOI: 10.1016/j.chom.2024.07.007
{"title":"Bacterial homologs of innate eukaryotic antiviral defenses with anti-phage activity highlight shared evolutionary roots of viral defenses","authors":"","doi":"10.1016/j.chom.2024.07.007","DOIUrl":"https://doi.org/10.1016/j.chom.2024.07.007","url":null,"abstract":"<p>Prokaryotes have evolved a multitude of defense systems to protect against phage predation. Some of these resemble eukaryotic genes involved in antiviral responses. Here, we set out to systematically project the current knowledge of eukaryotic-like antiviral defense systems onto prokaryotic genomes, using <em>Pseudomonas aeruginosa</em> as a model organism. Searching for phage defense systems related to innate antiviral genes from vertebrates and plants, we uncovered over 450 candidates. We validated six of these phage defense systems, including factors preventing viral attachment, R-loop-acting enzymes, the inflammasome, ubiquitin pathway, and pathogen recognition signaling. Collectively, these defense systems support the concept of deep evolutionary links and shared antiviral mechanisms between prokaryotes and eukaryotes.</p>","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"69 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141862427","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}
引用次数: 0
Viral hijacking of hnRNPH1 unveils a G-quadruplex-driven mechanism of stress control 病毒对 hnRNPH1 的劫持揭示了一种由 G 型四联体驱动的应激控制机制
IF 30.3 1区 医学
Cell host & microbe Pub Date : 2024-08-01 DOI: 10.1016/j.chom.2024.07.006
{"title":"Viral hijacking of hnRNPH1 unveils a G-quadruplex-driven mechanism of stress control","authors":"","doi":"10.1016/j.chom.2024.07.006","DOIUrl":"https://doi.org/10.1016/j.chom.2024.07.006","url":null,"abstract":"<p>Viral genomes are enriched with G-quadruplexes (G4s), non-canonical structures formed in DNA or RNA upon assembly of four guanine stretches into stacked quartets. Because of their critical roles, G4s are potential antiviral targets, yet their function remains largely unknown. Here, we characterize the formation and functions of a conserved G4 within the polymerase coding region of orthoflaviviruses of the <em>Flaviviridae</em> family. Using yellow fever virus, we determine that this G4 promotes viral replication and suppresses host stress responses via interactions with hnRNPH1, a host nuclear protein involved in RNA processing. G4 binding to hnRNPH1 causes its cytoplasmic retention with subsequent impacts on G4-containing tRNA fragments (tiRNAs) involved in stress-mediated reductions in translation. As a result, these host stress responses and associated antiviral effects are impaired. These data reveal that the interplay between hnRNPH1 and both host and viral G4 targets controls the integrated stress response and viral replication.</p>","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"45 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141862426","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}
引用次数: 0
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