Cell host & microbe最新文献_第2页

Maternal gut microbiome during early pregnancy predicts preterm birth. 妊娠早期孕妇肠道微生物组预测早产。

IF 18.7

Cell host & microbe Pub Date : 2025-09-10 DOI: 10.1016/j.chom.2025.08.004

Zelei Miao, Shijia Hu, Ping Wu, Yuwei Lai, Leo Tianlai Chen, Mingxi Huang, Ke Zhang, Hang He, Fengzhe Xu, Fan Li, Jiaying Yuan, Yayi Hu, Gang Liu, Kailang Huang, Menglei Shuai, Meng Ye, Xinxiu Liang, Congmei Xiao, Wanglong Gou, Ruiqi Shi, Xinyu Wang, Zengliang Jiang, Mei-Qi Shi, Ying-Ying Wu, Xu-Hong Wang, Sha Lu, Yuanqing Fu, Wensheng Hu, Xiu Qiu, An Pan, Xiong-Fei Pan, Ju-Sheng Zheng

{"title":"Maternal gut microbiome during early pregnancy predicts preterm birth.","authors":"Zelei Miao, Shijia Hu, Ping Wu, Yuwei Lai, Leo Tianlai Chen, Mingxi Huang, Ke Zhang, Hang He, Fengzhe Xu, Fan Li, Jiaying Yuan, Yayi Hu, Gang Liu, Kailang Huang, Menglei Shuai, Meng Ye, Xinxiu Liang, Congmei Xiao, Wanglong Gou, Ruiqi Shi, Xinyu Wang, Zengliang Jiang, Mei-Qi Shi, Ying-Ying Wu, Xu-Hong Wang, Sha Lu, Yuanqing Fu, Wensheng Hu, Xiu Qiu, An Pan, Xiong-Fei Pan, Ju-Sheng Zheng","doi":"10.1016/j.chom.2025.08.004","DOIUrl":"10.1016/j.chom.2025.08.004","url":null,"abstract":"Preterm birth, the leading cause of infant mortality and morbidity, lacks robust biomarkers for early risk prediction. Here, we characterized the maternal gut microbiome in 5,313 Chinese pregnant women from two independent cohorts and identified eleven genera and one species associated with preterm birth during early pregnancy. We demonstrated that microbial risk scores (MRSs), generated from selected microbial genera or species, could effectively segregate pregnant women with shorter gestational duration and at higher preterm birth risk. The MRS showed interaction with host polygenic susceptibility to amplify preterm birth risk. Among bacteria comprising the MRS, Clostridium innocuum exhibited the most promising replicable microbial feature for preterm birth. The C. innocuum exhibited 17β-estradiol-degrading activity, and the estradiol-degrading gene k141_29441_57, validated through functional prediction and heterologous expression in E. coli, was enriched in women with preterm birth. These findings open new avenues for microbiome-targeted predictive and therapeutic strategies to mitigate adverse pregnancy outcomes.","PeriodicalId":93926,"journal":{"name":"Cell host & microbe","volume":"33 9","pages":"1623-1639.e8"},"PeriodicalIF":18.7,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145042556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

When predators meet the matrix: Natural resistance via amyloid fibers. 当捕食者遇到基质时：通过淀粉样蛋白纤维产生自然抗性。

IF 18.7

Cell host & microbe Pub Date : 2025-09-10 DOI: 10.1016/j.chom.2025.07.023

Yoann G Santin

引用次数: 0

Microbial matchmakers: Bifidobacterium evolution across animal hosts. 微生物配对者：双歧杆菌在动物宿主中的进化。

IF 18.7

Cell host & microbe Pub Date : 2025-09-10 DOI: 10.1016/j.chom.2025.08.009

Phillip B Pope, Gene W Tyson

引用次数: 0

From poo to promise: Fecal microbiota transplants support immunotherapy re-sensitization in solid tumors. 从 "便便 "到 "希望"：粪便微生物群移植支持实体瘤免疫疗法的再敏感化。

Cell host & microbe Pub Date : 2024-08-14 DOI: 10.1016/j.chom.2024.07.015

Laura Chambers, Dennis Grencewicz, Daniel Spakowicz

引用次数: 0

Brucella-driven host N-glycome remodeling controls infection. 布鲁氏菌驱动的宿主 N-糖蛋白重塑控制着感染。

Cell host & microbe Pub Date : 2024-04-10 Epub Date: 2024-03-25 DOI: 10.1016/j.chom.2024.03.003

Ana-Lucia Cabello, Kelsey Wells, Wenjing Peng, Hui-Qiang Feng, Junyao Wang, Damien F Meyer, Christophe Noroy, En-Shuang Zhao, Hao Zhang, Xueqing Li, Haowu Chang, Gabriel Gomez, Yuxin Mao, Kristin L Patrick, Robert O Watson, William K Russell, Aiying Yu, Jieqiang Zhong, Fengguang Guo, Mingqian Li, Mingyuan Zhou, Xiaoning Qian, Koichi S Kobayashi, Jianxun Song, Suresh Panthee, Yehia Mechref, Thomas A Ficht, Qing-Ming Qin, Paul de Figueiredo

{"title":"Brucella-driven host N-glycome remodeling controls infection.","authors":"Ana-Lucia Cabello, Kelsey Wells, Wenjing Peng, Hui-Qiang Feng, Junyao Wang, Damien F Meyer, Christophe Noroy, En-Shuang Zhao, Hao Zhang, Xueqing Li, Haowu Chang, Gabriel Gomez, Yuxin Mao, Kristin L Patrick, Robert O Watson, William K Russell, Aiying Yu, Jieqiang Zhong, Fengguang Guo, Mingqian Li, Mingyuan Zhou, Xiaoning Qian, Koichi S Kobayashi, Jianxun Song, Suresh Panthee, Yehia Mechref, Thomas A Ficht, Qing-Ming Qin, Paul de Figueiredo","doi":"10.1016/j.chom.2024.03.003","DOIUrl":"10.1016/j.chom.2024.03.003","url":null,"abstract":"Many powerful methods have been employed to elucidate the global transcriptomic, proteomic, or metabolic responses to pathogen-infected host cells. However, the host glycome responses to bacterial infection remain largely unexplored, and hence, our understanding of the molecular mechanisms by which bacterial pathogens manipulate the host glycome to favor infection remains incomplete. Here, we address this gap by performing a systematic analysis of the host glycome during infection by the bacterial pathogen Brucella spp. that cause brucellosis. We discover, surprisingly, that a Brucella effector protein (EP) Rhg1 induces global reprogramming of the host cell N-glycome by interacting with components of the oligosaccharide transferase complex that controls N-linked protein glycosylation, and Rhg1 regulates Brucella replication and tissue colonization in a mouse model of brucellosis, demonstrating that Brucella exploits the EP Rhg1 to reprogram the host N-glycome and promote bacterial intracellular parasitism, thereby providing a paradigm for bacterial control of host cell infection.","PeriodicalId":93926,"journal":{"name":"Cell host & microbe","volume":" ","pages":"588-605.e9"},"PeriodicalIF":0.0,"publicationDate":"2024-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140295569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Human cytomegalovirus degrades DMXL1 to inhibit autophagy, lysosomal acidification, and viral assembly. 人类巨细胞病毒会降解 DMXL1，从而抑制自噬、溶酶体酸化和病毒组装。

IF 18.7

Cell host & microbe Pub Date : 2024-04-10 Epub Date: 2024-03-12 DOI: 10.1016/j.chom.2024.02.013

Hanqi Li, Alice Fletcher-Etherington, Leah M Hunter, Swati Keshri, Ceri A Fielding, Katie Nightingale, Benjamin Ravenhill, Luis Nobre, Martin Potts, Robin Antrobus, Colin M Crump, David C Rubinsztein, Richard J Stanton, Michael P Weekes

{"title":"Human cytomegalovirus degrades DMXL1 to inhibit autophagy, lysosomal acidification, and viral assembly.","authors":"Hanqi Li, Alice Fletcher-Etherington, Leah M Hunter, Swati Keshri, Ceri A Fielding, Katie Nightingale, Benjamin Ravenhill, Luis Nobre, Martin Potts, Robin Antrobus, Colin M Crump, David C Rubinsztein, Richard J Stanton, Michael P Weekes","doi":"10.1016/j.chom.2024.02.013","DOIUrl":"10.1016/j.chom.2024.02.013","url":null,"abstract":"Human cytomegalovirus (HCMV) is an important human pathogen that regulates host immunity and hijacks host compartments, including lysosomes, to assemble virions. We combined a quantitative proteomic analysis of HCMV infection with a database of proteins involved in vacuolar acidification, revealing Dmx-like protein-1 (DMXL1) as the only protein that acidifies vacuoles yet is degraded by HCMV. Systematic comparison of viral deletion mutants reveals the uncharacterized 7 kDa US33A protein as necessary and sufficient for DMXL1 degradation, which occurs via recruitment of the E3 ubiquitin ligase Kip1 ubiquitination-promoting complex (KPC). US33A-mediated DMXL1 degradation inhibits lysosome acidification and autophagic cargo degradation. Formation of the virion assembly compartment, which requires lysosomes, occurs significantly later with US33A-expressing virus infection, with reduced viral replication. These data thus identify a viral strategy for cellular remodeling, with the potential to employ US33A in therapies for viral infection or rheumatic conditions, in which inhibition of lysosome acidification can attenuate disease.","PeriodicalId":93926,"journal":{"name":"Cell host & microbe","volume":" ","pages":"466-478.e11"},"PeriodicalIF":18.7,"publicationDate":"2024-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140121586","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cytoplasmic calcium influx mediated by plant MLKLs confers TNL-triggered immunity. 由植物 MLKLs 介导的细胞质钙离子流入赋予 TNL 触发的免疫力。

Cell host & microbe Pub Date : 2024-04-10 Epub Date: 2024-03-20 DOI: 10.1016/j.chom.2024.02.016

Qiaochu Shen, Keiichi Hasegawa, Nicole Oelerich, Anna Prakken, Lea Weiler Tersch, Junli Wang, Frowin Reichhardt, Alexandra Tersch, Je Cuan Choo, Ton Timmers, Kay Hofmann, Jane E Parker, Jijie Chai, Takaki Maekawa

{"title":"Cytoplasmic calcium influx mediated by plant MLKLs confers TNL-triggered immunity.","authors":"Qiaochu Shen, Keiichi Hasegawa, Nicole Oelerich, Anna Prakken, Lea Weiler Tersch, Junli Wang, Frowin Reichhardt, Alexandra Tersch, Je Cuan Choo, Ton Timmers, Kay Hofmann, Jane E Parker, Jijie Chai, Takaki Maekawa","doi":"10.1016/j.chom.2024.02.016","DOIUrl":"10.1016/j.chom.2024.02.016","url":null,"abstract":"The plant homolog of vertebrate necroptosis inducer mixed-lineage kinase domain-like (MLKL) contributes to downstream steps in Toll-interleukin-1 receptor domain NLR (TNL)-receptor-triggered immunity. Here, we show that Arabidopsis MLKL1 (AtMLKL1) clusters into puncta at the plasma membrane upon TNL activation and that this sub-cellular reorganization is dependent on the TNL signal transducer, EDS1. We find that AtMLKLs confer TNL-triggered immunity in parallel with RPW8-type HeLo-domain-containing NLRs (RNLs) and that the AtMLKL N-terminal HeLo domain is indispensable for both immunity and clustering. We show that the AtMLKL HeLo domain mediates cytoplasmic Ca2+ ([Ca2+]cyt) influx in plant and human cells, and AtMLKLs are responsible for sustained [Ca2+]cyt influx during TNL-triggered, but not CNL-triggered, immunity. Our study reveals parallel immune signaling functions of plant MLKLs and RNLs as mediators of [Ca2+]cyt influx and a potentially common role of the HeLo domain fold in the Ca2+-signal relay of diverse organisms.","PeriodicalId":93926,"journal":{"name":"Cell host & microbe","volume":" ","pages":"453-465.e6"},"PeriodicalIF":0.0,"publicationDate":"2024-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140186604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Opposing diet, microbiome, and metabolite mechanisms regulate inflammatory bowel disease in a genetically susceptible host. 饮食、微生物组和代谢物的对立机制调节易感基因宿主的炎症性肠病。

Cell host & microbe Pub Date : 2024-04-10 Epub Date: 2024-03-20 DOI: 10.1016/j.chom.2024.03.001

Gabriel Vasconcelos Pereira, Marie Boudaud, Mathis Wolter, Celeste Alexander, Alessandro De Sciscio, Erica T Grant, Bruno Caetano Trindade, Nicholas A Pudlo, Shaleni Singh, Austin Campbell, Mengrou Shan, Li Zhang, Qinnan Yang, Stéphanie Willieme, Kwi Kim, Trisha Denike-Duval, Jaime Fuentes, André Bleich, Thomas M Schmidt, Lucy Kennedy, Costas A Lyssiotis, Grace Y Chen, Kathryn A Eaton, Mahesh S Desai, Eric C Martens

{"title":"Opposing diet, microbiome, and metabolite mechanisms regulate inflammatory bowel disease in a genetically susceptible host.","authors":"Gabriel Vasconcelos Pereira, Marie Boudaud, Mathis Wolter, Celeste Alexander, Alessandro De Sciscio, Erica T Grant, Bruno Caetano Trindade, Nicholas A Pudlo, Shaleni Singh, Austin Campbell, Mengrou Shan, Li Zhang, Qinnan Yang, Stéphanie Willieme, Kwi Kim, Trisha Denike-Duval, Jaime Fuentes, André Bleich, Thomas M Schmidt, Lucy Kennedy, Costas A Lyssiotis, Grace Y Chen, Kathryn A Eaton, Mahesh S Desai, Eric C Martens","doi":"10.1016/j.chom.2024.03.001","DOIUrl":"10.1016/j.chom.2024.03.001","url":null,"abstract":"Inflammatory bowel diseases (IBDs) are chronic conditions characterized by periods of spontaneous intestinal inflammation and are increasing in industrialized populations. Combined with host genetics, diet and gut bacteria are thought to contribute prominently to IBDs, but mechanisms are still emerging. In mice lacking the IBD-associated cytokine, interleukin-10, we show that a fiber-deprived gut microbiota promotes the deterioration of colonic mucus, leading to lethal colitis. Inflammation starts with the expansion of natural killer cells and altered immunoglobulin-A coating of some bacteria. Lethal colitis is then driven by Th1 immune responses to increased activities of mucin-degrading bacteria that cause inflammation first in regions with thinner mucus. A fiber-free exclusive enteral nutrition diet also induces mucus erosion but inhibits inflammation by simultaneously increasing an anti-inflammatory bacterial metabolite, isobutyrate. Our findings underscore the importance of focusing on microbial functions-not taxa-contributing to IBDs and that some diet-mediated functions can oppose those that promote disease.","PeriodicalId":93926,"journal":{"name":"Cell host & microbe","volume":" ","pages":"527-542.e9"},"PeriodicalIF":0.0,"publicationDate":"2024-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11064055/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140186605","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A specific enterotype derived from gut microbiome of older individuals enables favorable responses to immune checkpoint blockade therapy. 从老年人肠道微生物组中提取的特异性肠型可对免疫检查点阻断疗法产生良好反应。

Cell host & microbe Pub Date : 2024-04-10 Epub Date: 2024-03-20 DOI: 10.1016/j.chom.2024.03.002

Xiaoqiang Zhu, Xiaowen Huang, Muni Hu, Rongrong Sun, Jiantao Li, Hai Wang, Xuefeng Pan, Yanru Ma, Lijun Ning, Tianying Tong, Yilu Zhou, Jinmei Ding, Ying Zhao, Baoqin Xuan, Jing-Yuan Fang, Jie Hong, Jason Wing Hon Wong, Youwei Zhang, Haoyan Chen

{"title":"A specific enterotype derived from gut microbiome of older individuals enables favorable responses to immune checkpoint blockade therapy.","authors":"Xiaoqiang Zhu, Xiaowen Huang, Muni Hu, Rongrong Sun, Jiantao Li, Hai Wang, Xuefeng Pan, Yanru Ma, Lijun Ning, Tianying Tong, Yilu Zhou, Jinmei Ding, Ying Zhao, Baoqin Xuan, Jing-Yuan Fang, Jie Hong, Jason Wing Hon Wong, Youwei Zhang, Haoyan Chen","doi":"10.1016/j.chom.2024.03.002","DOIUrl":"10.1016/j.chom.2024.03.002","url":null,"abstract":"Immunotherapy has revolutionized cancer treatment, but inconsistent responses persist. Our study delves into the intriguing phenomenon of enhanced immunotherapy sensitivity in older individuals with cancers. Through a meta-analysis encompassing 25 small-to-mid-sized trials of immune checkpoint blockade (ICB), we demonstrate that older individuals exhibit heightened responsiveness to ICB therapy. To understand the underlying mechanism, we reanalyze single-cell RNA sequencing (scRNA-seq) data from multiple studies and unveil distinct upregulation of exhausted and cytotoxic T cell markers within the tumor microenvironment (TME) of older patients. Recognizing the potential role of gut microbiota in modulating the efficacy of immunotherapy, we identify an aging-enriched enterotype linked to improved immunotherapy outcomes in older patients. Fecal microbiota transplantation experiments in mice confirm the therapeutic potential of the aging-enriched enterotype, enhancing treatment sensitivity and reshaping the TME. Our discoveries confront the prevailing paradox and provide encouraging paths for tailoring cancer immunotherapy strategies according to an individual's gut microbiome profile.","PeriodicalId":93926,"journal":{"name":"Cell host & microbe","volume":" ","pages":"489-505.e5"},"PeriodicalIF":0.0,"publicationDate":"2024-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140186603","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Plant cellular messengers mobilized to defend. 调动植物细胞信使进行防御。

Cell host & microbe Pub Date : 2024-03-13 DOI: 10.1016/j.chom.2024.02.005

Lifan Sun, Jie Zhang

引用次数: 0