Cell host & microbe最新文献_第9页

Transcriptional repressor Capicua is a gatekeeper of cell-intrinsic interferon responses 转录抑制因子Capicua是细胞内生性干扰素反应的守门人

IF 30.3 1区医学

Cell host & microbe Pub Date : 2025-03-24 DOI: 10.1016/j.chom.2025.02.017

Senthamizharasi Manivasagam, Julianna Han, Athmane Teghanemt, Henry Keen, Boopathi Sownthirarajan, Boyang Cheng, Abhiraj Singh, Abigail Lewis, Olivia A. Vogel, Gayathri Loganathan, Lei Huang, Maryline Panis, David K. Meyerholz, Benjamin tenOever, Jasmine T. Perez, Santhakumar Manicassamy, Priya D. Issuree, Balaji Manicassamy

{"title":"Transcriptional repressor Capicua is a gatekeeper of cell-intrinsic interferon responses","authors":"Senthamizharasi Manivasagam, Julianna Han, Athmane Teghanemt, Henry Keen, Boopathi Sownthirarajan, Boyang Cheng, Abhiraj Singh, Abigail Lewis, Olivia A. Vogel, Gayathri Loganathan, Lei Huang, Maryline Panis, David K. Meyerholz, Benjamin tenOever, Jasmine T. Perez, Santhakumar Manicassamy, Priya D. Issuree, Balaji Manicassamy","doi":"10.1016/j.chom.2025.02.017","DOIUrl":"https://doi.org/10.1016/j.chom.2025.02.017","url":null,"abstract":"Early detection of viral infection and rapid activation of host antiviral defenses through transcriptional upregulation of interferons (IFNs) and IFN-stimulated genes (ISGs) are critical for controlling infection. However, aberrant production of IFN in the absence of viral infection leads to auto-inflammation and can be detrimental to the host. Here, we show that the DNA-binding transcriptional repressor complex composed of Capicua (CIC) and Ataxin-1 like (ATXN1L) binds to an 8-nucleotide motif near IFN and ISG promoters and prevents erroneous expression of inflammatory genes under homeostasis in humans and mice. By contrast, during respiratory viral infection, activation of the mitogen-activated protein kinase (MAPK) pathway results in rapid degradation of the CIC-ATXN1L complex, thereby relieving repression and allowing for robust induction of IFN and ISGs. Together, our studies define a new paradigm for host regulation of IFN and ISGs through the evolutionarily conserved CIC-ATXN1L transcriptional repressor complex during homeostasis and viral infection.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"94 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143677858","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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METs, NETs, and UTIs METs， NETs和uti

IF 30.3 1区医学

Cell host & microbe Pub Date : 2025-03-12 DOI: 10.1016/j.chom.2025.02.014

Thomas J. Hannan

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The African gut microbiome: A window into the hidden human microbial diversity 非洲人的肠道微生物群：一扇窥视隐藏的人类微生物多样性的窗口

IF 30.3 1区医学

Cell host & microbe Pub Date : 2025-03-12 DOI: 10.1016/j.chom.2025.02.015

Shuqin Zeng, Hua Wang, Dezhi Mu, Shaopu Wang

引用次数: 0

It takes three: A cocktail of protists, bacterial sphingolipids and an inflammasome 它需要三种物质：原生生物、细菌鞘脂和炎性体的混合物

IF 30.3 1区医学

Cell host & microbe Pub Date : 2025-03-12 DOI: 10.1016/j.chom.2025.02.013

Michael E. Grigg, Eliza V.C. Alves-Ferreira

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Boosting endosymbiosis in plants for future self-sustained crop production 促进植物内共生，为未来作物自给生产做准备

IF 30.3 1区医学

Cell host & microbe Pub Date : 2025-03-12 DOI: 10.1016/j.chom.2025.02.011

Ariane Kemen, Eric Kemen

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Plant growth promotion through repression of defenses by leaf microbiota 通过抑制叶片微生物群的防御来促进植物生长

IF 30.3 1区医学

Cell host & microbe Pub Date : 2025-03-12 DOI: 10.1016/j.chom.2025.02.010

Benjamin Gourion

引用次数: 0

Rewild your gut: Fighting modern diseases with ancient microbes 重新放飞你的肠道：用古老的微生物对抗现代疾病

IF 30.3 1区医学

Cell host & microbe Pub Date : 2025-03-12 DOI: 10.1016/j.chom.2025.02.012

Gwenn Pinel, André Marette

引用次数: 0

Plant cell-cycle regulators control the nuclear environment for viral pathogenesis 植物细胞周期调节器控制病毒致病的核环境

IF 30.3 1区医学

Cell host & microbe Pub Date : 2025-03-04 DOI: 10.1016/j.chom.2025.02.006

Xu Zhang, Ge Wang, Peng Zhang, Chunyan Chen, Jiucheng Zhang, Yumei Bian, Minmin Liu, Chenxu Niu, Fengze Sun, Yahui Wang, Genzhong Liu, Zhimin Wang, Fangfang Ma, Zhilong Bao

{"title":"Plant cell-cycle regulators control the nuclear environment for viral pathogenesis","authors":"Xu Zhang, Ge Wang, Peng Zhang, Chunyan Chen, Jiucheng Zhang, Yumei Bian, Minmin Liu, Chenxu Niu, Fengze Sun, Yahui Wang, Genzhong Liu, Zhimin Wang, Fangfang Ma, Zhilong Bao","doi":"10.1016/j.chom.2025.02.006","DOIUrl":"https://doi.org/10.1016/j.chom.2025.02.006","url":null,"abstract":"The proper regulation of cell-cycle regulators is curial for both viral replication and host-plant adaptive growth during the viral pathogenesis. Mechanisms on reorchestrating RETINOBLASTOMA-RELATED 1 (RBR1), repressor of E2F transcription factor, and downstream genes in host-virus interactions are unclear. Here, we discover that anaphase-promoting complex/cyclosome (APC/C) E3 ligase activator cell division cycle 20 (CDC20) in tomato binds RBR1 or mediates cyclin D1 depletion to preserve RBR1-E2F complexes, while geminivirus or crinivirus repurposes APC/CCDC20 activities to liberate E2Fs in two ways: activating APC/CCDC20 to deplete RBR1 or blocking APC/CCDC20 to stimulate cyclin-D1-mediated RBR1 depletion. The liberated E2Fs activate DNA polymerase or heat shock protein 70 gene transcription to favor virus propagation. The improper disruption of RBR1-E2F complexes via hijacking APC/CCDC20 causes the host growth repression. We uncover a scenario in which the virus co-opts host APC/CCDC20 to reprogram RBR1-E2F complex to favor its propagation while dampening host vitality.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"9 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143539116","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

Cross-kingdom-mediated detection of intestinal protozoa through NLRP6 通过 NLRP6 跨领域检测肠道原生动物

IF 30.3 1区医学

Cell host & microbe Pub Date : 2025-03-04 DOI: 10.1016/j.chom.2025.02.008

Nathaniel J. Winsor, Giuliano Bayer, Ojas Singh, Jeremy K. Chan, Lu Yi Li, Brandon Y. Lieng, Elisabeth Foerster, Ana Popovic, Boyan K. Tsankov, Heather Maughan, Paul Lemire, Elaine Tam, Catherine Streutker, Lina Chen, Stacey L. Heaver, Ruth E. Ley, John Parkinson, J. Rafael Montenegro-Burke, George M.H. Birchenough, Dana J. Philpott, Stephen E. Girardin

{"title":"Cross-kingdom-mediated detection of intestinal protozoa through NLRP6","authors":"Nathaniel J. Winsor, Giuliano Bayer, Ojas Singh, Jeremy K. Chan, Lu Yi Li, Brandon Y. Lieng, Elisabeth Foerster, Ana Popovic, Boyan K. Tsankov, Heather Maughan, Paul Lemire, Elaine Tam, Catherine Streutker, Lina Chen, Stacey L. Heaver, Ruth E. Ley, John Parkinson, J. Rafael Montenegro-Burke, George M.H. Birchenough, Dana J. Philpott, Stephen E. Girardin","doi":"10.1016/j.chom.2025.02.008","DOIUrl":"https://doi.org/10.1016/j.chom.2025.02.008","url":null,"abstract":"Intestinal protists are detected by the host innate immune system through mechanisms that remain poorly understood. Here, we demonstrate that Tritrichomonas protozoa induce thickening of the colonic mucus in an NLRP6-, ASC-, and caspase-11-dependent manner, consistent with the activation of sentinel goblet cells. Mucus growth is recapitulated with cecal extracts from Tritrichomonas-infected mice but not purified protozoa, suggesting that NLRP6 may detect infection-induced microbial dysbiosis. In agreement, Tritrichomonas infection causes a shift in the microbiota with the expansion of Bacteroides and Prevotella, and untargeted metabolomics reveals a dramatic increase in several classes of metabolites, including sphingolipids. Finally, using a combination of gnotobiotic mice and ex vivo mucus analysis, we demonstrate that wild-type, but not sphingolipid-deficient, B. thetaiotaomicron is sufficient to induce NLRP6-dependent sentinel goblet cell function, with the greatest effect observed in female mice. Thus, we propose that NLRP6 is a sensor of intestinal protozoa infection through monitoring microbial sphingolipids.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"29 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143539117","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

Innate immune sensing of rotavirus by intestinal epithelial cells leads to diarrhea 肠道上皮细胞对轮状病毒的先天免疫感应导致腹泻

IF 30.3 1区医学

Cell host & microbe Pub Date : 2025-03-03 DOI: 10.1016/j.chom.2025.02.005

Gaopeng Hou, Juhee Son, Maria Florencia Gomez Castro, Takahiro Kawagishi, Xingxing Ren, Alexa N. Roth, Avan Antia, Qiru Zeng, Anna L. DeVeaux, Ningguo Feng, Hinissan P. Kohio, Megan T. Baldridge, Terence S. Dermody, Shu Zhu, Siyuan Ding

{"title":"Innate immune sensing of rotavirus by intestinal epithelial cells leads to diarrhea","authors":"Gaopeng Hou, Juhee Son, Maria Florencia Gomez Castro, Takahiro Kawagishi, Xingxing Ren, Alexa N. Roth, Avan Antia, Qiru Zeng, Anna L. DeVeaux, Ningguo Feng, Hinissan P. Kohio, Megan T. Baldridge, Terence S. Dermody, Shu Zhu, Siyuan Ding","doi":"10.1016/j.chom.2025.02.005","DOIUrl":"https://doi.org/10.1016/j.chom.2025.02.005","url":null,"abstract":"Diarrhea is the predominant symptom of acute gastroenteritis resulting from enteric infections and a leading cause of death in infants and young children. However, the role of the host response in diarrhea pathogenesis is unclear. Using rotavirus and neonatal mice as a model, we found that oral inoculation of UV-inactivated replication-defective rotavirus consistently induced watery diarrhea by robust activation of cytosolic double-stranded RNA sensing pathways and type III interferon (IFN-λ) secretion. Diarrhea was significantly diminished in mice lacking the IFN-λ receptor. Mechanistically, IFN-λ signaling downregulates the expression of Dra, a chloride and bicarbonate exchanger, which contributes to reduced water absorption. We confirmed these findings in mice inoculated with reovirus, as well as in donor-derived human intestinal organoids and human biopsy samples. Our data highlight a mechanism of rapid diarrhea induction by host innate immune sensing in the gastrointestinal tract and suggest that diarrhea induction is an active host defense strategy to eliminate the pathogen.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"5 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143532405","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