Cell host & microbe最新文献_第3页

The HY5-NPR1 module governs light-dependent virulence of a plant bacterial pathogen HY5-NPR1模块控制植物细菌病原体的光依赖性毒力

IF 30.3 1区医学

Cell host & microbe Pub Date : 2025-09-02 DOI: 10.1016/j.chom.2025.08.007

Pengtao Liu, Zhao Zhao, Yaqi Tang, Yangyang Zhou, Jie Liu, Kaiqi Xu, Yaxin Chen, Xiaoting Li, Yaru Tang, Li Yang

{"title":"The HY5-NPR1 module governs light-dependent virulence of a plant bacterial pathogen","authors":"Pengtao Liu, Zhao Zhao, Yaqi Tang, Yangyang Zhou, Jie Liu, Kaiqi Xu, Yaxin Chen, Xiaoting Li, Yaru Tang, Li Yang","doi":"10.1016/j.chom.2025.08.007","DOIUrl":"https://doi.org/10.1016/j.chom.2025.08.007","url":null,"abstract":"Light is essential for plant development, but its influence on pathogen virulence and immunity remains poorly understood. Here, we found that the Pseudomonas syringae DC3000 type III effector, AvrPtoB, exhibits virulence exclusively upon light exposure. This light-dependent regulation is controlled by the Arabidopsis transcription factor ELONGATED HYPOCOTYL 5 (HY5), a central regulator of photomorphogenesis. AvrPtoB targets HY5 in the nucleus, facilitating its ubiquitination and degradation. Genetic disruption of HY5 eliminates susceptibility to AvrPtoB and compromises plant immunity upon light exposure. HY5 enhances immunity by binding promoters of defense-related genes, activating their expression, and stabilizing the transcriptional coregulator NONEXPRESSOR OF PATHOGENESIS-RELATED (PR) GENES 1 (NPR1) by inhibiting its negative regulators NPR3/4. Both HY5-mediated immunity and light-dependent AvrPtoB virulence require NPR1. By contrast, during darkness, CONSTITUTIVELY PHOTOMORPHOGENIC 1 (COP1)-mediated HY5 degradation suppresses AvrPtoB virulence and HY5-enhanced immunity. These findings elucidate a mechanism in which light modulates bacterial virulence and plant immunity via an HY5-NPR1 module, advancing our understanding of light-pathogen-host interactions.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"50 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144928634","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

pH-induced conformational changes and inhibition of the Lassa virus spike complex ph诱导的拉沙病毒刺突复合体的构象变化和抑制

IF 30.3 1区医学

Cell host & microbe Pub Date : 2025-09-01 DOI: 10.1016/j.chom.2025.07.020

Michael Katz, Hadas Cohen-Dvashi, Sarah Borni, John Ruedas, Greg Henkel, Ken McCormack, Ron Diskin

{"title":"pH-induced conformational changes and inhibition of the Lassa virus spike complex","authors":"Michael Katz, Hadas Cohen-Dvashi, Sarah Borni, John Ruedas, Greg Henkel, Ken McCormack, Ron Diskin","doi":"10.1016/j.chom.2025.07.020","DOIUrl":"https://doi.org/10.1016/j.chom.2025.07.020","url":null,"abstract":"Lassa virus (LASV) is a devastating human pathogen with no vaccines and limited therapeutics. The LASV class-I spike complex engages target cells via binding its primary host receptor, matriglycan, followed by macropinocytosis and binding of its secondary receptor, lysosomal-associated membrane protein 1 (LAMP1), to trigger virus fusion. This process occurs across multiple pH-dependent steps, but the molecular events remain largely unknown. Through high-resolution structures, we study the pH-induced conformational changes of the spike preceding membrane fusion. We reveal pH-sensitive metal coordination sites that control the integrity of the spike's native state, elucidate a reorganization of the spike's transmembrane region, and provide a mechanism for dissociation from its primary receptor. Using the entry inhibitor ARN-75039, we validate our findings and establish the molecular basis for the binding and function of this investigational drug. These data define the molecular basis for the cell entry of LASV and will promote efforts in combating this virus and potentially related viral pathogens.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"91 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144924413","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

Macrophages orchestrate elimination of Shigella from the intestinal epithelial cell niche via TLR-induced IL-12 and IFN-γ 巨噬细胞通过tlr诱导的IL-12和IFN-γ从肠上皮细胞龛中协调消除志贺氏菌

IF 30.3 1区医学

Cell host & microbe Pub Date : 2025-08-29 DOI: 10.1016/j.chom.2025.08.001

Kevin D. Eislmayr, Charlotte A. Nichols, Fitty L. Liu, Sudyut Yuvaraj, Janet Peace Babirye, Justin L. Roncaioli, Jenna Vickery, Gregory M. Barton, Cammie F. Lesser, Russell E. Vance

{"title":"Macrophages orchestrate elimination of Shigella from the intestinal epithelial cell niche via TLR-induced IL-12 and IFN-γ","authors":"Kevin D. Eislmayr, Charlotte A. Nichols, Fitty L. Liu, Sudyut Yuvaraj, Janet Peace Babirye, Justin L. Roncaioli, Jenna Vickery, Gregory M. Barton, Cammie F. Lesser, Russell E. Vance","doi":"10.1016/j.chom.2025.08.001","DOIUrl":"https://doi.org/10.1016/j.chom.2025.08.001","url":null,"abstract":"Bacteria of the genus Shigella replicate in intestinal epithelial cells and cause shigellosis, a severe diarrheal disease that resolves spontaneously in most healthy individuals. During shigellosis, neutrophils are abundantly recruited to the gut and have long been thought to be central to Shigella control and pathogenesis. However, how shigellosis resolves remains poorly understood due to the longstanding lack of a tractable and physiological animal model. Here, using our newly developed Nlrc4–/–Casp11–/– mouse model of shigellosis, we unexpectedly find no major role for neutrophils in limiting Shigella or in disease pathogenesis. Instead, we uncover an essential role for macrophages in the host control of Shigella. Macrophages respond to Shigella via Toll-like receptors (TLRs) to produce IL-12, which then induces IFN-γ, a cytokine that is essential to control Shigella replication in intestinal epithelial cells. Collectively, our findings reshape our understanding of the innate immune response to Shigella.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"37 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144915924","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

Cryptosporidium parvum multidrug resistance protein confers resistance to toxic gut microbial metabolite 小隐孢子虫多药耐药蛋白赋予对有毒肠道微生物代谢物的抗性

IF 30.3 1区医学

Cell host & microbe Pub Date : 2025-08-27 DOI: 10.1016/j.chom.2025.07.024

Wanyi Huang, Rui Xu, Abigail Kimball, William H. Witola, Megan T. Baldridge, Yaoyu Feng, Lihua Xiao, L. David Sibley

{"title":"Cryptosporidium parvum multidrug resistance protein confers resistance to toxic gut microbial metabolite","authors":"Wanyi Huang, Rui Xu, Abigail Kimball, William H. Witola, Megan T. Baldridge, Yaoyu Feng, Lihua Xiao, L. David Sibley","doi":"10.1016/j.chom.2025.07.024","DOIUrl":"https://doi.org/10.1016/j.chom.2025.07.024","url":null,"abstract":"Cryptosporidium parvum subtypes differ in pathogenicity, but the underlying factors are largely unknown. We show that two genetically similar C. parvum isolates grow equally well in vitro but differ in pathogenicity in immunocompromised mice. Reduced oocyst shedding of the avirulent strain was restored by antibiotic treatment, suggesting susceptibility to colonization resistance imparted by the microbiota. This resistance was associated with a gene encoding a parasite ABC transporter and enhanced infectivity. Molecular analyses indicate that the ABC transporter belongs to a multidrug resistance protein (MRP) family. CpMRP1 binds bacterial metabolites, notably deoxycholic acid (DCA) that inhibits C. parvum growth. CpMRP1 is exported from small granules to the parasite-host interface, potentially mediating the export of xenobiotics. Loss of CpMRP1 reduces infectivity and DCA resistance in mice, and CpMRP1 polymorphisms across isolates determine susceptibility to DCA. These results define CpMRP1 as a determinant of C. parvum sensitivity to microbiome-mediated inhibition, thereby influencing infectivity.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"23 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144906040","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

Veillonella intestinal colonization promotes C. difficile infection in Crohn’s disease 细孔菌肠道定植促进克罗恩病难辨梭菌感染

IF 30.3 1区医学

Cell host & microbe Pub Date : 2025-08-22 DOI: 10.1016/j.chom.2025.07.019

Ziyu Yang, Jilin Wang, Yifan Chen, Tianchi Chen, Zhen Shen, Yanan Wang, Ying Jian, Guoxiu Xiang, Xiaowei Ma, Na Zhao, Yan Song, Bisheng Shi, Juanxiu Qin, Qian Liu, Zhijun Cao, Michael Otto, Min Li

{"title":"Veillonella intestinal colonization promotes C. difficile infection in Crohn’s disease","authors":"Ziyu Yang, Jilin Wang, Yifan Chen, Tianchi Chen, Zhen Shen, Yanan Wang, Ying Jian, Guoxiu Xiang, Xiaowei Ma, Na Zhao, Yan Song, Bisheng Shi, Juanxiu Qin, Qian Liu, Zhijun Cao, Michael Otto, Min Li","doi":"10.1016/j.chom.2025.07.019","DOIUrl":"https://doi.org/10.1016/j.chom.2025.07.019","url":null,"abstract":"Crohn’s disease is a severe inflammatory disorder of the intestine for which there is no cure. Individuals suffering from Crohn’s disease are at an increased risk of developing <ce:italic>Clostridioides difficile</ce:italic> infection (CDI), which considerably exacerbates symptoms. Using a prospective observational clinical study combined with animal models of intestinal inflammation, we show that intestinal colonization by <ce:italic>Veillonella</ce:italic>, an oral commensal, promotes CDI in Crohn’s disease. In mice, <ce:italic>Veillonella parvula</ce:italic> suppresses expression of the main bile acid transporter, ASBT, thus preventing bile acid reabsorption. Similarly, <ce:italic>Veillonella</ce:italic> abundance is associated with increased bile acid metabolism in Crohn’s disease patients. This increase in bile acid availability within the intestinal lumen triggers <ce:italic>C. difficile</ce:italic> germination. <ce:italic>V. parvula</ce:italic> expresses a highly pro-inflammatory lipopolysaccharide that triggers the transcription factors c-Jun and c-Fos regulating ASBT expression. These findings highlight that oral commensals can exacerbate intestinal disease, providing pathways to design therapeutics to treat CDI in Crohn’s disease patients.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"52 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144900128","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

Born to rewild: Reconnecting beneficial plant-microbiome alliances for resilient future crops 为重新野生而生：重新连接有益的植物-微生物联盟，以实现有弹性的未来作物

IF 30.3 1区医学

Cell host & microbe Pub Date : 2025-08-13 DOI: 10.1016/j.chom.2025.06.017

Dario X. Ramirez-Villacis, Antonio Leon-Reyes, Corné M.J. Pieterse, Jos M. Raaijmakers

{"title":"Born to rewild: Reconnecting beneficial plant-microbiome alliances for resilient future crops","authors":"Dario X. Ramirez-Villacis, Antonio Leon-Reyes, Corné M.J. Pieterse, Jos M. Raaijmakers","doi":"10.1016/j.chom.2025.06.017","DOIUrl":"https://doi.org/10.1016/j.chom.2025.06.017","url":null,"abstract":"Plant domestication is a coevolutionary process shaped by human selection, favoring traits supporting modern-day agriculture. This process has reduced genetic diversity and fixed alleles for desirable traits, coinciding with changes in agricultural practices, particularly soil tilling, crop monocultures, and the (over)use of fertilizers and pesticides. The combined effects—collectively termed “domestication syndrome”—have contributed to the homogenization of soil and plant-associated microbial communities, reducing diversity and disrupting beneficial plant-microbiome alliances. Microbiome rewilding has uncovered ecological, genetic, and molecular principles underlying these depleted plant-microbiome partnerships. Studies have revealed ancestral microbial taxa enriched in wild crop relatives, plant genes, and metabolites critical for microbial recruitment, as well as the potential of reintroducing microbes to enhance nutrient uptake, pathogen resistance, and stress tolerance. These findings offer models for restoring such interactions in modern crops. We review the current state of crop microbiome rewilding and highlight how these discoveries are instrumental for designing resilient crop systems.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"37 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144825136","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

A. baumannii’s nutrient tug-of-war 鲍曼杆菌的营养拔河

IF 30.3 1区医学

Cell host & microbe Pub Date : 2025-08-13 DOI: 10.1016/j.chom.2025.07.010

Ashley R. Wolf

引用次数: 0

Breaking open the taxonomic boundaries of plant NLR immunity 突破植物NLR免疫的分类学界限

IF 30.3 1区医学

Cell host & microbe Pub Date : 2025-08-13 DOI: 10.1016/j.chom.2025.07.006

Xander C.L. Zuijdgeest, Farid El Kasmi

引用次数: 0

Immune cell states: Critical building blocks of the plant immune system 免疫细胞状态：植物免疫系统的关键组成部分