Pub Date : 2026-02-03DOI: 10.1016/j.chom.2026.01.008
Anne-Marie C. Overstreet, McKenzie Burge, Brady Anderson, Xiaorong Zhu, Yun Tao, Candace M. Cham, Brenna Michaud, Soyar Horam, Naseer Sangwan, Mohammed Dwidar, Xuefeng Liu, Akeem Santos, Vartika Srivastava, Chelsea Finney, Christopher M. Goins, Zhanghan Dai, B. Ben Koff, Shaun R. Stauffer, Vanessa A. Leone, Jeannette S. Messer
{"title":"HMGB1 functions as a critical mediator of host defense at the gut mucosal barrier","authors":"Anne-Marie C. Overstreet, McKenzie Burge, Brady Anderson, Xiaorong Zhu, Yun Tao, Candace M. Cham, Brenna Michaud, Soyar Horam, Naseer Sangwan, Mohammed Dwidar, Xuefeng Liu, Akeem Santos, Vartika Srivastava, Chelsea Finney, Christopher M. Goins, Zhanghan Dai, B. Ben Koff, Shaun R. Stauffer, Vanessa A. Leone, Jeannette S. Messer","doi":"10.1016/j.chom.2026.01.008","DOIUrl":"https://doi.org/10.1016/j.chom.2026.01.008","url":null,"abstract":"","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"43 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2026-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146110542","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 : 2026-01-30DOI: 10.1016/j.chom.2026.01.007
Stav Kabel, Shira Omer Bendori, Tom Borenstein, Polina Guler, Claudia Martinez-Alonso, Javier Mancheño-Bonillo, Francisca Gallego-del-Sol, Alberto Marina, Avigdor Eldar
{"title":"A widespread extended arbitrium system controls lysis/lysogeny through antirepression","authors":"Stav Kabel, Shira Omer Bendori, Tom Borenstein, Polina Guler, Claudia Martinez-Alonso, Javier Mancheño-Bonillo, Francisca Gallego-del-Sol, Alberto Marina, Avigdor Eldar","doi":"10.1016/j.chom.2026.01.007","DOIUrl":"https://doi.org/10.1016/j.chom.2026.01.007","url":null,"abstract":"","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"56 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2026-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146089428","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 : 2026-01-30DOI: 10.1016/j.chom.2026.01.003
Zhiyu Zang, Olivia K. Duncan, Dziugas Sabonis, Iana Fedorova, Yun Shi, Gause Miraj, Shuai Le, Jun Deng, Yuhao Zhu, Yanyao Cai, Chengqian Zhang, Garima Arya, Shelley A.H. Dixon, Steven P. Angus, Breck A. Duerkop, Haihua Liang, Robert H. Pepin, Thomas Ve, Joseph Bondy-Denomy, Giedre Tamulaitiene, Joseph P. Gerdt
{"title":"Chemical inhibition of a bacterial immune system","authors":"Zhiyu Zang, Olivia K. Duncan, Dziugas Sabonis, Iana Fedorova, Yun Shi, Gause Miraj, Shuai Le, Jun Deng, Yuhao Zhu, Yanyao Cai, Chengqian Zhang, Garima Arya, Shelley A.H. Dixon, Steven P. Angus, Breck A. Duerkop, Haihua Liang, Robert H. Pepin, Thomas Ve, Joseph Bondy-Denomy, Giedre Tamulaitiene, Joseph P. Gerdt","doi":"10.1016/j.chom.2026.01.003","DOIUrl":"https://doi.org/10.1016/j.chom.2026.01.003","url":null,"abstract":"","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"58 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2026-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146089426","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 : 2026-01-30DOI: 10.1016/j.chom.2026.01.012
Cora Chmielowska, Sara Zamora-Caballero, Javier Mancheño-Bonillo, Yuyi Li, Daniel Sin, Tom Borenstein, Shira Omer Bendori, Avigdor Eldar, Alberto Marina, José R. Penadés
{"title":"A DNA recognition-mimicry switch governs induction in arbitrium phages","authors":"Cora Chmielowska, Sara Zamora-Caballero, Javier Mancheño-Bonillo, Yuyi Li, Daniel Sin, Tom Borenstein, Shira Omer Bendori, Avigdor Eldar, Alberto Marina, José R. Penadés","doi":"10.1016/j.chom.2026.01.012","DOIUrl":"https://doi.org/10.1016/j.chom.2026.01.012","url":null,"abstract":"","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"389 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2026-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146089427","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 : 2026-01-29DOI: 10.1016/j.chom.2026.01.001
Hui Liu, Ling Hou, Liying Lan, Rong Zhang, Ding-Jie Wang, Huan Feng, Chun-Yan Chen, Jun-Jie Ye, Oyetola O. Oyebanji, Emmanuel C. Chukwuma, Si-Yun Chen, Yi-Xiao Tong, Jun-Bo Yang, Jun Yang, Jeremy D. Murray, Pamela S. Soltis, Douglas E. Soltis, Xiao-Wei Zhang, De-Zhu Li, Ting-Shuang Yi, Ertao Wang
The evolution of root nodule symbiosis (RNS), a key innovation for plant nitrogen acquisition, has long been studied but lacks a mechanistic, gene-level evolutionary framework. Here, we reconstruct the gene regulatory network underlying RNS (GRN-RNS) at single-gene resolution using comparative genomic and phylogenomic analyses of 10 newly sequenced and published genomes across all RNS families. We discover that symbiosis-related gene families originated from γ paleohexaploidy in core eudicots, fueling the molecular foundation for network assembly. The initial GRN-RNS emerged at the crown node of the nitrogen-fixing clade through the recruitment and rewiring of genes from three pathways: arbuscular mycorrhizal symbiosis, nitrate response, and stress response. In legumes, GRN-RNS was further refined to enable symbiosome formation via convergent recruitment of modules for cell wall remodeling and kinase signaling. Our work resolves the temporal and regulatory architecture of RNS, providing a unifying framework to understand the evolution of this complex trait.
{"title":"Evolution of root nodule symbiosis via paleopolyploidy and modular pathway rewiring","authors":"Hui Liu, Ling Hou, Liying Lan, Rong Zhang, Ding-Jie Wang, Huan Feng, Chun-Yan Chen, Jun-Jie Ye, Oyetola O. Oyebanji, Emmanuel C. Chukwuma, Si-Yun Chen, Yi-Xiao Tong, Jun-Bo Yang, Jun Yang, Jeremy D. Murray, Pamela S. Soltis, Douglas E. Soltis, Xiao-Wei Zhang, De-Zhu Li, Ting-Shuang Yi, Ertao Wang","doi":"10.1016/j.chom.2026.01.001","DOIUrl":"https://doi.org/10.1016/j.chom.2026.01.001","url":null,"abstract":"The evolution of root nodule symbiosis (RNS), a key innovation for plant nitrogen acquisition, has long been studied but lacks a mechanistic, gene-level evolutionary framework. Here, we reconstruct the gene regulatory network underlying RNS (GRN-RNS) at single-gene resolution using comparative genomic and phylogenomic analyses of 10 newly sequenced and published genomes across all RNS families. We discover that symbiosis-related gene families originated from γ paleohexaploidy in core eudicots, fueling the molecular foundation for network assembly. The initial GRN-RNS emerged at the crown node of the nitrogen-fixing clade through the recruitment and rewiring of genes from three pathways: arbuscular mycorrhizal symbiosis, nitrate response, and stress response. In legumes, GRN-RNS was further refined to enable symbiosome formation via convergent recruitment of modules for cell wall remodeling and kinase signaling. Our work resolves the temporal and regulatory architecture of RNS, providing a unifying framework to understand the evolution of this complex trait.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"20 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146070699","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 : 2026-01-28DOI: 10.1016/j.chom.2026.01.004
Bradley Allen Weiler, Nicholas Kron, Anthony Mario Bonacolta, Mark J.A. Vermeij, Andrew Charles Baker, Javier del Campo
Diel rhythms align physiological processes with light/dark cycles, driving predictable oscillations in gene expression and protein activity through tightly controlled transcriptional-translational feedback loops. This study presents in situ transcriptomic analyses of the stony coral Pseudodiploria strigosa and its photosymbionts, Breviolum sp., at key daily time points. P. strigosa shows precise transcriptional control: dawn triggers a molecular reset marked by RNA metabolism and protein turnover; midday emphasizes anabolic and phosphate-regulated pathways; dusk reflects transitional lipid and amino acid metabolism; and midnight reveals stress responses, mRNA catabolism, and mitochondrial organization. Photosymbionts display subtler diel patterns, with photoprotection at dawn, metabolite transport and nitrogen cycling through midday/dusk, and cell cycle and ion homeostasis at night. Microbial communities show time-dependent restructuring of co-occurrence networks, driving diel-related functional consequences like changes in microbial metabolism. These findings present a system-level molecular framework of diel regulation across the coral-photosymbiont-microbe holobiont, revealing time-specific transcriptional control of coordinated function and homeostasis.
{"title":"Temporal transcriptional rhythms govern coral-symbiont function and microbiome dynamics","authors":"Bradley Allen Weiler, Nicholas Kron, Anthony Mario Bonacolta, Mark J.A. Vermeij, Andrew Charles Baker, Javier del Campo","doi":"10.1016/j.chom.2026.01.004","DOIUrl":"https://doi.org/10.1016/j.chom.2026.01.004","url":null,"abstract":"Diel rhythms align physiological processes with light/dark cycles, driving predictable oscillations in gene expression and protein activity through tightly controlled transcriptional-translational feedback loops. This study presents <em>in situ</em> transcriptomic analyses of the stony coral <em>Pseudodiploria strigosa</em> and its photosymbionts, <em>Breviolum</em> sp., at key daily time points. <em>P. strigosa</em> shows precise transcriptional control: dawn triggers a molecular reset marked by RNA metabolism and protein turnover; midday emphasizes anabolic and phosphate-regulated pathways; dusk reflects transitional lipid and amino acid metabolism; and midnight reveals stress responses, mRNA catabolism, and mitochondrial organization. Photosymbionts display subtler diel patterns, with photoprotection at dawn, metabolite transport and nitrogen cycling through midday/dusk, and cell cycle and ion homeostasis at night. Microbial communities show time-dependent restructuring of co-occurrence networks, driving diel-related functional consequences like changes in microbial metabolism. These findings present a system-level molecular framework of diel regulation across the coral-photosymbiont-microbe holobiont, revealing time-specific transcriptional control of coordinated function and homeostasis.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"40 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2026-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146070559","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}
Glioblastoma (GBM) remains a highly lethal form of cancer due to its molecular heterogeneity and the immunosuppressive microenvironment surrounding the tumor. Here, we report a modular immunotherapy platform characterized by its flexibility to simultaneously target multiple antigens. Specifically, we utilize engineered E. coli Nissle to colonize tumors and produce bispecific engagers that simultaneously target EGFRvIII and interleukin (IL)-13Rα2. These tags direct in situ-reprogrammed chimeric antigen receptor (CAR) macrophages, which are edited using nanoparticles and delivered within a shear-thinning hydrogel, to execute targeted phagocytosis. This probiotic-macrophage crosstalk eliminates tumor cells while converting protumor M2 macrophages into immunostimulatory M1 effectors. In aggressive orthotopic GBM mouse models, this strategy achieves 83% survival at the 120-day endpoint, representing a 5-fold improvement over single-target controls and establishing durable immunological memory that effectively combats recurrence. By functioning as multifunctional immune hubs, this platform offers a versatile framework designed to overcome the antigenic complexity of solid tumors.
{"title":"Engineered probiotics recruit CAR macrophages and establish immune memory to eradicate heterogeneous glioblastoma in mice","authors":"Yulin Zhang, Jianyu Shen, Yu Xu, Fan Feng, Xu Han, Kaiyan Xi, Zezheng Fang, Yi Zhang, Mingrui Wang, Zixu Wang, Pengfei Zhu, Qikang Zhang, Zhiqiang Li, Baichuan Liu, Zeyue Cao, Chaoqun Wang, Qianen Xu, Yang Yu, Chengpeng Sun, Xinrui Wang, Jingjing Wang, Jiaojiao Pang, Zimei Wu, Huimin Geng, Ahmet Acar, Thomas Daubon, Wenli Zhang, Yanrong Zhang, Xingang Li, Yuguo Chen, Shilei Ni, Xinyi Jiang","doi":"10.1016/j.chom.2025.12.014","DOIUrl":"https://doi.org/10.1016/j.chom.2025.12.014","url":null,"abstract":"Glioblastoma (GBM) remains a highly lethal form of cancer due to its molecular heterogeneity and the immunosuppressive microenvironment surrounding the tumor. Here, we report a modular immunotherapy platform characterized by its flexibility to simultaneously target multiple antigens. Specifically, we utilize engineered E. coli Nissle to colonize tumors and produce bispecific engagers that simultaneously target EGFRvIII and interleukin (IL)-13Rα2. These tags direct in situ-reprogrammed chimeric antigen receptor (CAR) macrophages, which are edited using nanoparticles and delivered within a shear-thinning hydrogel, to execute targeted phagocytosis. This probiotic-macrophage crosstalk eliminates tumor cells while converting protumor M2 macrophages into immunostimulatory M1 effectors. In aggressive orthotopic GBM mouse models, this strategy achieves 83% survival at the 120-day endpoint, representing a 5-fold improvement over single-target controls and establishing durable immunological memory that effectively combats recurrence. By functioning as multifunctional immune hubs, this platform offers a versatile framework designed to overcome the antigenic complexity of solid tumors.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"43 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2026-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146071652","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 : 2026-01-27DOI: 10.1016/j.chom.2026.01.002
Ronni A.G. da Silva, Brenda Yin Qi Tien, Patrick Hsien Neng Kao, Haris Antypas, Cenk Celik, Ai Zhu Casandra Tan, Muhammad Hafiz Ismail, Guangan Hu, Kelvin Kian Long Chong, Guillaume Thibault, Jianzhu Chen, Kimberly A. Kline
Macrophage activation is essential for innate immunity and antimicrobial defense. We show that Enterococcus faecalis suppresses macrophage activation through lactic-acid-mediated acidification of the extracellular environment, enabling pathogen persistence. E. faecalis-derived lactic acid acts via the lactate transporter monocarboxylate transporter 1 (MCT-1) and the sensor GPR81 to initiate complementary mechanisms that collaboratively reduce nuclear factor κB (NF-κB) activity. Lactic acid acts through MCT-1 to inhibit extracellular signal-regulated kinase and STAT3 phosphorylation, leading to reduced levels of the adaptor MyD88 involved in NF-κB activation. Lactic acid signaling to GPR81 induces phosphorylation of the transcription factor YAP, ultimately attenuating NF-κB signaling. A bacterial mutant lacking lactate dehydrogenase is unable to acidify the environment and thus fails to inhibit NF-κB. In a murine wound infection model, lactic-acid-driven immunosuppression enables prolonged E. faecalis persistence and enhances the fitness of co-infecting bacteria such as Escherichia coli. These findings reveal how bacterial lactic acid subverts innate immunity to support chronic and polymicrobial infections.
{"title":"Enterococcus faecalis-derived lactic acid suppresses macrophage activation to facilitate persistent and polymicrobial wound infections","authors":"Ronni A.G. da Silva, Brenda Yin Qi Tien, Patrick Hsien Neng Kao, Haris Antypas, Cenk Celik, Ai Zhu Casandra Tan, Muhammad Hafiz Ismail, Guangan Hu, Kelvin Kian Long Chong, Guillaume Thibault, Jianzhu Chen, Kimberly A. Kline","doi":"10.1016/j.chom.2026.01.002","DOIUrl":"https://doi.org/10.1016/j.chom.2026.01.002","url":null,"abstract":"Macrophage activation is essential for innate immunity and antimicrobial defense. We show that <em>Enterococcus faecalis</em> suppresses macrophage activation through lactic-acid-mediated acidification of the extracellular environment, enabling pathogen persistence. <em>E. faecalis-</em>derived lactic acid acts via the lactate transporter monocarboxylate transporter 1 (MCT-1) and the sensor GPR81 to initiate complementary mechanisms that collaboratively reduce nuclear factor κB (NF-κB) activity. Lactic acid acts through MCT-1 to inhibit extracellular signal-regulated kinase and STAT3 phosphorylation, leading to reduced levels of the adaptor MyD88 involved in NF-κB activation. Lactic acid signaling to GPR81 induces phosphorylation of the transcription factor YAP, ultimately attenuating NF-κB signaling. A bacterial mutant lacking lactate dehydrogenase is unable to acidify the environment and thus fails to inhibit NF-κB. In a murine wound infection model, lactic-acid-driven immunosuppression enables prolonged <em>E. faecalis</em> persistence and enhances the fitness of co-infecting bacteria such as <em>Escherichia coli</em>. These findings reveal how bacterial lactic acid subverts innate immunity to support chronic and polymicrobial infections.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"75 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2026-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146070574","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 : 2026-01-14DOI: 10.1016/j.chom.2025.12.012
Shiwei Xiao, Qinglu Zeng
Auxiliary metabolic genes, acquired by cyanobacterial viruses (cyanophages) from their hosts, are thought to manipulate host metabolism during infection. A recent study by Nadel et al. performed in vivo experiments to reveal how cyanophages use a viral nblA gene to accelerate infection by degrading the photosynthetic machinery of marine cyanobacteria.
{"title":"Viral theft of light: A cyanophage protein dismantles cyanobacterial photosynthesis to accelerate infection","authors":"Shiwei Xiao, Qinglu Zeng","doi":"10.1016/j.chom.2025.12.012","DOIUrl":"https://doi.org/10.1016/j.chom.2025.12.012","url":null,"abstract":"Auxiliary metabolic genes, acquired by cyanobacterial viruses (cyanophages) from their hosts, are thought to manipulate host metabolism during infection. A recent study by Nadel et al. performed <em>in vivo</em> experiments to reveal how cyanophages use a viral <em>nblA</em> gene to accelerate infection by degrading the photosynthetic machinery of marine cyanobacteria.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"265 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145962141","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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