Hao Liu, Huiling Shang, Hui Chen, Chuhui Zhou, Bin Luo, Di Zhao, Zhengxiu Xiao, Yimin Cui, Yuhang Zhang, Ri-hua Xie
{"title":"Vaginal microbiota transfer ameliorates cesarean-associated neurodevelopmental deficits in mice via N-bc2S1P synthesis on neonatal skin","authors":"Hao Liu, Huiling Shang, Hui Chen, Chuhui Zhou, Bin Luo, Di Zhao, Zhengxiu Xiao, Yimin Cui, Yuhang Zhang, Ri-hua Xie","doi":"10.1016/j.chom.2026.03.023","DOIUrl":"https://doi.org/10.1016/j.chom.2026.03.023","url":null,"abstract":"Cesarean section (CS) bypasses neonatal exposure to maternal vaginal microbiota, leaving the metabolic contribution of skin microbiota to neurodevelopment unclear. In CS neonates receiving vaginal microbiota transfer, skin multi-omics at 24 h identified restoration of β-carboline-sphingosine-1-phosphate (<em>N</em>-bc2S1P), whose levels correlated with ASQ-3 scores at 3 and 6 months. In mice, <em>N</em>-bc2S1P assembled on neonatal skin by <em>Lactobacillus crispatus</em> and <em>Bacteroides fragilis</em> reaches the brain and selectively triggers β-arrestin1-biased S1PR2 signaling in forebrain excitatory neurons. This pathway promotes AP-1/CBP recruitment, increases H3K27 acetylation at Notch loci, and transiently ameliorates CS-associated early-life neurodevelopmental impairments. Because <em>N-</em>bc2S1P is rapidly cleared, we engineered the skin commensal <em>Staphylococcus epidermidis</em> to co-synthesize β-carboline and S1P, sustaining cutaneous <em>N</em>-bc2S1P production, prolonging brain exposure, and improving neurodevelopmental outcomes. These findings identify a microbe-derived, arrestin-biased S1PR2 agonist and show that engineered skin commensals extend transient maternal microbial signals into more durable neurodevelopmental benefit in mice.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"142 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147732281","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}
Ruth Steinberg, Marie-Madlen Pust, Aranzazu Arias-Rojas, Gleb Pishchany, Kathryn A. Ramsey, Elisabeth Kieninger, Alexander Moeller, Carmen Casaulta, Markus Hilty, Philipp Latzin, SCILD Study Group, BILD Study Group, Insa Korten, Ramnik J. Xavier
{"title":"An infant nasal microbial gene atlas uncovers intervention-driven microbiome shifts and salt-resistant pathogen expansion","authors":"Ruth Steinberg, Marie-Madlen Pust, Aranzazu Arias-Rojas, Gleb Pishchany, Kathryn A. Ramsey, Elisabeth Kieninger, Alexander Moeller, Carmen Casaulta, Markus Hilty, Philipp Latzin, SCILD Study Group, BILD Study Group, Insa Korten, Ramnik J. Xavier","doi":"10.1016/j.chom.2026.03.019","DOIUrl":"https://doi.org/10.1016/j.chom.2026.03.019","url":null,"abstract":"Functional studies of how early-life interventions shape the airway microbiome remain scarce. Here, we performed metagenomic sequencing of 704 longitudinal nasal swabs from infants with and without cystic fibrosis (CF) to construct and characterize a non-redundant gene atlas of the infant nasal microbiome. We aimed to determine how the nasal microbiome is perturbed by early therapies, as CF is commonly treated with inhaled hypertonic saline to improve mucociliary clearance. We found functional and compositional microbiome changes linked to inhalation therapy, including an expansion of salt-associated transporter genes and a community shift toward CF-associated microbial opportunists, including <ce:italic>Haemophilus influenzae</ce:italic> and fungi, carrying the identified salt-associated transporter genes with high sequence and structural identity. Hypertonic, compared with isotonic, saline accelerates <ce:italic>H. influenzae</ce:italic> growth and induces efflux pumps linked to antibiotic tolerance <ce:italic>in vitro</ce:italic>. This study establishes a reference framework for functional airway microbiome research, enabling the examination of therapeutic perturbations and their impact on microbial adaptation.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"11 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147736467","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}
{"title":"Gut microbiota-derived ergothioneine alleviates antipsychotic-induced synaptic and cognitive impairments","authors":"Mingxuan Zheng, Hanrong Yan, Wenting Hao, Huimei An, Xi Chen, Qingyuan Wu, Xing Ge, Huaiyu Ye, Menglu Zhou, Guorong Zhou, Xiaoying Yang, Minmin Hu, Peng Zhang, Wei Pan, Renxian Tang, Kuiyang Zheng, Xu-Feng Huang, Yinghua Yu","doi":"10.1016/j.chom.2026.03.020","DOIUrl":"https://doi.org/10.1016/j.chom.2026.03.020","url":null,"abstract":"Chronic antipsychotic use is associated with neuronal damage and cognitive impairment, with the gut microbiome increasingly implicated. However, the specific microbial metabolites and mechanisms involved remain unknown. Here, we demonstrate that chronic olanzapine treatment induces gut microbial dysbiosis, compromises intestinal barrier integrity, and causes cognitive deficits in mice. Multi-omics analyses reveal profound depletion of the microbiota-associated metabolite ergothioneine in blood and brain, a finding validated in the blood of olanzapine-treated patients and risperidone- and clozapine-treated mice. This deficiency correlates with a loss of ergothioneine-producing bacteria (Cyanobacteria and subordinate taxa). Fecal microbiota transplantation from olanzapine-treated mice confers cognitive impairment, while ergothioneine supplementation mitigates it. Mechanistically, ergothioneine attenuates hippocampal oxidative stress and inhibits the redox-sensitive phosphatase protein tyrosine phosphatase 1B (PTP1B). Furthermore, hippocampal neuronal-specific PTP1B deletion abolishes olanzapine-induced synaptic and cognitive deficits. Our findings identify depletion of microbiota-derived ergothioneine as a mechanism underlying antipsychotic-induced cognitive impairment, highlighting therapeutic strategies to mitigate this side effect.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"15 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147732282","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}
Chao Xiong, Manuel Delgado-Baquerizo, Jinsong Liang, Juntao Wang, Zhenzhen Yan, Slade O. Jensen, Min Gao, Tadeo Sáez-Sandino, Emilio Guirado, Miriam Muñoz-Rojas, Raul Román, Fernando T. Maestre, Brajesh K. Singh
{"title":"Soil microbial diversity associates with lower prevalence of human bacterial pathogens across global soils","authors":"Chao Xiong, Manuel Delgado-Baquerizo, Jinsong Liang, Juntao Wang, Zhenzhen Yan, Slade O. Jensen, Min Gao, Tadeo Sáez-Sandino, Emilio Guirado, Miriam Muñoz-Rojas, Raul Román, Fernando T. Maestre, Brajesh K. Singh","doi":"10.1016/j.chom.2026.03.011","DOIUrl":"https://doi.org/10.1016/j.chom.2026.03.011","url":null,"abstract":"Soil-inhabiting pathogens threaten human health, but their biogeography and associations with soil biodiversity remain poorly understood. Here, we present global patterns of dominant human bacterial pathogens by integrating 1,602 soil metagenomes from 59 countries across continents. We show that dominant human pathogens are more prevalent (i.e., relative abundance) in wet (tropical and temperate) ecosystems and are particularly abundant in cropland soils. We find a global negative association between soil microbiome diversity and pathogen prevalence. We further reveal a significant and positive correlation between the abundance of dominant human pathogens and both disease virulence and global patterns of mortality associated with infectious diseases. Many dominant pathogens are likely to increase their proportion under global change scenarios. Our work provides a global atlas of dominant soil-inhabiting human pathogens and reveals their biogeography and ecology. These findings can guide the development of effective surveillance and risk management strategies to reduce outbreaks and pandemics.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"18 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147587883","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}
Junxia Zhang, Changyun Liu, Yupeng Wang, Yusi Chen, Haibao Shang, Wen Zheng, Li Jin, Peng Xie, Yingjia Li, Yahan Liu, Yunxiao Zhang, Yang Wang, Wei Zhao, Han Xiao, Guisong Wang, Xin Zhang, Xiaolei Yang, Erdan Dong, Yan Zhang
{"title":"Bacteroides acidifaciens exacerbates cardiac ischemia/reperfusion injury via the microbial-host isozyme DPP4","authors":"Junxia Zhang, Changyun Liu, Yupeng Wang, Yusi Chen, Haibao Shang, Wen Zheng, Li Jin, Peng Xie, Yingjia Li, Yahan Liu, Yunxiao Zhang, Yang Wang, Wei Zhao, Han Xiao, Guisong Wang, Xin Zhang, Xiaolei Yang, Erdan Dong, Yan Zhang","doi":"10.1016/j.chom.2026.03.012","DOIUrl":"https://doi.org/10.1016/j.chom.2026.03.012","url":null,"abstract":"Ischemia/reperfusion (I/R) injury is a key driver in cardiomyocyte loss and cardiac dysfunction in ischemic heart disease. Here, we uncover a previously unrecognized gut microbiota-mediated mechanism that contributes to myocardial I/R injury. Using murine I/R models and fecal microbiota transplantation, we demonstrate that the gut microbiota mediates cardiac damage through selective enrichment of <em>Bacteroides acidifaciens</em> (<em>B. acidifaciens</em>) following I/R-induced intestinal hypoxia and elevated luminal lactate levels. <em>B. acidifaciens</em> produces dipeptidyl peptidase 4 (BaDPP4), which degrades cardioprotective peptides (e.g., glucagon-like peptide-1 [GLP-1]) in the plasma, amplifying myocardial injury. Pharmacological inhibition of BaDPP4 with daurisoline, a microbial DPP4-specific inhibitor, mitigates cardiac dysfunction. In acute myocardial infarction patients with I/R injury, <em>B. acidifaciens</em> abundance and BaDPP4 levels correlate with clinical markers of cardiac damage. Together, these findings reveal a gut-heart axis whereby microbial-derived DPP4 exacerbates cardiac I/R injury and highlight the hypoxia-lactate-BaDPP4 axis as a promising target for microbiota-based cardioprotection.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"19 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147586419","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}
Dora Čerina, Matthieu Rousseau, Carla Hart Olaiz, Gerben Marsman, Arturo Zychlinsky, Molly A. Ingersoll
{"title":"The DanRI regulatory system in uropathogenic Escherichia coli subverts neutrophil responses","authors":"Dora Čerina, Matthieu Rousseau, Carla Hart Olaiz, Gerben Marsman, Arturo Zychlinsky, Molly A. Ingersoll","doi":"10.1016/j.chom.2026.03.013","DOIUrl":"https://doi.org/10.1016/j.chom.2026.03.013","url":null,"abstract":"Uropathogenic <em>Escherichia coli</em> (UPEC) is the primary cause of urinary tract infections (UTIs). To establish an infection, UPEC must evade infiltrating neutrophils and their antimicrobial neutrophil extracellular traps (NETs). In this study, we identify a previously uncharacterized two-gene regulatory system within the pathogenicity island PAI<sub>UTI89</sub>II, which we named DanRI (defense against neutrophil regulator and inhibitor). DanRI is induced by nucleosomes present in NETs and enables UPEC to suppress neutrophil responses by attenuating reactive oxygen species production and subsequent NET formation. Mechanistically, DanI functions as an antagonist to the transcriptional regulator DanR, thereby modulating key bacterial processes, including metabolic, flagellar biosynthesis, and stress response pathways. DanRI enhances UPEC fitness by dampening the early host inflammatory response during UTI in a mouse model. Taken together, these findings reveal DanRI as a regulatory system that promotes UPEC pathogenesis by facilitating immune evasion.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"192 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2026-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147586420","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}
{"title":"Diversity-triggered 2-naphthoic acid exudation recruits keystone microbial taxa to promote soybean drought tolerance","authors":"Shi Chen, Yang Wang, Beibei Chen, Xinyi Hou, Siyu Liu, Sihan He, Jiejun Qi, Ziheng Peng, Haibo Pan, Chunling Liang, Gehong Wei, Shuo Jiao","doi":"10.1016/j.chom.2026.03.002","DOIUrl":"https://doi.org/10.1016/j.chom.2026.03.002","url":null,"abstract":"Rhizosphere microbiomes are essential for plant growth and stress tolerance, yet how microbial diversity shapes drought resilience in soybean remains unclear. Here, we demonstrate that high rhizosphere microbial diversity, generated via dilution-to-extinction manipulation of soil microbiome diversity, improves soybean performance under drought. Integrated metabolomic and transcriptomic analyses identify 2-naphthoic acid as a diversity-induced root exudate that accumulates exclusively under drought. This metabolite selectively recruits <ce:italic>Sinorhizobium</ce:italic> CS204 via chemotaxis and ATP-binding cassette (ABC) transporter-mediated uptake, as confirmed by <ce:italic>in vitro</ce:italic> substrate utilization assays and targeted mutant construction. Molecular docking and microscale thermophoresis reveal direct interactions between this metabolite and nitrogen-cycling proteins, enhancing denitrification and nitrogen fixation of <ce:italic>S</ce:italic>.CS204. Co-application of 2-naphthoic acid and <ce:italic>S</ce:italic>.CS204 significantly improves plant nutrient acquisition and photosynthesis under drought. Collectively, our study underscores the pivotal role of rhizosphere microbial diversity in triggering the exudation of root metabolites to recruit keystone taxa, establishing microbe-plant synergies that bolster drought tolerance.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"19 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2026-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147587884","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}
Seth M. Bloom, Laura Symul, Joseph Elsherbini, Jiawu Xu, Salina Hussain, Johnathan Shih, Ashley Sango, Caroline M. Mitchell, Anke Hemmerling, Thomas P. Parks, Aditi Kannan, Fatima A. Hussain, Craig R. Cohen, Susan P. Holmes, Douglas S. Kwon
{"title":"Vaginal microbiota impacts of a Lactobacillus crispatus live biotherapeutic and predictors of colonization in randomized controlled trial","authors":"Seth M. Bloom, Laura Symul, Joseph Elsherbini, Jiawu Xu, Salina Hussain, Johnathan Shih, Ashley Sango, Caroline M. Mitchell, Anke Hemmerling, Thomas P. Parks, Aditi Kannan, Fatima A. Hussain, Craig R. Cohen, Susan P. Holmes, Douglas S. Kwon","doi":"10.1016/j.chom.2026.03.003","DOIUrl":"https://doi.org/10.1016/j.chom.2026.03.003","url":null,"abstract":"Bacterial vaginosis (BV) affects >25% of women worldwide and often recurs after standard-of-care metronidazole (MTZ) treatment. LACTIN-V, a live biotherapeutic product (LBP) containing <em>Lactobacillus crispatus</em> strain CTV-05, significantly reduced recurrent BV in a phase 2b clinical trial, but efficacy was incomplete. Here, we characterize microbiota and immune effects using multi-omics and define correlates of treatment success. By week 12, an <em>L. crispatus</em>-dominant microbiota was achieved in 30% of LBP recipients compared with 9% of placebo recipients (benefit ratio: 3.31; <em>p</em> < 0.005). This is primarily due to CTV-05, but native <em>L. crispatus</em> strains are also present and increase over time. Inflammatory cytokines decrease in both arms after MTZ but return to baseline in placebo recipients. Successful <em>L. crispatus</em> colonization is associated with pre-MTZ microbiota, baseline inflammatory profiles, post-MTZ bacterial load, and clinical and behavioral variables. These findings elucidate LBP microbiota effects and identify predictors of treatment success, informing improved intervention strategies to advance women’s health.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"101 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2026-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147518840","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}
Uday Tak, Kate Schinkel, Peace Walth, Jian Wei Tay, Erik W. Hartwick, Aaron T. Whiteley
{"title":"Bacterial 2′,3′-cGAMP activates a SAVED effector to form membrane-disrupting filaments and restrict phage replication","authors":"Uday Tak, Kate Schinkel, Peace Walth, Jian Wei Tay, Erik W. Hartwick, Aaron T. Whiteley","doi":"10.1016/j.chom.2026.03.004","DOIUrl":"https://doi.org/10.1016/j.chom.2026.03.004","url":null,"abstract":"Mammalian cells initiate antiviral signaling when cyclic GMP-AMP synthase (cGAS) detects cytoplasmic DNA and synthesizes 2′,3′-cyclic GMP-AMP (2′,3′-cGAMP), which activates stimulator of interferon genes (STING). Similarly, bacteria use cyclic oligonucleotide-based antiphage signaling systems (CBASS) to detect phage using ancestral cGAS/DncV-like nucleotidyltransferases (CD-NTases), but they are not known to use 2′,3′-cGAMP. Here, we discover a bacterial CD-NTase that produces 2′,3′-cGAMP to activate a Saf-2TM-SMODS-associated fused to various effector domains (SAVED) effector (CD-NTase-associated protein 14 [Cap14]), which initiates membrane disruption to restrict phage replication. Cryo-electron microscopy (cryo-EM) reveals that Cap14 binds 2′,3′-cGAMP to form a filament, while electrophysiology suggests that cGAMP activates membrane disruption. Swapping the Cap14 transmembrane domain with a nuclease domain yields a functional chimera that exclusively responds to 2′,3′-cGAMP. We hypothesize that other predicted transmembrane effectors in CBASS operons disrupt membranes, and we confirm this by showing that bacterial STING homologs with transmembrane domains restrict phage through membrane disruption. These findings expand our understanding of cGAS-STING-like pathways in bacterial immunity.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"58 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2026-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147518841","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}
Vanessa Salazar, Scott T. Espenschied, Anthony P. Fernandez, Paul E. Karell, Naseer Sangwan, Thaddeus S. Stappenbeck
{"title":"The skin microbiota drives cutaneous immune checkpoint inhibitor toxicity in genetically susceptible mice","authors":"Vanessa Salazar, Scott T. Espenschied, Anthony P. Fernandez, Paul E. Karell, Naseer Sangwan, Thaddeus S. Stappenbeck","doi":"10.1016/j.chom.2026.03.008","DOIUrl":"https://doi.org/10.1016/j.chom.2026.03.008","url":null,"abstract":"Immune checkpoint inhibitors (ICIs) show increasing promise for cancer therapy. However, patients can experience adverse events, particularly those with pre-existing autoimmune disease. We determined that the microbiome can drive ICI-induced systemic toxicity in a mouse model of autoimmune susceptibility. Specifically, ICI treatment of specific pathogen-free (SPF) <em>Act1</em><sup>−/−</sup> mice, which develop spontaneous autoimmunity due to a deficiency in an immune adaptor, resulted in systemic adverse events that were ameliorated by topical antibiotics. Moreover, germ-free (GF) <em>Act1</em><sup>−/−</sup> mice failed to develop ICI toxicity. Transfer of gut or skin microbiota from SPF <em>Act1</em><sup>−/−</sup> mice to GF <em>Act1</em><sup>−/−</sup> mice showed that only the skin microbiota rendered exGF mice sensitive to ICI toxicity. Notably, therapeutic application of topical antibiotics decoupled ICI-induced toxicity from anti-tumor efficacy in SPF <em>Act1</em><sup>−/−</sup> mice. This model provides a paradigm for future translational studies in cancer patients to mitigate adverse effects of ICIs and maximize their efficacy by targeting skin microbes.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"31 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2026-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147518839","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}
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号
