{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE322nnn/GSE322583/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE322583"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"mtROS-NF-κB signaling promotes ILC3 protective function and survival during sepsis-induced intestinal injury","description":"Group 3 innate lymphoid cells (ILC3s) are key regulators of mucosal immunity,yet their role in sepsis-associated colon injury remains unclear.Peripheral blood from healthy volunteers and septic patients was analyzed for ILC subset alterations.A LPS-induced murine sepsis model,combined with ILC3-deficient mice,was employed to assess ILC3 dynamic,function,metabolic features and impact on colon barrier interity using flow cytometry,histopathology,ELISA,RT-qPCR and in vitro co-culture experiments.Septic patients exhibited significantly reduced circulating ILC3 proportions.In mice,sepsis decreased colonic ILC3 numbers but enhanced IL-22 and GM-CSF production.ILC3 deficiency increased mortality and exacerbated intestinal barrier disruption,while exogenous IL-22/GM-CSF administration ameliorated colonic pathology.Mechanistically,sepsis induced metabolic reprogramming in ILC3,characteristiced by enhanced glycolysis,reduced mitochondrial mass and ATP producton,which led to mitochondrial ROS accumulation.ROS activated the NF-κB pathway to drive IL-22 and GM-CSF production.However,ROS scavening or NF-κB inhibition unexpectedly increased ILC3 apoptosis,revealing that ROS-NF-κB axis also conveys pro-survival signals.Despite enhanced function,the repair capacity of residual ILC3s was outpaced by ongoing intestinal destruction.Our finding provided insight into the relation of ROS-NF-κB axis with IL-22/GM-CSF production and the survival of remaining colonic ILC3s in sepsis.Thereby targeting this metabolic-immune crosstalk may present a therapeutic strategy to sepsis associated intestinal injury.","dates":{"publication":"2026/09/02"},"accession":"GSE322583","cross_references":{"GSM":["GSM9555220","GSM9555221","GSM9555222","GSM9555223","GSM9555224","GSM9555219"],"GPL":["24247"],"GSE":["322583"],"taxon":["Mus musculus"]}}