{"database":"GEO","file_versions":[],"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=GSE300863"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Immature neutrophils promote sepsis in hereditary hemochromatosis hosts infected with hyper-yersiniabactin-producing Yersinia pseudotuberculosis","description":"Hereditary hemochromatosis (HH) increases susceptibility to bacterial infections, often leading to sepsis, but underlying mechanisms are unclear. Here, we show that HH mice infected with a hyper–yersiniabactin-producing Yersinia pseudotuberculosis Δfur mutant (Δfur) rapidly develop sepsis, marked by an influx of immature, pro-inflammatory CD101⁻ neutrophils with impaired bacterial killing and enhanced NETosis, unlike mature CD101⁺ neutrophils in wild-type mice. We further demonstrate that type I interferon (IFN-I) signaling impairs neutrophil bactericidal function, increasing bacterial burden and driving emergency granulopoiesis in HH mice, in turn which results in systemic recruitment of immature CD101⁻ neutrophils. Blocking IFNAR signaling restores neutrophil function, reduces bacterial loads, limits neutrophil recruitment, and promotes a shift toward mature CD101⁺ neutrophils, ultimately reducing sepsis severity and improving survival. These findings reveal a pathogenic role for immature CD101⁻ neutrophils in driving sepsis and identify IFN-I signaling as a key regulator of this dysfunctional immune response in HH. ","dates":{"publication":"2026/05/26"},"accession":"GSE300863","cross_references":{"GSM":["GSM9069820","GSM9069821","GSM9069822","GSM9069817","GSM9069818","GSM9069819"],"GPL":["19057"],"GSE":["300863"],"taxon":["Mus musculus"]}}