{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE328nnn/GSE328605/"]},"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=GSE328605"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Myeloid Cell States in Influenza-Associated Pulmonary Aspergillosis are Shaped by Iron Overload and Metabolic Reprogramming","description":"We performed single-cell RNA sequencing using the 10x Genomics platform to define how prior influenza A virus (IAV) infection reshapes pulmonary monocyte and macrophage responses during secondary Aspergillus fumigatus infection in a murine model of influenza-associated pulmonary aspergillosis (IAPA). IAPA is a severe complication of influenza ICU-admitted patients, but the host mechanisms that drive susceptibility remain incompletely understood. To address this, we profiled CD11b+ monocyte/macrophage-enriched lung cells from naïve mice, IAV-only mice, A. fumigatus (CEA10)-only mice, and IAV+A. fumigatus (Coinfection) mice. This dataset provides a high-resolution view of how prior influenza infection reshapes innate immune cell states during secondary A. fumigatus infection. These data establish a resource for investigating innate immune dysregulation in IAPA and offer new insight into how influenza-driven remodeling of the lung myeloid compartment impairs monocyte and macrophage responses to secondary fungal challenge.","dates":{"publication":"2026/08/30"},"accession":"GSE328605","cross_references":{"GSM":["GSM9685927","GSM9685926","GSM9685925","GSM9685924"],"GPL":["19057"],"GSE":["328605"],"taxon":["Mus musculus"]}}