{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE327nnn/GSE327879/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Other"],"species":["Homo sapiens"],"gds_type":["Other"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE327879"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Single-cell spatial transcriptomic analyses of severe Covid-19 lungs identifies disease-associated spatial niches","description":"Severe COVID-19 is characterized by marked heterogeneity in lung pathology, yet how spatially organized cellular interactions shape disease progression remains unclear. Here, we applied imaging-based single-cell spatial transcriptomics to post-mortem lung samples from severe COVID-19 patients and controls. We identified distinct cellular niches associated with specific histopathological states, including fibrotic and alveolar remodeling regions. Fibrotic niches were enriched in CHI3L1/MMP9hi macrophages spatially associated with COL1A1+ fibroblasts and predicted to drive pathogenic fibroblast reprogramming through Tgf-β and galectin-3 signaling. In contrast, alveolar niches contained SPP1hi macrophages exposed to epithelial-derived cues, including WNT ligands and GM-CSF, consistent with differentiation toward an alveolar macrophage-like state. These findings reveal that severe COVID-19 lungs are organized into discrete, macrophage-centered microenvironments that differentially regulate tissue remodeling, providing a spatial framework to understand divergent immunopathological trajectories.  ","dates":{"publication":"2026/09/21"},"accession":"GSE327879","cross_references":{"GSM":["GSM9667708","GSM9667707"],"GPL":["33484"],"GSE":["327879"],"taxon":["Homo sapiens"]}}