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Human Immuno-Lung Organoid Model to Study Macrophage-Mediated Lung Cell Senescence Upon SARS-CoV-2 Infection [snMultiomics]

GSE287113 Homo sapiens Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing 8 samples Submitted 2025/11/14 Platform GPL34284
Summary
In this study, we utilized spatial transcriptional assays (NanoString CosMx) to analyze both explant and autopsy samples from non-COVID and COVID-19 lungs, identifying activation of proinflammatory macrophages. We then created macrophage-alveolar and macrophage-airway organoid models, integrating hPSC-derived macrophages with alveolar or airway organoids, and discovered that proinflammatory macrophages induce lung cell senescence through via the THBS1-(ITGA3+ITGB1) pathway. This study not only establishes immune-lung organoid models for studying macrophage-mediated host damage but also highlights the previously unrecognized role of the THBS1-(ITGA3+ITGB1) pathway in lung cell senescence during infectious diseases.
Published in
A Human Immuno-Lung Organoid Model to Study Macrophage-Mediated Lung Cell Senescence Upon SARS-CoV-2 Infection
Han Y, Leng D, Zhang T et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) 2025 · PMID 40712141 · doi:10.1002/advs.202503932
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Direct links to NCBI, no account and no request form: the whole study as GSE287113_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 8 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1211144 and SRA study SRP557625. Searching any of these in the dataset finder brings you back here.

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