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Macrophage-derived oncostatin M repairs the lung epithelial barrier during inflammatory damage

GSE291698 Mus musculus Expression profiling by high throughput sequencing 8 samples Submitted 2025/07/10 Platform GPL24247
Summary
Tissue repair programs must function alongside antiviral immunity to restore the lung epithelial barrier following infection. We found that macrophage-derived oncostatin M (OSM) counteracted the pathological effects of type I interferon (IFN- I) during infection and damage in mice. At baseline, OSM-deficient mice exhibited altered alveolar type II (ATII) epithelial cell states. In response to influenza or viral mimic challenge, mice lacking OSM exhibited heightened IFN-I responses and increased mortality. OSM delivery to the lung induced ATII proliferation and was sufficient to protect deficient mice against morbidity. Furthermore, OSM promoted organoid formation despite the growth- inhibitory effects of IFN- I. These findings identify OSM as an indispensable macrophage-derived growth factor that maintains the homeostasis of lung epithelial cells and promotes their proliferation to overcome IFN-I–mediated immunopathology.
Published in
Macrophage-derived oncostatin M repairs the lung epithelial barrier during inflammatory damage
Hoagland DA, Rodríguez-Morales P, Mann AO et al. · Science (New York, N.Y.) 2025 · PMID 40638741 · doi:10.1126/science.adi8828
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Also filed as BioProject PRJNA1234675 and SRA study SRP569685. Searching any of these in the dataset finder brings you back here.

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