Integrated histopathology, spatial and single cell transcriptomics resolve cellular drivers of early and late alveolar damage in COVID-19.

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Tác giả: Alexander Aivazidis, Vincenzo Arena, Helen Ashwin, Sam N Barnett, Omer Ali Bayraktar, Patricia Chaves, Jae-Won Cho, Andrew Filby, Andrew J Fisher, Brian Hanley, Martin Hemberg, Alik Huseynov, Zuzanna Jablonska, Paul M Kaye, Jimmy Tsz Hang Lee, Michael Lee, Tong Li, Joaquim Majo, Gary R McLean, Luke Milross, Antonio M A Miranda, Michela Noseda, Michael Osborn, Anna M Randi, Kenny Roberts, Sarah A Teichmann, Virginie Uhlmann, Benjamin Woodhams, Xiao-Ning Xu

Ngôn ngữ: eng

Ký hiệu phân loại:

Thông tin xuất bản: England : Nature communications , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 686036

The most common cause of death due to COVID-19 remains respiratory failure. Yet, our understanding of the precise cellular and molecular changes underlying lung alveolar damage is limited. Here, we integrate single cell transcriptomic data of COVID-19 and donor lung tissue with spatial transcriptomic data stratifying histopathological stages of diffuse alveolar damage. We identify changes in cellular composition across progressive damage, including waves of molecularly distinct macrophages and depletion of epithelial and endothelial populations. Predicted markers of pathological states identify immunoregulatory signatures, including IFN-alpha and metallothionein signatures in early damage, and fibrosis-related collagens in late damage. Furthermore, we predict a fibrinolytic shutdown via endothelial upregulation of SERPINE1/PAI-1. Cell-cell interaction analysis revealed macrophage-derived SPP1/osteopontin signalling as a key regulator during early steps of alveolar damage. These results provide a comprehensive, spatially resolved atlas of alveolar damage progression in COVID-19, highlighting the cellular mechanisms underlying pro-inflammatory and pro-fibrotic pathways in severe disease.
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