Disruption in lung cell repair may underlie acute respiratory distress syndrome in COVID-19 and other respiratory diseases (IMAGE)
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Fatal COVID-19 (and non--COVID-19) acute respiratory distress syndrome (ARDS) is characterized by diffuse injury to epithelial cells, including type 1 alveolar epithelial cells (AEC1), indicated by HTI-56 and tomato lectin staining in (A) and AEC2, indicated by proSPC staining shown in (B). Progenitor cells proliferate and assume the AEC transitional state, indicated by KRT8 staining shown in (B). Transitional cells line structurally normal alveolar septa filling gaps denuded of AEC1. They are sometimes cuboidal (open yellow arrowheads), sometimes partially spread (open white arrowheads, and sometimes assume a flat AEC1 morphology (closed yellow arrowheads), as shown in (C). Taken together, these data suggest that to replace damaged epithelial cells, AEC2 proliferate and assume the transitional state, and that AEC1 differentiation from the transitional state is ongoing but incomplete without scarring, leading to fatal acute respiratory failure. In contrast, fibrosis is associated with a permanent arrest in the transitional state (D). An improved understanding of the mechanisms by which transitional cells differentiate into AEC1 may ultimately lead to the development of new treatments to accelerate lung regeneration and prevent mortality and lung scarring in COVID-19 and ARDS due to other causes.
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The American Journal of Pathology
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