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Hu, Y.* ; Hu, Q.* ; Ansari, M. ; Riemondy, K.* ; Pineda, R.H.* ; Sembrat, J.* ; Leme, A.S.* ; Ngo, K.* ; Morgenthaler, O.* ; Ha, K.* ; Gao, B.* ; Janssen, W.J.* ; Basil, M.C.* ; Kliment, C.R.* ; Morrisey, E.* ; Lehmann, M. ; Evans, C.M.* ; Schiller, H. ; Königshoff, M.*

Airway derived emphysema-specific alveolar type II cells exhibit impaired regenerative potential in COPD.

Eur. Respir. J. 64:2302071 (2024)

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Emphysema, the progressive destruction of gas exchange surfaces in the lungs, is a hallmark of chronic obstructive pulmonary disease (COPD) that is presently incurable. This therapeutic gap is largely due to a poor understanding of potential drivers of impaired tissue regeneration, such as abnormal lung epithelial progenitor cells, including alveolar type II (ATII) and airway club cells. We discovered an emphysema-specific sub-population of ATII cells located in enlarged distal alveolar sacs, termed asATII cells. Single cell RNA-seq and in situ localisation revealed that asATII cells co-express the alveolar marker surfactant protein C (SPC) and the club cell marker secretaglobin-3A2 (SCGB3A2). A similar ATII sub-population derived from club cells was also identified in mouse COPD models using lineage labeling. Human and mouse ATII sub-populations formed 80-90% fewer alveolar organoids than healthy controls, indicating reduced progenitor function. Targeting asATII cells or their progenitor club cells could reveal novel COPD treatment strategies.

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