GSE162154
RNA-seq of human small airawy epithelial cells in patients with COPD and Never-smoker
Chronic obstructive pulmonary disease (COPD) is a progressive disease that obstructs the airflow from the lungs, and tobacco smoking is the major cause of COPD. Here, we applied single-cell RNA sequencing to analyze COPD pathogenesis in COPD patients, non-COPD smokers and never-smokers and investigated the disease progression at single-cell resolution. By single-cell transcriptome analysis, we identified a novel subpopulation of Alveolar Type 2 epithelial cells that emerged in smokers, such as COPD patients, and specifically expressed a series of chemokines and PD-L1. Since the number of cells in the basal cell clusters increased in only the COPD lungs but not in the non-COPD smoker or never-smoker lungs, we also tried to clarify the difference in phenotype between COPD and other basal cells with single-cell RNA-seq. However, due to the small number of cells in each, no clear difference could be found. To further investigate the functional properties of basal cells in COPD, we isolated small airway epithelial cells from surgical samples of COPD or never-smoker lungs and expanded the cells in vitro.Total RNA was extracted from early passaged cells , and bulk RNA-seq was performed to characterize these cells in detail. Finally, we found that the COPD basal cells retained the inflammatory response and basal/stem-related signals, even after a few passages in culture, and it might cause basal cell expansion in vivo. Overall design: Human small airway epithelial cell(HSAEC) were isolated from surgical samples of 3 COPD and 3 never-smoker lungs and expanded the cells in vitro. Morphologically, small airway epithelial cells from COPD and never-smokers were similar, and the expression patterns of basal cell markers such as Krt5 and p63 were similar. Total RNA was extracted from early passaged cells (less than passage 3), and bulk RNA-seq was performed to characterize these cells in detail.