Expression data from airway basal cells and mucociliary-differentiated epithelium of COPD patients and normal subjects

Continuous stress caused by smoking induces changes in the cell population of small airway epithelium, with basal cell hyperplasia and goblet cell metaplasia at the expense of ciliated cells, and there is now compiling evidence that basal cells play a key role in the early pathogenesis of Chronic Obtructive Pulmonary Disease (COPD). We hypothesized that COPD airway basal cells undergo transcriptomic changes during differentiation that are different from those observed in normal cells and can explain the formation of an abnormal epithelium. We performed microarray analysis of basal cells obtained from healthy non-smoker and COPD subjects and also mucociliary-differentiated cell cultures from the same basal cells. We compared the transcriptome of normal and COPD basal cells, mucociliary-differentiated normal and COPD cell cultures and also of basal cells with corresponding mucociliary-differentiated cultures for both normal and COPD. Basal cells were isolated from tracheobronchial segments of normal donor lungs and explanted lungs from COPD patients at the time of lung transplantation. Tissue was collected from 8 healthy non-smokers and 8 COPD patients. Basal cells were cultured in collagen coated dishes, flow sorted on the expression of a basal cell marker, and then seeded in transwell to promote mucociliary differentitation. Cells were harvested either at subconfluent stage that is 3-4 days after seeding (basal cells) or after 4 weeks of culturing at air-liquid interface (differentiated cells)