Anomalous Epithelial Variations and Ectopic Inflammatory Response in Chronic Obstructive Pulmonary Disease
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, COPD was characterized by shifts in the stromal, immune system and epithelial cell compositions. While epithelial components in never-smokers were relatively uniform, the smoker groups presented with extensive heterogeneity in epithelial cells, particularly in the alveolar type II (AT2) lineages. We identified a subpopulation of AT2 epithelial cells that emerged in smokers, such as COPD patients, and specifically expressed a series of chemokines and PD-L1. A trajectory analysis revealed that the inflammatory AT2 cell subpopulation followed a unique differentiation path, and a prediction model of cell-to-cell interactions inferred increased intercellular networks of inflammatory AT2 cells with immune and stromal cell populations. Thus, our analysis reveals a unique cellular differentiation pathway and function underlying the biological and clinical characteristics of COPD pathogenesis. Overall design: single-cell transcriptome profiling from human lung tissues of 6 COPD, 3 non-COPD smoker, and 3 never-smoker samples.
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Atlas

Analysis Portals
Project Label
SingleCellTranscriptomeCOPDSpecies
Homo sapiens
Sample Type
specimens
Anatomical Entity
lung
Organ Part
Unspecified
Selected Cell Types
Unspecified
Disease Status (Specimen)
Disease Status (Donor)
Development Stage
human adult stage
Library Construction Method
Nucleic Acid Source
single cell
Paired End
falseAnalysis Protocol
analysis_protocol_1, analysis_protocol_2File Format
Cell Count Estimate
57.5kDonor Count
12