Abstract
BackgroundThe human small airway epithelium (SAE) plays a central role in the early events in the pathogenesis of most inherited and acquired lung disorders. Little is known about the molecular phenotypes of the specific cell populations comprising the SAE in humans, and the contribution of SAE specific cell populations to the risk for lung diseases.MethodsDrop-seq single-cell RNA-sequencing was used to characterize the transcriptome of single cells from human SAE of nonsmokers and smokers by bronchoscopic brushing.ResultsEleven distinct cell populations were identified, including major and rare epithelial cells, and immune/inflammatory cells. There was cell type-specific expression of genes relevant to the risk of the inherited pulmonary disorders, genes associated with risk of chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis and (non-mutated) driver genes for lung cancers. Cigarette smoking significantly altered the cell type-specific transcriptomes and disease risk-related genes.ConclusionsThis data provides new insights into the possible contribution of specific lung cells to the pathogenesis of lung disorders.
Highlights
The small airway epithelium (SAE), a single layer of cells covering the branching airways from the 6th-23rd generations, plays a central role in the early events in the pathogenesis of most lung disorders, including hereditary lung disorders, chronic obstructive pulmonary disease (COPD), Using single-cell RNA-sequencing, we defined the transcriptomes of eleven small airway cell populations recovered by brushing the 10th–12th order bronchi ofZuo et al Respiratory Research (2020) 21:200 nonsmokers and smokers
Little is known about the molecular phenotypes of the specific cell populations comprising the SAE, and the contribution of specific SAE cell populations to the pathogenesis of human lung disorders
The data demonstrate cellspecific differences in genes essential to the risk for lung-related hereditary monogenic disorders, COPD, idiopathic pulmonary fibrosis (IPF), and lung cancers. For many of these hereditary and acquired disorders, the analysis uncovered unexpected cell specificity in both major and rare small airway cell types modulated by cigarette smoking
Summary
The small airway epithelium (SAE), a single layer of cells covering the branching airways from the 6th-23rd generations, plays a central role in the early events in the pathogenesis of most lung disorders, including hereditary lung disorders, chronic obstructive pulmonary disease (COPD), Using single-cell RNA-sequencing, we defined the transcriptomes of eleven small airway cell populations recovered by brushing the 10th–12th order bronchi ofZuo et al Respiratory Research (2020) 21:200 nonsmokers and smokers. The small airway epithelium (SAE), a single layer of cells covering the branching airways from the 6th-23rd generations, plays a central role in the early events in the pathogenesis of most lung disorders, including hereditary lung disorders, chronic obstructive pulmonary disease (COPD), Using single-cell RNA-sequencing, we defined the transcriptomes of eleven small airway cell populations recovered by brushing the 10th–12th order bronchi of. The data demonstrate cellspecific differences in genes essential to the risk for lung-related hereditary monogenic disorders, COPD, IPF, and lung cancers. For many of these hereditary and acquired disorders, the analysis uncovered unexpected cell specificity in both major and rare small airway cell types modulated by cigarette smoking. The human small airway epithelium (SAE) plays a central role in the early events in the pathogenesis of most inherited and acquired lung disorders. Little is known about the molecular phenotypes of the specific cell populations comprising the SAE in humans, and the contribution of SAE specific cell populations to the risk for lung diseases
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