Abstract
Chronic Lung Allograft Dysfunction (CLAD) is characterized by airway epithelial cell damage followed by airway and parenchymal fibrosis. The origin and initiation of fibrosis are notunderstood. To understand how cells differ from each other, we need to understand which genes are transcribed at a single-cell level. The purpose of pilot to: 1) determine if AECs can be analyzed with scRNAseq 2) what cell populations can we identify 3) can we find rare AEC pops METHODS: 5 ml BAL aliquots from surveillance procedures in 3 patients. Cells plated onto plates (10,000 wells). Beads with cell- and transcript-barcodes added alongside 1 cell to specifically label. cells lysed, mRNAs hybridized to beads, RT, amplified, and sequenced RESULTS: gene expression profile for each cell is reconstructed to the cell of origin. Figure presents the various cell types found in tSNE plot. Same cells close to one another in the 2D data space, each dot a cell. optimized to yield the highest number of AECs, but AM are present in abundance. Gene expression patterns were quantified. Each cluster a cell type. Cells with similar HLA expression profiles are the same color. rare cell types can be isolated and studied with scRNAseq. gene expression reveal T-cells in acute rejection, AECs involved in tissue remodeling and rare AEC progenitor cells (Table) implying EMT. This discovery pilot demonstrates the power to delve into cell-specific activity and can be further pursued to discover pathways that lead to CLAD long before graft dysfunction is measured.
Published Version
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