Rescue Of Dysfunctional Autophagy By Peptide IDR-1018 Attenuates Hyperinflammatory Phenotype Of Cystic Fibrosis Cells. Homo sapiens

Genome-wide gene expression was measured in two cell lines: CF bronchial epithelial cell line IB3-1 (compound heterozygote for the ΔF508 and W1282X CFTR mutations) and the isogenic, CFTR-corrected C38 cell line, after treatment with the flagellin protein FliC, and/or synthetic peptide IDR-1018. Overall design: Total RNA was obtained from cell lines representing CF and normal epithelial cells after treatment with the fliC protein (that is known to play a role in CF lung inflammation), and/or the peptide IDR-1018 that has anti-inflammatory properties. Comparison of genes and pathways affected by these treatments indicated the role of autophagy process in CF disease.