Immune response of polarized cystic fibrosis airway epithelial cells infected with Influenza A virus.

摘要: Abstract Background Cystic fibrosis (CF), a genetic disease caused by mutations of the cystic transmembrane conductance regulator (CFTR) gene, is characterized dysfunction immune response in airway epithelium that leads to prolonged infection, colonization and exacerbated inflammation. In this study, we determined gene expression profile epithelial cells knockdown for CFTR (CFTR KD) bacterial viral challenges. Methods first approach, polarized KD their control counterpart CTL) were stimulated with P. aeruginosa-derived virulence factor flagellin. Next, developed model Influenza A virus (IAV) infection CTL cells. mRNA was collected transcriptome analysis. Results Beside expected pro-inflammatory response, Gene Set Enrichment Analysis highlighted key molecular pathways players involved IAV anti-viral interferon signaling. Although replication similar both cell types, multiplex analysis revealed changes genes dependent on time found be CFTR-dependent and/or IAV-dependent. Interferons are signaling proteins/cytokines antibacterial antiviral response. To evaluate impact altered responses pathogens, measured after exposure Type I-, II- III-interferons. Conclusions Our findings reveal target understanding defective CF context infection. Information provided study would useful understand dysfunctional during