Respiratory viral infections cause lung epithelial damage, barrier dysfunction and severe disease. Type I interferons (IFN-a/b) are antiviral cytokines whose therapeutic use is limited by well-characterized pleiotropic effects. Type III IFNs (IFN-) are less pro-inflammatory and regarded a superior treatment option. Here, we show that IFN signalling reduces lung epithelial proliferation and differentiation and increases epithelial apoptosis during recovery from viral infection. This delays epithelial repair, increasing disease severity and the risk of bacterial superinfection. IFN-a has least effects, with IFN-b intermediate and IFN- strongest action. SOURCE: Andreas Wack (andreas.wack@crick.ac.uk) - Immunoregulation Laboratory The Francis Crick Institute

Pluto Bioinformatics

GSE148709: Interferons disrupt lung epithelial repair during recovery from respiratory infection [RN19197]