GSE193160
Arhgdia regulates disease tolerance in IAV-infected epithelial cells
When challenged with an invading pathogen, host defense mechanisms are engaged to eliminate the pathogen (resistance) and limit tissue damage that results from host-pathogen interactions (disease tolerance). We identified Arhgdia as a driver of the molecular disease-tolerance response in epithelial cells. The effect of Arhgdia on disease tolerance and resistance was evaluated at early stages of influenza A virus (IAV) infection. Our observations indicates that Arhgdia has an effect on disease tolerance during IAV infection. Overall design: To test the role of Arhgdia in the regulation of disease-tolerance state, we deleted Arhgdia in mouse epithelial cells (LET1 and MLE cells) by CRISPR-Cas9 editing, and then tested the effect of this deletion on the host response to infection. Control (non-targeting sgRNA) and Arhgdia-deleted (Arhgdia-targeted sgRNA) cells, with and without IAV infection, were analyzed.