Influenza virus infection modulates expression of the anti-inflammatory mucin 1 in both epithelial and immune cells

Abstract Cell-associated mucin 1(MUC1/Muc1) is a component of the mucus barrier in respiratory tract that acts as physical and signaling molecule. Our prior work shows MUC1 expression increased during influenza virus (IAV) infection human airway epithelial (HAE) cultures vitro. Here we further detail patterns report IAV-induced cytokines, including type I interferons (IFNs), trigger low-molecular-weight form which localizes to cytoplasm nucleus, expressed different cell types. Further, IFN-driven changes cellular composition HAE toward more secretory phenotype require MUC1, suggesting plays an important role shaping response viral infection. Using mouse model IAV infection, confirmed upregulation Muc1 throughout epithelium vivoand observed altered levels lung immune cells. Specifically, was upregulated interstitial macrophages but downregulated antigen-presenting cells (APCs) alveolar dendritic early 2 days post-infection (dpi). By 5 dpi, significantly various T subsets their effector counterparts CD4 +, CD8 double-negative We also found negative correlation between APCs expansion populations, supporting putative immunoregulatory roles MUC1/Muc1. ongoing explores impact specific on pathogenesis. This supported by National Heart, Lung, Blood Institute (R01HL151840, MAS)