Influenza A virus (IAV) is a highly contagious virus that causes respiratory infections in up to 40% of children each year. Both the virus and the immune system’s response to the virus can damage the lungs in IAV infection. We found that young mice infected with IAV show activation of two signaling pathways, NLRP3 and NOD2, even after the virus is eliminated. Our goal is to determine how NLRP3 and NOD2 contribute to IAV-induced lung injury in juvenile mice and to identify the cell type governing the juvenile response to IAV. We hypothesize that robust and sustained activation of the NLRP3 inflammation pathway exacerbates IAV-induced lung injury in juvenile mice and may contribute to morbidity and mortality in children infected with IAV.
|Effective start/end date||7/1/16 → 6/30/17|
- Respiratory Health Association of Metropolitan Chicago (RHA2016-01-ARDS)