Infection with Influenza A virus (IAV) continues to cause morbidity and mortality in children across the globe, in part due to the excessive inflammatory response during pathogen clearance. Using a murine model of IAV infection, this study focuses on the role of the innate immune system in IAV infection through the scope of NLRP3 inflammasome protein activation and assembly. We were able to detect the presence of the NLRP3-inflammasome target proteins ASC, Pro-caspase-1, NLRP3, RIG-1, and IL-1β in both juvenile and adult mice. Notably, we found significantly increased levels of ASC and RIG-1 protein in juveniles compared to adults. This suggests that ASC and RIG-1 are related to the observed excessive inflammatory response upon IAV infection in juveniles. To examine NLRP3-inflammasome assembly, we created multiple mutant constructs of the inflammasome scaffolding protein Vimentin as well as vimentin-/- cells. IL-1β production was greatly inhibited in vimentin-/- cells compared to the wild type upon activation of the NLRP3 inflammasome. The same trend was seen when only the head region of the protein was present. We suggest that the intermediate filament (IF) Vimentin serves as a protein scaffold for inflammasome assembly, and that expression of Vimentin is a necessary checkpoint in the innate immune response. Furthermore, we propose the Vimentin-targeting drug withaferin A as a potential treatment for IAV induced acute lung injury. Further studies are to be conducted to compare age-related differences in expression of other inflammasome-related proteins as well as the effect of other Vimentin constructs on IL-1β production. A better understanding of age-related differences in innate immune signaling as well as the overall structure of the inflammasome will be essential to improve care of and treatment for this high-risk population.