Influenza A virus (IAV) is an infectious respiratory pathogen that is estimated to affect at least 1 billion people worldwide every year, with the young, old and immunocompromised being at most risk. Detection of IAV by the host's immune system aids viral clearance, however, hyperinflammation can lead to the development of fatal lung disease. Gasdermin D is an executioner of pyroptosis, a lytic form of cell death which results following NLRP3 inflammasome activation. Gasdermin D forms a transmembrane pore, which is thought to promote the cellular release of pro-inflammatory cytokines including IL-1β and IL-18, as well as danger associated molecular patterns (DAMPs), promoting further inflammation. While Gasdermin D has been implicated in many inflammatory diseases, its role in IAV infection is not well characterised. Here, we showed that mice lacking gasdermin D (Gsdmd-/-) are less susceptible to HKx31 H3N2 IAV infection, displaying significantly improved survival in comparison to wildtype controls. Further, bronchoalveolar lavage fluid presented with a significant reduction in total cellularity, which correlated with fewer numbers of infiltrating neutrophils at day 3 and 5 post-infection. This was accompanied with a significant decrease in pro-inflammatory cytokines including CCL2/MCP-1, IL-6 and TNF at day 3. Interestingly, the number of infectious viral particles in lung tissue was reduced at day 3. Together, these results suggest that gasdermin D limits the severity of IAV infection. Inhibition of gasdermin D may provide a novel host-targeted IAV therapeutic strategy, which limits the development of fatal lung disease.