Indeed, while we demonstrate that neutrophils activate the inflammasome in macrophages during influenza infection, other studies have also shown that neutrophils can inhibit macrophage inflammatory responses to viruses.39 Regardless, in our physiologically relevant model, influenza elicited an early release of IL-1β that peaked at 24 hours post infection, which was completely dependent on neutrophil infiltrate. The gene discussed is IL1B; the disease is influenza.