Significance Pathogenic bacteria subvert host-defense mechanisms by injecting effector proteins into target cells to inhibit NF-κB and MAPK signaling. Detection of such effector proteins, such as YopJ from pathogenic Yersinia , activates RIPK1 and caspase-8–dependent cell death that promotes antibacterial defense. While recent studies demonstrate that caspase-8 cleaves the pore-forming protein gasdermin D to promote anti- Yersinia defense, whether RIPK1 activates other substrates is unclear. Here, we demonstrate that RIPK1 activates gasdermin D in macrophages and the related gasdermin E in neutrophils to promote host defense. Neutralization of IL-1β in vivo promoted host susceptibility to Yersinia infection in wild-type, but not Gsdme ^−/− , animals, revealing an unexpected role for gasdermin E in IL-1β secretion during bacterial infection.