The re-discovery of caspase-11 led to the refinement of the functions of both caspase-11 and caspase-1. The current consensus is that caspase-11 is both the initiator and executioner caspase for cell death upon binding by bacterial lipopolysaccharide present in the cytosol. Caspase-1, on the other hand, is the executioner caspase for cleavage and activation of various IL-1 family of cytokines. The actions of both caspases complete the host defense mechanism of pyroptosis, defined as a necrotic cell death process with concomitant release of mature IL-1 cytokines. Upstream and downstream players in the caspase-11 cascade have also been elucidated in rapid succession. The activation of caspase-11 upon Gram-negative bacterial infection require a family of proteins known as the Guanylate Binding Proteins (GBPs). Downstream of caspase-11, the pore forming protein GasderminD (GsdmD) oligomerizes to form plasma membrane pores, resulting in cell death. Detailed in this dissertation are two projects that I investigated on macrophage pyroptosis against two different bacterial pathogens. In the first project, I built upon existing knowledge of GBPs to refine their role and placement in the initiation of cytosolic pathogen sensing. Here, I used a mutant of Legionella pneumophila that shows inadvertent cytosol permeability to model the initial response of a naive macrophage to cytosol bacterial presence. I report that low levels of GBP expression are maintained by quiescent Interferon signaling, and is crucial for the timely release of bacterial contents to initiate downstream immune responses. In the second project, I explored the morphology of a rapid, necrotic cell death phenotype mediated by caspase-8 during Yersinia species infection. Using Y. pseudotuberculosis in conjunction with a small molecule inhibitor to mimic the virulence factor YopJ, I found that caspase-8 activation induced the cleavage of multiple gasdermins, resulting in a pyroptotic-like cell death morphology and IL-1 release. I am glad to have been able to first amend and then to add to our understanding of this rapidly evolving field of host defense known as pyroptosis.