Pyroptosis is a caspase-1-dependent inflammatory form of cell death that plays a crucial role in controlling microbial infections. It is distinct from apoptosis, which is non-inflammatory and involves programmed cell death without significant inflammation. Pyroptosis is characterized by rapid plasma membrane rupture, release of proinflammatory intracellular contents, and cell lysis. It is triggered by various stimuli, including microbial infections and host factors, and is essential for host defense against pathogens. Pathogens have evolved mechanisms to inhibit pyroptosis, enhancing their survival and virulence. The competition between host and pathogen in regulating pyroptosis determines the outcome for the host. Pyroptosis is initiated through the activation of caspase-1, which leads to the formation of inflammatory cytokines such as IL-1β and IL-18. This process is mediated by pattern recognition receptors, including Toll-like receptors (TLRs) and Nod-like receptors (NLRs), which recognize pathogen-associated molecular patterns. NLRs, such as NLRP3 and NLRC4, play a key role in sensing danger signals and triggering the formation of the inflammasome, a multiprotein complex that activates caspase-1. The inflammasome is crucial for the processing and secretion of inflammatory cytokines, which contribute to the inflammatory response. Caspase-1 activation also influences the development of adaptive immune responses by enhancing the production of T helper 1 (Th1) cells and promoting the production of IFN-γ. Additionally, caspase-1 is involved in the clearance of intracellular pathogens, such as Salmonella, Shigella, and Legionella, by facilitating their degradation within lysosomes. However, excessive or inappropriate caspase-1 activation can lead to detrimental outcomes, including excessive inflammation and tissue damage. Pathogens have evolved strategies to inhibit caspase-1 activation, thereby avoiding pyroptosis and enhancing their survival. The regulation of pyroptosis is a dynamic process involving the interplay between host and pathogen. Host cells can redirect cell death from apoptosis to pyroptosis in response to pathogen infection, which enhances the inflammatory response and facilitates pathogen clearance. However, excessive pyroptosis can lead to tissue damage and systemic inflammation. Understanding the mechanisms of pyroptosis and its regulation is essential for developing therapeutic strategies to combat infectious diseases and inflammatory conditions.Pyroptosis is a caspase-1-dependent inflammatory form of cell death that plays a crucial role in controlling microbial infections. It is distinct from apoptosis, which is non-inflammatory and involves programmed cell death without significant inflammation. Pyroptosis is characterized by rapid plasma membrane rupture, release of proinflammatory intracellular contents, and cell lysis. It is triggered by various stimuli, including microbial infections and host factors, and is essential for host defense against pathogens. Pathogens have evolved mechanisms to inhibit pyroptosis, enhancing their survival and virulence. The competition between host and pathogen in regulating pyroptosis determines the outcome for the host. Pyroptosis is initiated through the activation of caspase-1, which leads to the formation of inflammatory cytokines such as IL-1β and IL-18. This process is mediated by pattern recognition receptors, including Toll-like receptors (TLRs) and Nod-like receptors (NLRs), which recognize pathogen-associated molecular patterns. NLRs, such as NLRP3 and NLRC4, play a key role in sensing danger signals and triggering the formation of the inflammasome, a multiprotein complex that activates caspase-1. The inflammasome is crucial for the processing and secretion of inflammatory cytokines, which contribute to the inflammatory response. Caspase-1 activation also influences the development of adaptive immune responses by enhancing the production of T helper 1 (Th1) cells and promoting the production of IFN-γ. Additionally, caspase-1 is involved in the clearance of intracellular pathogens, such as Salmonella, Shigella, and Legionella, by facilitating their degradation within lysosomes. However, excessive or inappropriate caspase-1 activation can lead to detrimental outcomes, including excessive inflammation and tissue damage. Pathogens have evolved strategies to inhibit caspase-1 activation, thereby avoiding pyroptosis and enhancing their survival. The regulation of pyroptosis is a dynamic process involving the interplay between host and pathogen. Host cells can redirect cell death from apoptosis to pyroptosis in response to pathogen infection, which enhances the inflammatory response and facilitates pathogen clearance. However, excessive pyroptosis can lead to tissue damage and systemic inflammation. Understanding the mechanisms of pyroptosis and its regulation is essential for developing therapeutic strategies to combat infectious diseases and inflammatory conditions.