2009 February ; 7(2): 99–109. | Tessa Bergsbaken*, Susan L. Fink‡, and Brad T. Cookson*§
The article discusses the nature and mechanisms of pyroptosis, a form of host cell death that is characterized by inflammation. Pyroptosis, or caspase 1-dependent cell death, is triggered by various pathological stimuli and is crucial for controlling microbial infections. The process involves rapid plasma membrane rupture and the release of proinflammatory intracellular contents, leading to cell lysis and inflammation. Caspase 1, a cysteine protease, mediates this process by activating inflammatory cytokines such as interleukin-1β (IL-1β) and IL-18. Pathogens have evolved mechanisms to inhibit pyroptosis, enhancing their ability to persist and cause disease. The competition between host and pathogen to regulate pyroptosis ultimately determines the outcome of infection, which can be life or death for the host. The article also explores the role of toll-like receptors (TLRs) and nod-like receptors (NLRs) in sensing danger signals and activating caspase 1, as well as the involvement of the inflammasome in pyroptosis. Additionally, it highlights the multifaceted role of caspase 1 in host defense, including its impact on inflammatory cytokine production, pathogen growth, and immune response regulation.The article discusses the nature and mechanisms of pyroptosis, a form of host cell death that is characterized by inflammation. Pyroptosis, or caspase 1-dependent cell death, is triggered by various pathological stimuli and is crucial for controlling microbial infections. The process involves rapid plasma membrane rupture and the release of proinflammatory intracellular contents, leading to cell lysis and inflammation. Caspase 1, a cysteine protease, mediates this process by activating inflammatory cytokines such as interleukin-1β (IL-1β) and IL-18. Pathogens have evolved mechanisms to inhibit pyroptosis, enhancing their ability to persist and cause disease. The competition between host and pathogen to regulate pyroptosis ultimately determines the outcome of infection, which can be life or death for the host. The article also explores the role of toll-like receptors (TLRs) and nod-like receptors (NLRs) in sensing danger signals and activating caspase 1, as well as the involvement of the inflammasome in pyroptosis. Additionally, it highlights the multifaceted role of caspase 1 in host defense, including its impact on inflammatory cytokine production, pathogen growth, and immune response regulation.