Pyroptosis

Pyroptosis is a highly inflammatory form of programmed cell death that occurs most frequently upon infection with intracellular pathogens and is likely to form part of the antimicrobial response. In this process, immune cells recognize foreign danger signals within themselves, release pro-inflammatory cytokines, swell, burst and die. The released cytokines attract other immune cells to fight the infection and contribute to inflammation in the tissue. Pyroptosis promotes the rapid clearance of various bacterial and viral infections by removing intracellular replication niches and enhancing the host’s defensive responses. However, in pathogenic chronic diseases, the inflammatory response does not eradicate the primary stimulus, as would normally occur in most cases of infection or injury, and thus a chronic form of inflammation ensues that ultimately contributes to tissue damage. Some examples of pyroptosis include salmonella-infected macrophages and abortively HIV-infected T helper cells.

The initiation of pyroptosis in infected macrophages is caused by the recognition of flagellin components of salmonella and shigella species (and similar pathogen-associated molecular patterns (PAMPs) in other microbial pathogens) by NOD-like receptors (NLRs). These receptors function like plasma membrane toll-like receptors (TLRs), but recognise antigens located within the cell rather than outside of it.

In contrast to apoptosis, pyroptosis requires the function of the enzyme caspase-1. Caspase-1 is activated during pyroptosis by a large supramolecular complex termed the pyroptosome (also known as an inflammasome). Only one large pyroptosome is formed in each macrophage, within minutes after infection. Biochemical and mass spectroscopic analysis revealed that this pyroptosome is largely composed of dimers of the adaptor protein ASC (apoptosis-associated speck protein containing a CARD or Caspase activation and recruitment domain).

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