ABSTRACT
Pyroptosis is an inflammatory form of programmed cell death, first named in 2001 from the Greek words pyro (“fire” or “fever”) and ptosis (“to fall”). It is triggered by a variety of threats, including invading pathogens. Most often, this is an advantageous adaptation that removes intracellular pathogens from the host; infectious bacteria are removed from their replication niches and presented to neutrophils responding to released cytokines. Pyroptosis is mechanistically distinct from other types of regulated cell death, such as apoptosis and necroptosis, and is defined by its dependence on the inflammatory caspases 1, 4, 5, and 11 in humans and their orthologues in animals. Excessive activation of the pathway has been found to be associated with widespread cell death, causing tissue damage, organ failure, and lethal septic shock, inflammatory bowel disease, hair loss, neuronal damage, and cognitive impairment in aged mice, and bladder muscular hyperplasia, hepatitis, auto-inflammatory diseases, brucella joint infection, acute lung injury, acute respiratory distress syndrome, inflammatory demyelination, sepsis, and osteomyelitis in animals. This chapter, while describing the molecular mechanism, points to studies where pyroptosis has been identified as the underlying etiology of many animal diseases. The diagnostic potential of biomarkers of pyroptosis like caspase-1, interleukin-1β, interleukin-18, and gasdermin D have not been exploited enough. Along with challenges in the use of these biomarkers for diagnosis, they also present opportunities for future development of veterinary diagnostics.
