Fig. 1.

Type of cell death for neutrophil in organ injury. During solid organ injury, neutrophils could be prompted to undergo caspase-dependent apoptosis, which results in controlled dissolution of cell into apoptotic bodies containing cellular debris to prevent immune and inflammatory responses. Neutrophil extracellular traps (NETs) form via two pathways. The first is through lytic NETosis, a cell death pathway characterised by nuclear de-lobulation and disintegration of the nuclear envelope, which precedes loss of cellular polarisation, chromatin de-condensation and plasma membrane rupture. The second mechanism involves the non-lytic form of NETosis, which is not associated with cellular death but prompts expulsion of nuclear chromatin together with release of granule proteins through degranulation. These components can assemble in the extracellular space into NETs, leaving behind enucleated cytoplasts that continue to ingest microorganisms [4]. In addition, neutrophils could undergo unregulated necrosis that does not involve specific molecular pathways, with uncontrolled release of cellular debris acting as danger-associated molecular patterns (DAMPs) to trigger pro-inflammatory response.