Neutrophils and Apoptosis

Neutrophil function is tightly regulated, as the toxic metabolites intended to destroy invading microorganisms lack specificity and are therefore also damaging to host tissues. Once an inflammatory stimulus has been successfully cleared by the actions intended to destroy invading microorganisms, lack of specificity can also damage host tissues. Thus, once an inflammatory stimulus has been successfully cleared by the actions of recruited neutrophils, it is essential that these neutrophils are equally rapidly 'switched off' to prevent inadvertent damage to host tissues with unnecessary propagation of inflammation, as well as allowing restoration of organ homeostasis to occur. Key to the successful resolution of neutrophilic inflammation is the highly regulated and energy-dependent processes of neutrophil apoptosis and subsequent uptake and disposal of apoptotic neutrophils by tissue macrophages. In this chapter we will focus on our current understanding of the mechanisms governing neutrophil apoptosis under both basal and inflammatory conditions, as well as present and discuss evidence that driving neutrophil apoptosis is a possible strategy for inflammation resolution.