Abstract
Polymorphonuclear leukocytes or neutrophils are the main executors of cellular death, both in septic inflammation during bacterial infection and in strile inflammation during trauma or surgery. Whereas in septic inflammation neutrophils perform a useful function to fortify the host's defense against infection, in sterile inflammation, by contrast, they contribute to unwelcome tissue damage.
Regardless of the situation, activated neutrophils exhibit a prolonged lifespan and delayed apoptotic death which, under normal conditions, is a prerequisite for their natural renewal. Traditionally, delayed neutrophil apoptosis was considered to promote trauma or surgical injury.
According to the results of recent studies, however surprising they may appear, the reverse might be in keeping with what happens in vivo. Apoptotic signalizing in neutrophils could, by contrast, contribute to intrinsic protection of the host's tissue.