Regulation of PMN Apoptosis. Neutrophils, once mature, exhibit a constitutive form of programmed cell death with a life span between 6 to 12 h in circulation. Under normal circumstances, activated PMNs are eliminated fairly quickly once the invading pathogen has been cleared. Several inflammatory agents, such as LPS, TNF, IL-8, IL-6, IL-1, Granulocyte [macrophage] colony-stimulating factor (G [M] -CSF), etc., can inhibit PMN apoptosis (81) (82) (83) (84) . The delayed apoptotic response provides PMNs with a longer life span, which, in turn, allows them to accumulate at local tissue sites of inflammation/infection. In this respect, PMNs obtained from patients following major trauma (85, 86) , burn injury (87), sepsis (88) , and ARDS (89) all showed evidence of decreased apoptosis. The anti-apoptotic effect of ARDS plasma on PMNs appears to be mediated through the GM-CSF receptor (90) . In sepsis, the delay in apoptosis was associated with a decrease in caspase-3 and -9 activity and a prolonged maintenance of the mitochondrial membrane potential (88) . The delay of PMN apoptosis also involved the active regulation of CXC receptors by PMNs themselves (91) . However, controversy persists as to whether this sustained activation actually contributes to organ injury. Activated PMNs have been shown to exert damaging effects in the lungs (68, 92) . However, following G-CSF treatment in pneumonia patients, no differences in outcome or time of recovery were noted, while it appeared that complications such as ARDS were decreased (93) . These data were complemented by studies that indicated that GM-CSF in the air spaces was associated with improved survival in patients with ARDS (94) .