Once activated PMNs have reached the lungs, they possess the potential to induce tissue injury. The release of ROS/NOS has long been thought to be a central effector mechanism of PMNmediated lung injury (69) . In this regard, while the inhibition of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase attenuated sepsisassociated ALI (70) , surprisingly, NADPH oxidase-deficient animals were not protected from complement-induced ALI (71) . On the other hand, inhibition/ deficiency of the nitric oxide synthetase showed protection in complement-/ endotoxin-induced ALI (71, 72) . However, ROS and NOS also play additional roles as signaling molecules modulating kinases and phosphatases, receptors and transcription factors (reviewed in 73) complicating the interpretation as to whether their net pulmonary effect is one of harm or help.