Inhibition of human neutrophil reactive oxygen species production and p67phox translocation by cigarette smoke extract

These findings demonstrate that CS treatment reduced agonist-induced human neutrophil ROS production independent of p47phox phosphorylation and translocation from the cytosol to the membrane. However, this inhibition could be attributed to a reduction in translocation of another cytosolic NADPH oxidase protein, p67phox. Although neutrophil-generated ROS have been implicated in the pathogenesis of atherosclerosis, this does not appear to be the mechanism by which CS induces vascular injury.