NEUTROPHIL-PLATELET INTERACTIONS IN INFLAMMATION

Inflammation is a multicomponent system that involves a network of cel lular crosstalk and control. Many different cell types, including neut rophils and platelets, participate as both sources and targets of biol ogical mediators that are generated or released in acute and chronic i nflammatory states. Owing to the complex nature of inflammation the ma gnitude as well as the spatial and temporal characteristics of the res ponses are likely to vary with the type, concentration, and duration o f the inflammatory stimulus. Despite the potential variations in respo nses to diverse stimuli, a feature common to and responsible for the m ajor characteristics of inflammation (heat, pain, redness, swelling) i s proteases. In the early stages of inflammation, the neutrophil is th e predominant cell to infiltrate the tissue, and the extent of inflamm atory injury has been shown to be directly dependent on the extent of neutrophil infiltration. Since both cathepsin G and elastase are neutr al serine proteases present in large amounts in azurophilic granules a nd are known to affect platelet function, it is thus likely that these neutrophil enzymes are important contributing factors to inflammatory reactions in general and to neutrophil-platelet interactions specific ally.