Neutrophil-platelet interactions in inflammation.

Abstract

Inflammation is a multicomponent system that involves a network of cellular crosstalk and control. Many different cell types, including neutrophils and platelets, participate as both sources and targets of biological mediators that are generated or released in acute and chronic inflammatory states. Owing to the complex nature of inflammation, the magnitude as well as the spatial and temporal characteristics of the responses are likely to vary with the type, concentration, and duration of the inflammatory stimulus. Despite the potential variations in responses to diverse stimuli, a feature common to and responsible for the major characteristics of inflammation (heat, pain, redness, swelling) is proteases. In the early stages of inflammation, the neutrophil is the predominant cell to infiltrate the tissue, and the extent of inflammatory injury has been shown to be directly dependent on the extent of neutrophil infiltration. Since both cathepsin G and elastase are neutral serine proteases present in large amounts in azurophilic granules and 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 specifically.