Abstract

The manifestation of platelet 'satallitism' around neutrophils in whole blood is a long acknowledged phenomenon [1]. Circulating platelet-neutrophil complexes (PNC) occur in a diverse range of inflammatory disorders and infections that affect numerous organs of the body. Animal models have revealed that the formation of PNC is required for the recruitment of neutrophils to inflamed tissue, since platelets 'prime' neutrophils for efficient adhesion to vascular endothelium via the up-regulation of integrins and enhanced responsiveness to chemokines (Fig.1). Perhaps surprisingly, the surface contact between platelets and neutrophils additionally enhances other neutrophil functions, such as chemotaxis that is required for migration into tissues, trans-cellular production of eicosanoids, phagocytosis and trapping of pathogens, increased respiratory burst leading to the production of reactive oxygen species (ROS), and modulation of neutrophil apoptosis (Fig.1). Platelet P-selectin appears to have a particular role in enhancing the majority of these activities, and the influence of platelet P-selectin is not therefore confined to the initial rolling events in the process of neutrophil extravasation.

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