Adhesion between neutrophils and platelets: a modulator of thrombotic and inflammatory events?

Abstract

Recent studies have demonstrated that neutrophilic granulocytes and platelets have the capability to interact with each other. Either type of cell may release soluble factors, which either activate the other or increase its response to separate stimulating agents. Direct contact between the two types of cell generally increases the response, and it may be predicted that neutrophil-platelet adhesion will augment the potential for biochemical interaction in vivo. Adhesion may also promote immobilisation of neutrophils or platelets in thrombotic or inflamed tissue, while circulation aggregates could cause vascular blockage. Adhesion between neutrophils and platelets is dependent on P-selectin on activated platelets and sialyated carbohydrate moieties on the neutrophil, although other molecular mechanisms could stabilise the interaction. The adhesive interaction is strong enough to allow flowing neutrophils to adhere to immobilised platelets, and induce formation of aggregates in vivo. Thus, inhibition of neutrophil-platelet adhesion and modulation of their biochemical interactions could be a novel approach to treatment of thrombotic, ischaemic or inflammatory disorders.