Author(s): Faint RW
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Abstract In the vicinity of an acute inflammatory response both cellular and non-cellular elements may interact to modify the overall response. Evidence suggests that leukocytes may play an active role in the modulation of platelet function and vice-versa. This interaction may be abnormal in certain pathological states. Neutrophils have been found to alter platelet behaviour by several mechanisms. These include transcellular metabolism of eicosanoids. Neutrophils utilize platelet-derived arachidonate to increase leukotriene synthesis. Other arachidonate metabolites result from platelet-neutrophil interaction and these differ quantitatively and qualitatively from those arising from either cell-type alone. Another mechanism is the release of a nitric oxide-like factor by neutrophils. Nitric oxide inhibits platelet adhesion and aggregation via guanylate cyclase stimulation. Neutrophils, under different conditions, are potent inducers of platelet calcium flux, aggregation and secretion. This activity is mediated by a neutrophil-derived protease, most likely to be cathepsin G. The interaction of platelets with neutrophils may help to explain some of the pathophysiological events associated with different clinical states.
This article was published in Blood Rev
and referenced in Biochemistry & Pharmacology: Open Access