Platelet-neutrophil interactions. Possible relevance in the pathogenesis of thrombosis and inflammation.
Evidence indicates that complex interactions occur between platelets and neutrophils. Mediators released by activated platelets may act as stimuli for neutrophils, but platelets may also limit neutrophil activation. Similarly, neutrophils, depending upon their degree of activation, may bring about both enhancement and inhibition of platelet responses. The elaborate cross-talk among platelets and neutrophils, cells involved in hemostatic and phlogistic reactions, may condition the development and the course of thrombotic and inflammatory diseases; therefore, modulation of platelet-neutrophil interactions may represent a therapeutic target in these conditions. In this review, the mediators involved in the platelet-dependent modulation of neutrophil activation and, conversely, the mechanisms whereby neutrophils modify platelet responses are described. Moreover, the possible relevance of these interactions in the pathogenesis of thrombosis and inflammation is discussed.
Bazzoni
G
G
Laboratorio di Biologia Vascolare, Istituto di Ricerche Farmacologiche Mario Negri, Milano, Italy.
Dejana
E
E
Del Maschio
A
A
D016718:Arachidonic Acid / Q000378:metabolism; D001792:Blood Platelets / Q000502:physiology*; D002450:Cell Communication; D002630:Chemotactic Factors / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D004730:Endothelium, Vascular / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000209:etiology* / Q000503:physiopathology; D009504:Neutrophils / Q000502:physiology*; D010100:Oxygen / Q000378:metabolism; D015539:Platelet Activation; D013927:Thrombosis / Q000209:etiology* / Q000503:physiopathology
D002630:Chemotactic Factors; D016207:Cytokines; D016718:Arachidonic Acid; D010100:Oxygen