Mechanisms of blood clotting activation in inflammation: the role of mononuclear phagocytes.
The authors review the procoagulant role of mononuclear phagocytes in the activation of blood clotting. Although the intrinsic pathway via the contact system has been considered the most important mechanism leading to fibrin formation, at least in acute inflammation, recent studies strongly suggest a role for the cells of the monocyte-macrophage series, which accumulate in the inflamed areas. These cells, when triggered in vitro by various stimuli (endotoxin, antigens, immune complexes, complement proteolytic products C5a and C3b, allogeneic leucocytes, lymphokines and others), respond with the production of selected procoagulant activities, thereby initiating the coagulation pathways. The most commonly described procoagulant activity has been identified as tissue factor, although prothrombinases and factor X activators have been reported. In addition mononuclear phagocytes can also produce and/or assemble on their surface coagulation factors including f. II, VII/VIIa, IX, X/Xa and V. Available evidence indicates that monocytes/macrophages can respond to appropriate signals and acquire the capacity to activate blood coagulation in vivo also. These "activated" cells expressing procoagulant activity appear to be directly responsible for the local fibrin deposition observed at sites of endotoxin-induced inflammation, of tumours, of cell-mediated immune reactions and possibly of other inflammatory processes.
D001777:Blood Coagulation; D005770:Gastrointestinal Neoplasms / Q000503:physiopathology; D006084:Graft Rejection; D006801:Humans; D006968:Hypersensitivity, Delayed; D007249:Inflammation / Q000209:etiology / Q000503:physiopathology*; D008264:Macrophages / Q000502:physiology; D009000:Monocytes / Q000502:physiology; D010586:Phagocytes / Q000502:physiology*; D014115:Toxemia / Q000503:physiopathology; D014184:Transplantation, Homologous