The plasminogen activation system in inflammation
Mario Del Rosso1, Gabriella Fibbi, Marco Pucci
1Department of Experimental Pathology and Oncology, University of Florence, Viale G.B. Morgagni, 50, 50134, Florence, Italy. delrosso@unifi.it
Abstract:
Inflammation is an adaptive response to damage of vascularized tissues, which develops according to a stereotyped sequence governed by the local production of the so-called "chemical mediators of inflammation". Here we review the evidences indicating a role of the plasminogen activation system in the regulation of all the phases of the inflammation process. Plasminogen activation controls the formation of complement anaphylotoxins (responsible for vasodilatation, increase of venular permeability and leukocyte chemotaxis) and of bradykinin (which accounts for vasodilatation, increase of venular permeability and pain) by regulating the plasma contact system. The urokinase plasminogen activator and its cellular receptor, expressed on the surface of human leukocytes, provide a functional unit that, by regulating interaction of leukocytes with extracellular matrix, as well as its degradation, is critical for the migration of leukocytes and for their movement in the damaged tissues. By preventing excess fibrin accumulation in inflamed tissues, the plasminogen activation system also governs the proper evolution of the inflammatory exudates and prevents the possibility of a shift from acute to chronic inflammation.
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