Streptococcal plasminogen activator, triggers the activation of the human contact system. Activation of contact system factors at the surface of the Streptococcus pyogenes serotype M49 is dependent on streptokinase and plasminogen. Our results also show that secreted streptokinase is an efficient contact system activator, independent from a contact surface. This results in the processing of high-m
Rome and necrotizing fasciitis are associated with high morbidity and mortality (1). Although GAS virulence factors have been studied intensively, the mechanisms by which local infections progress to severe systemic infections are not yet fully understood. The systemic activation of host immune responses has been reported to account for several symptoms seen in septic patients, i.e., hypotension,
System comprises four plasma proteins, circulating as zymogens in the bloodstream or being assembled on various cell types: the serine proteases factor XII (FXII), factor XI (FXI), and prekallikrein (PKK) and the nonenzymatic cofactor high-molecularweight kininogen (HK). The latter forms equimolar complexes with plasma kallikrein (PK) or FXI. The cascade is initiated upon contact to a negatively c
Secrete streptokinase in order to accelerate the conversion of human plasminogen to plasmin (12). Lacking enzymatic activity itself, streptokinase evolves its function by forming a stoichiometric 1:1 complex with plasminogen or a trimolecular complex with plasminogen and fibrinogen. The activator complexes can bind at the bacterial surface via host factor receptors and convert other plasminogen mo
System comprises four plasma proteins, circulating as zymogens in the bloodstream or being assembled on various cell types: the serine proteases factor XII (FXII), factor XI (FXI), and prekallikrein (PKK) and the nonenzymatic cofactor high-molecularweight kininogen (HK). The latter forms equimolar complexes with plasma kallikrein (PK) or FXI. The cascade is initiated upon contact to a negatively c