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
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
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
E bradykinin. The nonapeptide has a very short half-life (a matter of seconds) and exhibits its functions via the B1 and B2 receptors (3). Generating other mediators such as nitric oxide, prostaglandins, and leukotrienes, bradykinin is involved in the regulation of blood pressure, the induction of fever and pain, vascular leakage, and the chemotaxis of immune cells (4). In addition, further proces
E bradykinin. The nonapeptide has a very short half-life (a matter of seconds) and exhibits its functions via the B1 and B2 receptors (3). Generating other mediators such as nitric oxide, prostaglandins, and leukotrienes, bradykinin is involved in the regulation of blood pressure, the induction of fever and pain, vascular leakage, and the chemotaxis of immune cells (4). In addition, further proces
Ons trigger an activation of the contact system more potently than strains isolated from noninvasive infections. The present study gives new insights into the mechanisms by which S. pyogenes triggers the human contact system and stresses the function of soluble and surface located plasmin exploited as a group A streptococcal virulence factor through the action of streptokinase. treptococcus pyogen
Ons trigger an activation of the contact system more potently than strains isolated from noninvasive infections. The present study gives new insights into the mechanisms by which S. pyogenes triggers the human contact system and stresses the function of soluble and surface located plasmin exploited as a group A streptococcal virulence factor through the action of streptokinase. treptococcus pyogen
Has been described for a number of bacterial species (for a review, see reference 7). In the case of S. pyogenes, the secreted streptococcal cysteine protease SpeB was found to cleave HK directly (8). In addition, the surface-bound M protein, one of the classical virulence determinants of GAS, has been demonstrated to bind HK, followed by bradykinin generation (9, 10). Binding and assembly of cont