Aline (PBS), and diluted (final, concentration 5 107 CFU/ml) in PBS. Next, 200- l bacterial suspensions were mixed with 200 l of plasma or buffer, followed by incubation for 3 h in human plasma. After three further washing steps with PBS, the pellet was suspended in Tris-NaCl buffer (19.2 mM/1.062 M; pH 7.5) containing 20 g/ml of the chromogenic substrate S-2251 (H-D-Val-Leu-Lys-pNA?HCl; Sigma), f
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
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
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
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
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,
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
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