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
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
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,
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