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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
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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
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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
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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,
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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
1
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
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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
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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
1
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,
1
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