Figure 1.

Schematic model of a window section through a microvessel, presenting different functional mechanisms induced by interaction of streptococci with plasminogen and plasmin. In the upper left site, binding of tPA to the pneumococcal PGK and binding of PLG to surface displayed moonlighting proteins is shown. Subsequent recruitment of PLG and a plasminogen activator leads to generation of plasmin activity on the bacterial surface. Similarly, PLG binding to streptococcal M-and M-like-proteins is followed by activation to plasmin via host-derived activators (upper right). Plasminogen binding also protects against phagocytic killing by granulocytes and macrophages and promotes adherence to endothelial cells (bottom right). Dissolution of fibrin thrombi by surface-bound plasmin-activity facilitating streptococcal transmigration is depicted on the lower left. Proteolytic degradation of extracellular matrix by recruited plasmin activity promotes bacterial-cell contact and pericellular transmigration as illustrated at the bottom center.