| Receptor | Primary bacteria | Possible physiological function | Reference |
| Enolase/SEN | Streptococcus | Plg binding and uPA/tPA-mediated activation Fibrinolysis, subsequent extracellular matrix degradation, and transmigration. Involved in tumorigenesis, cancer proliferation, invasion, specific humoral and cellular immune response, myogenesis as well as hypoxic stress response | [10] | GAPDH/SDH/Plr | Streptococcus | Plg binding and activation by uPA/tPA. Adhesion to uPAR, fibronectin | [11, 12] | M proteins, PAM | Streptococcus | Major virulence factor, promote fibrinolysis, antiphagocytosis, vascular leakage and tissue injury, proinflammatory properties, adhesion to host cell and tissues, transmigration and deep tissue invasion, immunoglobulin binding, acute rheumatic fever | [13, 14] | OspA, OspC | Borrelia | Plg activation by host uPA, increased MMP expression, degradation of soluble and insoluble ECM components, endothelial monolayer penetration including blood-brain barrier, effective dissemination in host | [15–17] | HP-NAP | Helicobacter pylori | Fibrin clot stabilization, inhibition of fibrinolysis, possibly antiphagocytic, tissue factor synthesis and PAI2 stimulation | [18] | PgbA/PgbB | Helicobacter pylori | Lysine-dependent Plg binding, tPA-mediated Plg activation | [19] | DnaK | Bifidobacterium animalis subsp. lactis | Plg binding; upregulated in response to bile salts | [20] | Flagella | Escherichia coli | Plg binding and activation by host PAs | [21] | Fimbriae | Escherichia coli Salmonella | Fibronectin binding, adhesion to ECM components/BM, facilitate penetration | [22] |
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