Table 1.

Bacterial plasminogen receptors.

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]