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. Author manuscript; available in PMC: 2020 Jul 25.
Published in final edited form as: Periodontol 2000. 2020 Feb;82(1):42–64. doi: 10.1111/prd.12311

TABLE 2.

Major virulence determinants of Porphyromonas gingivalisa

Virulence determinants Function
FimA Adherence to biotic and abiotic surfaces; binding to salivary proteins, epithelial cells, fibrinogen, fibronectin, lactoferrin, erythrocytes, oral streptococci; binding of chemokine (C-X-C motif) receptor 4 to suppress toll-like receptor 2/1-mediated proinflammatory and antimicrobial responses; binding of complement receptor 3 to inhibit interleukin-12 production to promote intracellular survival of bacteria, without affecting tumor necrosis factor-alpha-mediated destructive inflammation
Mfa1 pili Adherence to oral streptococci; binding to dendritic cell-specific intercellular adhesion molecule-3 grabbing nonintegrin of dendritic cells to initiate the entry and the survival of the bacteria
Hemagglutinins HagA, B, and C Hemolysis for iron acquisition as a nutrient; adherence to epithelial cells; induction of platelet aggregation
Hemoglobulin binding protein Binding of hemoglobin for nutrient acquisition
Gingipains (RgpA, RgpB, Kgp) Degradation of host tissue and antibodies; activation of the complement system, or inactivation of the complement system by degradation of its components; generating C5a to initiate C5aR toll-like receptor-2 crosstalk to promote bacterial survival in neutrophils and macrophages; degradation of toll-like coreceptors to suppress immune response
Capsule Antiphagocytosis
Lipid A of lipopolysaccharide Weak agonist or antagonist of toll-like receptor-4 to induce or inhibit inflammatory response
Phosphoserine phosphatase SerB Suppress interleukin-8 production to induce host defense paralysis
a

References:145,178,189,191.