General Information and Genome of Porphyromonas gingivalis
- Nonmotile, Gram-negative, rod-shaped, anaerobic bacterium
- Forms black colonies on blood agar
- Found in the oral cavity, upper gastrointestinal tract, respiratory tract, and colon
- Implicated in periodontal disease and bacterial vaginosis
- Linked to Alzheimer's disease and rheumatoid arthritis
- Described in 2003
- Contains 1,990 open reading frames
- Encoded by 2,343,479 bp
- Average G+C content of 48.3%
- Estimated 463 essential genes

Virulence Factors of Porphyromonas gingivalis
- Gingipain enzymes (Arg-gingipain and Lys-gingipain)
- Gingipains contribute to survival, virulence, and nutrient collection
- Gingipains degrade host peptides and proteins for nitrogen and carbon sources
- Gingipains facilitate adhesion, invasion, and colonization
- Gingipains degrade host immune response signals and cytokines

Capsular Polysaccharide (CPS) of Porphyromonas gingivalis
- Encapsulated strain is more virulent than nonencapsulated strain
- CPS downregulates proinflammatory cytokine production
- CPS elicits host immune responses and inflammation in periodontitis
- Vaccines made from P. gingivalis CPS impair oral bone loss
- CPS-challenged macrophages express cell migration chemokines

Fimbriae of Porphyromonas gingivalis
- Fimbriae are appendages involved in cellular attachment
- Fimbriae contribute to adhesion, invasion, and colonization
- Fimbriae bind to integrins and impair host cell homeostatic controls
- Long fimbriae mediate initial attachment and biofilm organization
- Short fimbriae are essential for cell-cell aggregation and microcolony formation

Evasion of Host Defenses and Immune Responses
- P. gingivalis evades host immune responses through gingipain proteases.
- P. gingivalis uses a capsular polysaccharide to evade host immune responses.
- P. gingivalis induces host cell proliferation to evade immune responses.
- P. gingivalis cleaves chemokines responsible for neutrophil recruitment, affecting immune response.
- P. gingivalis down-regulates IL-8 induction, causing delayed neutrophil recruitment.
- P. gingivalis modulates leukocyte recruitment by proteolysis of cytokines and chemokines.
- Arg-gingipain and lys-gingipains are responsible for proteolysis of cytokines and chemokines.
- P. gingivalis impairs signaling by cleaving IgG 1 and 3, evading opsonophagocytosis from PMNs.
- P. gingivalis subverts the complement pathway through C5αR and C3αR, modulating leukocyte killing capacity.
- P. gingivalis inhibits pro-inflammatory and antimicrobial responses in human monocytes and mouse macrophages.
- P. gingivalis inhibits apoptosis by modulating the JAK/Stat pathway.
- P. gingivalis compromises the integrity of the epithelial cell layer, allowing for invasion and colonization.
- P. gingivalis causes a microbial shift in the oral cavity, leading to uncontrolled growth of commensal bacteria.
- P. gingivalis colocalizes with CD4+ T cells in human biopsies, indicating a potential infection mechanism.
- P. gingivalis increases the virulence of other commensal bacteria in both in vivo and in vitro experiments.
- P. gingivalis plays an important role in the onset of chronic adult periodontitis.
- P. gingivalis disrupts host tissue homeostasis and adaptive immune response.
- Laser capture microdissection plus qRT-PCR detects P. gingivalis in human biopsies.
- The infection mechanism of T cells by P. gingivalis remains unknown.
- P. gingivalis alone cannot induce periodontitis.