Anticardiolipin in porphyromonas gingivalis antisera causes fetal loss in mice

Area of Science:

• Immunology
• Periodontology
• Reproductive Biology

Background:

• β2-glycoprotein I (β2GPI)-dependent anticardiolipin autoantibodies (aCl) are linked to thrombosis and fetal loss.
• Periodontitis patients often have aCl, and periodontal pathogens may possess antigens similar to β2GPI.

Purpose of the Study:

• To investigate if antibodies against Porphyromonas gingivalis (aPg) contain pathogenic aCl that induce fetal resorption.
• To identify potential antigens within P. gingivalis responsible for inducing these pathogenic antibodies.

Main Methods:

• Mice were immunized with β2GPI, P. gingivalis W83, or an arg-gingipain-defective mutant (HF18).
• IgG fractions from aPg were treated to remove aCl-like antibodies (abs-aPg).
• Mated female mice received IgG fractions intravenously, and fetal resorptions were assessed at day 15.

Main Results:

• Mice treated with aPg showed significantly higher fetal loss compared to controls (21.2% vs. 5.3%).
• Abs-aPg treatment resulted in less fetal loss than aPg (12% vs. 21.2%).
• No fetal resorptions occurred in the aPgHF18 group, indicating the arg-gingipain protease may be involved.

Conclusions:

• Antibodies against P. gingivalis possess activity consistent with pathogenic aCl.
• The arg-gingipain protease of P. gingivalis may harbor antigens that induce antibodies leading to increased fetal loss.
• This suggests a potential mechanism linking periodontal disease to adverse pregnancy outcomes.