Distinct Immune Responses to Oral Infection Among Porphyromonas Gingivalis Strains

Objective:  Clinical studies associate oral infection with multiple systemic diseases such as cardiovascular disease and rheumatoid arthritis. The determination of how bacteria involved in periodontitis pathogenesis may affect cells of the systemic immune response will assist in defining how periodontitis may impact other diseases. The goal of this study was to evaluate the systemic immune response of mice following a chronic oral infection with different strains of Porphyromonas gingivalis (Pg). 

Method:  DBA-1J mice received six oral inoculations over a 2-week period with 10⁹ CFU of Pg strains A7A1-28, W83, and W50. Periodontitis establishment was evaluated by both Pg presence in the oral microflora (by Pg gingipain expression via PCR) and alveolar bone resorption (via microcomputed tomography). At 42 d post-gavage, splenocytes were evaluated for gene expression, cellular proteins, and in vitro cytokine expression for markers of the acquired immune response. Protein expression for markers of the innate immune response by dendritic cells was evaluated in vitro. Differences among groups were assessed by ANOVA, with Tukey multiple comparison post-hoc test. 

Results: Pg presence in the oral cavity was confirmed and alveolar bone loss was established with all strains in varying degrees. Mouse exposure to Pg was sufficient to alter the pattern of cytokine expression by reactivated splenocytes in vitro. Mice infected with Pg strains W50 and W83 expressed higher levels of IL-4, while mice infected with A7A1-strain expressed higher levels of IFN-gamma and IL-10. Expression of IL-12, IL-6 and TGF-beta by dendritic cells in vitro was similar among strains.

Conclusion:  Mice infected with Pg strains W50 and W83 showed a predominant systemic Th2/B cell driven response and greater alveolar bone destruction, while animals infected with Pg A7A1-28 demonstrated a predominant Th1/Treg systemic response and more limited alveolar bone loss.