Premium
Divergence of the systemic immune response following oral infection with distinct strains of P orphyromonas gingivalis
Author(s) -
Marchesan J.T.,
Morelli T.,
Lundy S.K.,
Jiao Y.,
Lim S.,
Inohara N.,
Nunez G.,
Fox D.A.,
Giannobile W.V.
Publication year - 2012
Publication title -
molecular oral microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.18
H-Index - 77
eISSN - 2041-1014
pISSN - 2041-1006
DOI - 10.1111/omi.12001
Subject(s) - immune system , porphyromonas gingivalis , periodontitis , immunology , cytokine , biology , dental alveolus , microbiology and biotechnology , bone resorption , medicine , endocrinology , dentistry
Summary Periodontitis is a polymicrobial oral infection characterized by the destruction of tooth‐supporting structures that can be linked to systemic diseases such as cardiovascular disease, diabetes or rheumatoid arthritis. P orphyromonas gingivalis , a bacterium implicated in the etiology of periodontitis, has shown variation in inducing T ‐cell responses among different strains. Therefore, in this study we investigated the strain‐specific immune response using a murine experimental model of periodontitis. Periodontitis was induced by P . gingivalis strains A 7 A 1‐28, W 83 and W 50, and later confirmed by the presence of P . gingivalis in the oral microflora and by alveolar bone resorption. Splenocytes were evaluated for gene expression, cellular proteins and cytokine expression. Dendritic cells were stimulated in vitro for T helper cell–cytokine profiling. Results showed that P . gingivalis had the ability to alter the systemic immune response after bacterial exposure. Strains W 50 and W 83 were shown to induce alveolar bone loss, whereas the A 7 A 1‐28 strain did not significantly promote bone resorption in mice. Splenocytes derived from mice infected with strains W 50 and W 83 induced expression of high levels of interleukin‐4 ( IL ‐4) but A 7 A 1‐28 stimulated increased IL ‐10. Stimulation of dendritic cells in vitro showed a similar pattern of cytokine expression of IL ‐12p40, IL ‐6 and transforming growth factor‐β among strains. A distinct systemic response in vivo was observed among different strains of P . gingivalis, with IL ‐10 associated with the least amount of alveolar bone loss. Evaluation of pathogen‐driven systemic immune responses associated with periodontal disease pathogenesis may assist in defining how periodontitis may impact other diseases.