P. gingivalis has recently been associated with chronic inflammatory diseases such as atherosclerosis. Monocytes interact with endothelial cells at sites of vascular injury during both inflammatory responses and the development of atherosclerotic lesions and such close proximity leads to the modulation of the biological functions of these cells. We previously established that P. gingivalis temporally modulates the chemokine response in HUVEC cells through both fimbriae and gingipain-mediated mechanisms. Objective: We examined the IL-8 production in cocultures of monocytes with human aortic endothelial cells (HAEC) in response to P. gingivalis infection. Methods: Co cultures of HAEC and monocytes were challenged with P. gingivalis and supernatant fluids were collected and analyzed for IL-8 by ELISA. Results: We found that monocyte / HAEC cocultures infected with P. gingivalis381 at a multiplicity of infection (MOI) of 100 resulted in a 30-fold increase in IL-8 release when compared with HAEC alone, or a 4-fold increase when compared with monocytes alone. At a MOI of 500, the IL-8 responses in P. gingivalis381 infected monocyte / HAEC cocultures or monocytes alone was inhibited. Infection of the monocyte / HAEC cocultures with the P. gingivalis fimA mutant, DPG3 (MOI of 100), resulted in IL-8 levels which were only 0.25-fold of that induced with the wild type strain. Infection of the monocyte / HAEC cocultures or monocytes alone with P. gingivalis mutants deficient in the lysine- or arginine- specific cysteine proteinases (gingipains) resulted in increased IL-8 levels, when compared to the wild strain 33277. Conclusions: These results demonstrate that P. gingivalis invasion mediated via fimbriae induces higher IL-8 responses in monocyte / HAEC cocultures as compared to monocytes alone. Our results suggest a major role for P. gingivalis gingipains in the degradation of IL-8 in P. gingivalis infected monocyte / HAEC co-cultures.

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