Porphyromonas gingivalis and the Participatory Role of Interleukin-1beta in the Progression of Atherosclerosis

Abstract

Periodontal disease promotes atherosclerosis via a poorly defined mechanism. Our laboratory has previously shown that caspase-1, responsible for activating IL-1beta, is important in this process. We hypothesized that Porphyromonas gingivalis infection requires activated IL-1beta to promote atherosclerosis. Six-week old IL-1beta-/- apoE-/- mice of both genders received 15 oral inoculations of P.gingivalis. Detection of anti-P.gingivalis antibodies in serum of inoculated mice confirmed successful infection. Unexpectedly, atherosclerosis at age 17 weeks showed no effect of infection on IL-1beta+/+ mice. Moreover, contrary to our hypothesis, inoculated IL-1beta-/- females showed increased rather than decreased atherosclerosis compared to inoculated IL-1beta+/+ and non-inoculated IL-1beta-/-. Thus, either IL-1beta does not playa role in atherosclerosis development following P.gingivalis infection or there is a compensatory mechanism. IL-1beta deficiency may stimulate another pathway to promote P.gingivalis-induced atherosclerosis. Elucidation of the pathway by which P.gingivalis infection contributes to atherosclerosis development could reveal novel targets for therapy to impede disease progression.