Methods: In this study, atherogenesis was examined in ten-week old male apolipoprotein E-deficient (-/-) mice following weekly intraperitoneal immunization with P.gingivalis, C.pneumoniae or vehicle over 11 or 26 weeks. Mean cross sectional areas of atherosclerotic lesions from the proximal aorta and levels of serum antibodies to P.gingivalis, C.pneumoniae and GroEL, a bacterial heat shock protein (HSP), were measured. The nature of the inflammatory infiltrate as well as host HSP60 expression was determined.
Results: After 11 weekly injections, mice immunized with C.pneumoniae demonstrated increased atherogenesis compared with those immunized with P.gingivalis or vehicle. After 22 weekly immunizations however, atherosclerotic lesion areas were greater in mice immunized with P.gingivalis alone than in those mice immunized with P.gingivalis followed by C.pneumoniae, with either bacteria followed by vehicle or controls.
Conclusions: These results show that a high pathogen burden of P.gingivalis resulted in a continued immune response and increased atherogenesis which was of a similar magnitude to that of C.pneumoniae in this mouse model but which developed later. This study was supported by The Australian Dental Research Foundation: Project No 2003000266.