Abstract 9403: A Periodontal Pathogen Accelerates the Progression of Abdominal Aortic Aneurysm via Toll-Like Receptor-2 Signaling
Introduction-- Abdominal aortic aneurysm (AAA) is a life-threatening disorder. Periodontopathic bacteria have been detected at a high rate in specimens obtained from the aortic walls of AAA patients. It has been shown in an animal study that periodontopathic bacteria induce the progression of AAA. Toll-like receptors (TLRs) are key receptors of virulence factors of many periodontal bacteria.
Hypothesis-- We assessed the hypothesis that TLR plays a fundamental role in periodontopathic bacteria-accelerated AAA progression.
Methods-- AAA was experimentally produced with wild-type mice, TLR-2 deficient mice and TLR-4 deficient mice by the peri-aortic application of 0.25 mol/L CaCl2, while NaCl was used as a control. The mice were injected once per week with live Porphyromonas gingivalis (P.g.), which is a major periodontal pathogen, or vehicle. Four weeks after the application of either CaCl2 or NaCl, the aortic samples were obtained. Histological and immunohistochemical analyses were performed to assess the mechanism of AAA progression.
Results-- P.g.-injected and CaCl2-treated wild-type mice (n = 10) showed a larger increase (1.71 +/− 0.05-fold vs. before operation) than uninfected CaCl2-treated wild-type mice (n = 10) (1.51 +/− 0.09-fold vs. before). Although the aortic diameter of P.g.-injected and CaCl2-treated TLR-4 deficient mice (n = 11) showed a significant increase (1.28 +/− 0.20-fold vs. before, p < 0.05), the aortic diameter of P.g.-injected and CaCl2-treated TLR-2 deficient mice (n = 10) did not increase after the operation (1.07 +/− 0.19-fold vs. before). TLR-2 deficient mice which were injected with P.g. and treated with CaCl2 showed less elastic degradation than wild-type or TLR-4 deficient mice with histological analysis. Immunohistochemical analysis showed that the level of matrix metalloproteinase-2 in the aortic wall of the TLR-2 deficient mice was dramatically lower (1.0 +/− 0.4) than in the wild-type mice (3.0 +/− 0.6, p < 0.05).
Conclusion-- In conclusion, infection with P.g. could accelerate the progression of experimental AAA with TLR-2 signaling.
- © 2011 by American Heart Association, Inc.