Innate immune recognition of invasive bacteria accelerates atherosclerosis in apolipoprotein E-deficient mice

Article

关键词: TOLL-LIKE RECEPTOR-4;    PORPHYROMONAS-GINGIVALIS;    PERIODONTAL-DISEASE;    EXPRESSION;    INFECTION;    LESIONS;    MURINE;    PATHOGENESIS;    PROGRESSION;    PROTEIN;   

DOI  :  10.1161/01.CIR.0000129769.17895.F0

来源: SCIE

【 摘 要 】

Background - Infectious diseases have emerged as potential risk factors for cardiovascular disease (CVD). Epidemiological studies support a connection between periodontal disease, a chronic inflammatory disease of the supporting tissues of the teeth, and CVD. Methods and Results - To directly test the connection between periodontal disease and atherosclerosis, apoE(-/-) mice were orally challenged with the periodontal disease pathogen Porphyromonas gingivalis or an invasion-impaired P gingivalis fimbriae-deficient mutant (FimA-). Both wild-type P gingivalis and the FimA- mutant were detected in blood and aortic arch tissue of apoE(-/-) mice by PCR after challenge. ApoE(-/-) mice challenged with wild-type P gingivalis presented with increased atherosclerotic plaque and expressed the innate immune response markers Toll- like receptor (TLR)-2 and TLR-4 in aortic tissue. Despite detection of the FimA- mutant in the blood and in aortic arch tissue, apoE(-/-) mice challenged with the FimA(-) mutant did not present with periodontal disease, upregulation of TLRs, or accelerated atherosclerosis. Furthermore, we demonstrate that immunization to control P gingivalis - elicited periodontal disease concomitantly prevents P gingivalis - accelerated atherosclerosis. Conclusions - We conclude that invasive P gingivalis accelerates atherosclerosis.

【 授权许可】

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