CirculationMay 5, 2004

Immune response to invading bacteria speeds up artery plaque buildup in mice lacking apolipoprotein E

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Updated Mar 31, 2026

Abstract

ApoE-/- mice challenged with wild-type Porphyromonas gingivalis showed increased atherosclerotic plaque.

Detection of both wild-type and fimbriae-deficient strains of P gingivalis was confirmed in blood and aortic tissue.
Increased expression of immune response markers TLR-2 and TLR-4 was observed in the aortic tissue of mice challenged with wild-type P gingivalis.
Mice challenged with the fimbriae-deficient mutant did not show signs of periodontal disease, immune response upregulation, or accelerated atherosclerosis.
Immunization against P gingivalis-induced periodontal disease may prevent the acceleration of atherosclerosis associated with this pathogen.

Simplified

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.

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Immune response to invading bacteria speeds up artery plaque buildup in mice lacking apolipoprotein E

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