Clinical laboratoryOct 17, 2017

Porphyromonas gingivalis infection speeds up artery plaque buildup through oxidative stress and inflammation in mice lacking ApoE

Circadian Biology Weekly Brief ↗PubMed ↗DOI ↗

Updated Mar 31, 2026

Abstract

Chronic intravenous infection with P. gingivalis accelerated atherosclerosis development in ApoE-/- mice, confirmed by plaque formation in the aorta.

An abnormal lipid profile was observed, characterized by increased very low-density lipoprotein (vLDL) and oxidized low-density lipoprotein (oxLDL), alongside decreased high-density lipoprotein (HDL).
Higher levels of oxidative stress were indicated by increased reactive oxygen species (ROS) in serum and elevated mRNA levels of oxidized low-density lipoprotein receptor-1 (LOX-1) and fatty acid synthase (FAS) in several organs.
Enhanced inflammatory responses were noted, including increased C-reactive protein (CRP) expression and secretion, as well as elevated mRNA levels of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS).
Protein levels of inflammatory mediators, such as nuclear factor kappa B (NF-κB) and iNOS, were increased in key organs following P. gingivalis infection.

Simplified

BACKGROUND: The periodontal pathogen Porphyromonas gingivalis (P. gingivalis) has been proven to accelerate the development of atherosclerosis in apolipoprotein E (ApoE)-deficient mice. In this study, we used an ApoE knockout (ApoE-/-) mouse model with chronic intravenous infection with P. gingivalis to investigate the possible mechanisms of P. gingivalis-induced atherosclerosis.

METHODS: Eight-week-old ApoE-/- mice were randomly assigned to two groups: (a) ApoE-/- + PBS (n = 8); (b) ApoE-/- + P. gingivalis (n = 8). Both of the groups received intravenous injections 3 times per week. After 4 weeks, oxidative stress mediators in serum, heart, aorta, and liver tissues were analyzed by using histology, ELISA, realtime PCR, and Western blot.

RESULTS: Development of atherosclerosis as plaque formation in the aorta has been confirmed upon P. gingivalis infection. An abnormal lipid profile was found in the serum (increased amounts of very low-density lipoprotein [vLDL] and oxidized low-density lipoprotein [oxLDL], and decreased amount of HDL) and in some organs including heart, aorta or liver (increased mRNA levels of oxidized low-density lipoprotein receptor-1 [LOX-1] or fatty acid synthase [FAS]). Meanwhile, aggravated oxidative stress (higher level of reactive oxygen species [ROS] in the serum, and increased mRNA levels of nicotinamide adenine dinucleotide phosphate oxidase [NOX]-2 and/or NOX-4 in the three organs) was observed, as well as enhanced inflammatory responses (increased expression and secretion of C-reactive protein [CRP] in the liver and serum, and increased mRNA levels of cyclooxygenase-2 [NOX-2] and/or inducible nitric oxide synthase [iNOS] in the three organs). Besides, inflammatory mediators including nuclear factor of kappa B (NF-κB) and iNOS showed increased protein levels in the three organs after P. gingivalis infection.

CONCLUSIONS: These results suggest that chronic intravenous infection with P. gingivalis in ApoE-/- mice could accelerate the development of atherosclerosis, possibly associated with mediating oxidative stress as well as inflammatory responses and disturbing the lipid profile.

Porphyromonas gingivalis infection speeds up artery plaque buildup through oxidative stress and inflammation in mice lacking ApoE

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