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Updated: May 14, 2026
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A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites
Published on: August 8, 2014
Periodontal pathogen accelerates lipid peroxidation and atherosclerosis
R Jia1, T Kurita-Ochiai, S Oguchi
1Nihon University School of Dentistry at Matsudo, 2-870-1 Sakaecho-nishi, Matsudo, Chiba 271-8587, Japan.
Journal of Dental Research
|January 29, 2013
Summary
Aggregatibacter actinomycetemcomitans (Aa) infection, even with heat-killed cells or lipopolysaccharide (LPS) alone, accelerates atherosclerosis. This suggests Aa promotes immune signaling and LDL oxidation, contributing to atheroma development.
Area of Science:
- Microbiology
- Immunology
- Cardiovascular Science
Background:
- Periodontal disease is linked to cardiovascular disease.
- Aggregatibacter actinomycetemcomitans (Aa) accelerates atherosclerosis in Apoe(shl) mice.
Purpose of the Study:
- Investigate if live Aa cells or lipopolysaccharide (LPS) alone induce atherosclerosis.
- Determine the role of Aa components in atheroma development.
Main Methods:
- Mice were intravenously injected with live Aa, heat-killed (H.K.) Aa, or Aa LPS.
- Atherosclerotic plaque areas and immune gene expression were analyzed.
- LDL oxidation and reactive oxygen species (ROS) generation were assessed.
Main Results:
- Live Aa, H.K. Aa, and Aa LPS significantly increased atherosclerotic plaque areas.
- Atherosclerosis extent followed the order: live Aa > H.K. Aa > Aa LPS > sham.
- Aa challenge increased Toll and NOD-like receptor mRNA expression and promoted LDL oxidation via ROS.
Conclusions:
- Aa components, including LPS, are sufficient to induce atherosclerosis.
- Aa promotes innate immune signaling and LDL oxidation, facilitating atheroma development.
- These findings highlight Aa's role in cardiovascular disease pathogenesis.
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