Objectives: Increasing evidence suggests that bacterial lipopolysaccharide (LPS) plays a critical role in infection-associated atherogenesis by triggering foam cell formation, a feature of early fatty streak lesions in arterial wall. The aim of the study was to examine, if LPS isolated from A. actinomycetemcomitans (A.a.) is able to induce macrophage-derived foam cell formation. Methods: Mouse macrophages (RAW 264.7) were cultivated in the absence and presence of low density lipoprotein (LDL) and increasing concentrations of LPS (50, 150, and 300 ng/ml) isolated from A.a. strains JP2, Y4 (serotype b), and IDH781 (serotype d). LPS isolated from E. coli served as a positive control. After 12, 24, 48, and 72 hours the cells were stained for lipids with Oil Red O, and the proportions of stained cells were counted under a microscope. Results: In preparations where both LDL and LPS were present, lipid accumulation was evident after 24 hours in an LPS concentration-dependent manner. Longer incubation time led to increasing cell rupture with E. coli and A.a. serotype b, but not with serotype d LPS preparations. Both LPS preparations isolated from A.a. serotype b were as effective inducers of lipid accumulation as E. coli LPS, while A.a. serotype d LPS had a milder effect on the cells. In a typical experiment at 24 hours with 300 ng/ml of LPS, the proportion of foam cells was 40%, 38%, 39%, and 17% for E. coli, A.a. Y4 (b), A.a. JP2 (b), and A.a. IDH781 (d) LPS, respectively. Conclusions: A. actinomycetemcomitans LPS induces formation of macrophage-derived foam cells, which may promote atherogenesis and could be a mechanism behind an increased risk of coronary heart diseases in patients with periodontitis. The risk may depend on the colonizing A. actinomycetemcomitans serotype.

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