Anti-P. gingivalis Response Correlates with Atherosclerosis
P.J. Ford1,*,
E. Gemmell1,
P. Timms2,
A. Chan1,
F.M. Preston1, and
G.J. Seymour1
1 Oral Biology and Pathology, School of Dentistry, University of Queensland, Brisbane 4072, Australia; and
2 Infectious Diseases Program, Science Research Centre, School of Life Sciences, Queensland University of Technology, Brisbane 4001, Australia
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Figure 1. Mice immunized with P. gingivalis (A) and C. pneumoniae (B) demonstrated marked atherosclerotic lesions in the proximal aorta, as observed with Oil red O staining, compared with control mice (C) after 26 wks of immunizations. Dark-staining areas in the wall of the aorta are lipid-filled atherosclerotic lesions. Cross-sections of the proximal aorta show atherosclerotic lesions dominated by Mac-3 staining cells (D). Endothelial cells and some lesional cells stain positively for HSP60 (E). Original magnification 40X. Scale shown represents 100 µm.
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Figure 2. Mean cross-sectional atherosclerotic lesion area of the proximal aorta of mice immunized with P. gingivalis (Pg), C. pneumoniae (Cp), or vehicle (v). Results are mean ± SEM of 6 mice per group. *P < 0.001; **P < 0.036; ***P < 0.043.
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Figure 3. Serum antibody levels of immunized mice. (A) Anti-P. gingivalis; (B) anti-C. pneumoniae; and (C) anti-GroEL serum IgG antibody levels of mice immunized with P. gingivalis (Pg), C. pneumoniae (Cp), or vehicle (v). Results are mean ± SEM of 6 mice per group.
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