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aICC, immunocytochemistry; PCR, polymerase chain reaction; EM, electron microscopy; DIF, direct immunofluorescence; SVG, saphenous vein graft; IMAG, internal mammary arterial graft.

aICC, immunocytochemistry; PCR, polymerase chain reaction; EM, electron microscopy; DIF, direct immunofluorescence; SVG, saphenous vein graft; IMAG, internal mammary arterial graft.

of the rabbits had evidence of new or intermediate atherosclerotic lesions of the aorta. These results were also reproduced by Saikku and associates in Finland, but in each study the lesions were relatively minor (31). In a study by my group (32), rabbits fed 0.25% cholesterol diets were administered three separate intranasal inoculations of C. pneumoniae vs saline. The infected rabbits were then randomized to receive azithromycin, an antibiotic that is effective against C. pneumoniae, or placebo. This study demonstrated a significant acceleration of the development of atherosclerosis in the aortas of the infected/untreated rabbits tested compared with the other two groups (Fig. 3).

A variety of other animal models have also been tested. Mouse models using the Apo-E-deficient mouse (33), the low-density lipoprotein receptor-deficient mouse (34), as well as the C57BL/6J mouse (35) models have been successfully infected with C. pneumoniae through intranasal routes followed by successful detection of the organism within the arterial walls and the resultant acceleration of the development of atherosclerosis within these vessels. Likewise, some animal studies have documented worsening of endothelial function after repeated infection with C. pneumoniae (36).

Nevertheless, not all animal studies have been resoundingly positive, and it appears that some degree of hyperlipidemia is nearly always required before true atherosclerotic lesions can be produced (37,38). Additionally, no animal model of atherosclerosis exactly

Infected/no ABX Infected/ABX Noninfected

Fig. 3. Graph of mean intimal thickness of aortic sections from animals in the infected/untreated group, control (uninfected/untreated) group, and infected/treated group. ABX, antibiotics.

Infected/no ABX Infected/ABX Noninfected

Fig. 3. Graph of mean intimal thickness of aortic sections from animals in the infected/untreated group, control (uninfected/untreated) group, and infected/treated group. ABX, antibiotics.

mimics that ofthe human disease. Therefore, although generally supportive ofthe hypothesis, these studies, by themselves, do not yet prove that intravascular infection with C. pneumoniae plays a causative role in human CVD.

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