MURINE MODELS OF CHLAMYDIA-PNEUMONIAE INFECTION AND ATHEROSCLEROSIS

Chlamydia pneumoniae have been demonstrated in atherosclerotic lesions but not in normal arteries. An animal model of both C, pneumoniae and atherosclerosis is needed to investigate the role of the organism in atherosclerosis. Apolipoprotein (apo) E-deficient transgenic mice, whi ch spontaneously develop atherosclerosis, and C57BL/6J mice, which onl y develop atherosclerosis on an atherogenic diet, were evaluated. Foll owing single and multiple intranasal inoculations of apoE-deficient tr ansgenic mice, C. pneumoniae were detected in lung, aorta, and spleen for 20 weeks after inoculation in 25%-100% of mice, In the aorta, C. p neumoniae were detected within the atherosclerotic lesion. In C57BL/6J mice on a nonatherogenic diet, C. pneumoniae were detected in the aor ta only 2 weeks after a single intranasal inoculation in 8% of mice, T he persistence of C. pneumoniae in atheromas suggests a tropism of C. pneumoniae to the lesion. These mouse models should be useful for stud ying the pathogenic role of C. pneumoniae in atherosclerosis.