approved: ismnt.karin45

ISMNT NEWS: Disease Prevention by Exploring Molecular Mechanisms Linked to Nutrition

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ISMNT News #11 relates to recent intriguing findings that atherosclerosis might actually arise from infection with Chlamydia pneumoniae. If this explanation is indeed true, the impact of high cholesterol levels needs to be reevaluated. Obviously one might argue that the infection comes first and if there is no hypercholesterinemia, atherosclerosis would not become established. However, one might also argue that in the absence of an infection, hypercholesterinemia might not be a real problem. At the moment, these questions cannot be resolved. The Chlamydia story, however, shows that progress in a field totally unrelated to classical nutrition research could have a marked impact on nutritional guidelines.

The key reference is by:

Knoebel E; Vijayagopal P; Figueroa JE 2nd; Martin DH

IN VITRO INFECTION OF SMOOTH MUSCLE CELLS BY CHLAMYDIA PNEUMONIAE

from

Department of Medicine, Louisiana State University Medical Center, New Orleans 70112

in

Infect Immun, 1997 Feb, 65:2, 503-6

...Recent observations have shown that both Chlamydia pneumoniae antigens and DNA may be found within atherosclerotic lesions. In this study, we evaluated the ability of C. pneumoniae to infect cells that make up atherosclerotic lesions, including endothelial cells, smooth muscle cells, and cholesterol-loaded smooth muscle cells. The organism readily infected rabbit, bovine, and human aortic smooth muscle cells. Cholesterol-loaded smooth muscle cells were even more susceptible to C. pneumoniae infection. Chlamydia trachomatis inefficiently infected smooth muscle cells, demonstrating that this is not a characteristic of all members of the genus Chlamydia. C. pneumoniae infected bovine endothelial cells poorly.

This study demonstrates that C. pneumoniae readily infects one of the important types of cells found within atherosclerotic lesions, i.e., smooth muscle cells with and without cholesterol loading.