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The Role of Chlamydia pneumoniae and Inflammatory Proteins in Atherosclerosis

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Aristo Vojdani, Ph.D., M.T
Immunosciences Lab., Inc., 8730 Wilshire Boulevard, Suite 305
Beverly Hills, CA 90211
(310) 657-1077

SUMMARY

Chlamydia pneumoniae is a newly discovered third species of Chlamydia shown to cause pneumonia, bronchitis, pharyngitis, sinusitis, serious morbidity and mortality in nursing homes (Troy et al., JAMA 277:1214, 1997). C. pneumoniae has also been associated with coronary heart disease and myocardial infarction in serological studies. More specifically, C. pneumoniae antigen and elementary bodies have been found in atheromas from coronary arteries, carotid arteries, and aorta. In a preliminary study, researchers at St. George Hospital in London treated 46 survivors of heart attack with azithromycin. After six months, blood tests revealed that patients who were treated with this antibiotic produced a markedly decreased amount of inflammatory proteins (Northfield and Mendall, Lancet 343:1634, 1994).

However, it was not until recently that Muhlestein et al. (Circulation 1998; 97:633) demonstrated the casual role for C. pneumoniae in acceleration and development of atherosclerosis and its prevention by treatment with azithromycin. In this study, rabbits were fed a modestly cholesterol-enhanced diet and then infected intranasally with C. pneumoniae. In only a short time, the rabbits showed acceleration in the intimal thickening of the arteries. Uninfected control rabbits and infected rabbits receiving antibiotics did not show such pathological reaction of the arteries. These findings further strengthen the etiologic link between C. pneumoniae and atherosclerosis and should stimulate human studies and clinical antibiotic trials.

For the above reasons, we have developed methods for direct detection of C. pneumoniae genome as well as IgM antibody targeted at the major membrane protein peptide sequence of this organism in the blood of patients with confirmed atherosclerosis were examined for the presence of C. pneumoniae genome as well as for antibodies against the major outer membrane protein and were compared to one hundred healthy matched controls without evidence of arterial plaques. 35% of patients versus 6% of controls were positive for IgM antibodies against C. pneumoniae major membrane protein. Moreover, the bacterial genome was positive in more than half of the patients with elevated IgM, but not in those who had elevated IgG and IgA antibody titers or in control subjects (data in preparation for publication).

Detection of Chlamydia pneumoniae genome along with IgM specific antibodies in a significant percentage of patients with atherosclerosis, but not in control subjects, indicate involvement of this organism in atherosclerosis.

Moreover, in addition to C. pneumoniae, recent studies indicate a correlation between autoantibodies against oxidized LDL that mirrors the occurrence of oxidation process, and the progression of carotid atherosclerosis. Therefore, measurements of IgM antibodies against C. pneumoniae, and direct detection of its genome in the blood, along with antioxidized LDL, endothelial cell antibodies, fibrinogen, Protein-C, and C-Reactive protein are the best indicators of the involvement of infectious agents, inflammation, and immune reaction in atherosclerosis.

 

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