The Role of Chlamydia pneumoniae and
Inflammatory Proteins in Atherosclerosis
©
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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