JaLCDOI 10.18926/AMO/31958
FullText URL fulltext.pdf
Author Rota, Simin| Rota, Seyyal|
Abstract <p>In recent years, the results of some studies have revealed the possible potential role of several infectious agents in the inflammatory mechanism of atherosclerosis. The detection of specific antibodies against microorganisms such as and as well as Chlamydia pneumoniae and cytomegalovirus as well as antibodies directed to heat shock proteins in the sera of atherosclerotic patients and the presence of genomic material in atheromatous plaques all provide evidence supporting the presumptive role of infectious agents in atherosclerosis. There are some findings that can be accepted as clues for the possible involvement of Mycobacterium tuberculosis in atherosclerosis. These consist of the presence of high levels of mycobacterial heat shock protein 65 in atherosclerotic patients, and in animal studies, the detection of atherosclerotic changes in the vascular wall of animals vaccinated with recombinant heat shock protein 65, and Mycobacterium tuberculosis containing heat shock protein 65. The probable proatherogenic effect of the specific immune response to BCG-associated heat shock protein was also suggested. The mycobacterium cell wall contains a phospholipid, phosphatidylinositol, which was shown to have a procoagulant effect similar to that of a cytomegalovirus possessing phosphatidylserine, another phospholipid showing a procoagulant effect. These data suggest that Mycobacterium tuberculosis may also be involved in the pathogenesis of atherosclerosis.</p>
Keywords M. tuberculosis BCG phospholipid heat shock protein atherosclerosis
Amo Type Review
Published Date 2005-12
Publication Title Acta Medica Okayama
Volume volume59
Issue issue6
Publisher Okayama University Medical School
Start Page 247
End Page 251
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 16418767
Web of Sience KeyUT 000234176600002