Document Detail


Chlamydia pneumoniae and atherosclerosis: links to the disease process.
MedLine Citation:
PMID:  10539855     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Chlamydia pneumoniae is an obligate intracellular prokaryotic human pathogen responsible for a significant portion of atypical pneumonia and associated with a variety of chronic sequelae, the most significant of which is atherosclerosis. The organism is endowed with several attributes that may contribute to the development of atherosclerotic lesions or promote tissue damage at the site of an existing lesion. Two key events that are directly involved in the atherogenic process include the development of foam cells from macrophages and the oxidation of lipoproteins at the site of lesion development. The former process allows for deposition of cholesterol-containing low-density lipoprotein (LDL) and the latter can contribute directly to tissue damage locally. We have hypothesized that C pneumoniae may interact with mononuclear phagocytes in ways that are consistent with the view that this organism contributes to atherosclerotic lesion development. We have demonstrated that the presence of C pneumoniae causes macrophage foam cell formation and lipid oxidation with murine and human cells cocultured in the presence of LDL. In addition, we have provided evidence that implicates 2 putative chlamydial virulence factors in the development of these pathologic processes. Chlamydial lipopolysaccharide has been shown to cause macrophages to develop into foam cells in the presence of LDL, and the 60-kDa chlamydial heat shock protein (cHsp60), a known pathogenesis-inducing protein, has been found to contribute to oxidation of LDL in the presence of macrophages. Work is currently underway to define mechanisms involved in these processes and to further refine the putative role of C pneumoniae in atherogenesis and atherosclerotic lesion development.
Authors:
G I Byrne; M V Kalayoglu
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  American heart journal     Volume:  138     ISSN:  0002-8703     ISO Abbreviation:  Am. Heart J.     Publication Date:  1999 Nov 
Date Detail:
Created Date:  1999-12-02     Completed Date:  1999-12-02     Revised Date:  2014-03-21    
Medline Journal Info:
Nlm Unique ID:  0370465     Medline TA:  Am Heart J     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  S488-90     Citation Subset:  AIM; IM    
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MeSH Terms
Descriptor/Qualifier:
Arteriosclerosis / microbiology*
Cells, Cultured
Chaperonin 60 / pharmacology
Chlamydia Infections / complications*,  metabolism
Chlamydophila pneumoniae / pathogenicity*
Cholesterol Esters / biosynthesis
Foam Cells / cytology,  metabolism,  microbiology
Humans
Lipopolysaccharides / pharmacology
Lipoproteins, LDL / biosynthesis,  metabolism,  pharmacology
Macrophages / cytology,  drug effects,  metabolism,  microbiology
Monocytes / cytology,  drug effects,  metabolism
Oxidation-Reduction
Thiobarbituric Acid Reactive Substances / metabolism
Grant Support
ID/Acronym/Agency:
R01 AI042790/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Chaperonin 60; 0/Cholesterol Esters; 0/Lipopolysaccharides; 0/Lipoproteins, LDL; 0/Thiobarbituric Acid Reactive Substances; 0/oxidized low density lipoprotein

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