Induction of Macrophage Foam Cell Formation by Chlamydia pneumoniae

Foam cell formation is the hallmark of early atherosclerosis. It was found that the intracellular bacterium Chlamydia pneumoniae induces foam cell formation by human monocyte-derived macrophages. Exposure of macrophages to C. pneumoniae followed by low-density lipoprotein (LDL) caused a marked incre...

Full description

Saved in:
Bibliographic Details
Published in:The Journal of infectious diseases 1998-03, Vol.177 (3), p.725-729
Main Authors: Kalayoglu, Murat V., Byrne, Gerald I.
Format: Article
Language:English
Subjects:
Arteriosclerosis - etiology
Atherosclerosis
Bacteriology
Bacteriophages
Biological and medical sciences
Biological Transport
Cell Differentiation - drug effects
Cells, Cultured
Chlamydia Infections - etiology
Chlamydophila pneumoniae
Cholesterol - analysis
Cholesterol esters
Cholesterol Esters - analysis
Cholesterols
Foam cells
Foam Cells - drug effects
Foam Cells - metabolism
Foam Cells - microbiology
Fundamental and applied biological sciences. Psychology
Heparin
Heparin - pharmacology
Humans
LDL receptors
Lipids
Lipoproteins, LDL - metabolism
Macrophages
Macrophages - metabolism
Macrophages - microbiology
Major Articles
Microbiology
Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Foam cell formation is the hallmark of early atherosclerosis. It was found that the intracellular bacterium Chlamydia pneumoniae induces foam cell formation by human monocyte-derived macrophages. Exposure of macrophages to C. pneumoniae followed by low-density lipoprotein (LDL) caused a marked increase in the number of foam cells and accumulation of cholesteryl esters. Foam cell formation was not inhibited by the antioxidant butylated hydroxytoluene nor fucoidan, suggesting that lipid accumulation did not involve scavenger receptors. In contrast, addition of heparin, which blocks binding of LDL to the LDL receptor, inhibited C. pneumoniae-induced foam cell formation, suggesting that the pathogen induced lipid accumulation by dysregulating native LDL uptake or metabolism (or both). These data demonstrate that an infectious agent can induce macrophage foam cell formation and implicate C. pneumoniae as a causative factor in atherosclerosis.
ISSN:0022-1899
1537-6613
DOI:10.1086/514241