In:
Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 105, No. 16 ( 2002-04-23), p. 1976-1982
Abstract:
Background — It has not yet been determined whether lipid-loaded macrophages (foam cells), a major cellular component of atherosclerotic lesions, have the capacity to support growth of Chlamydia pneumoniae and be activated to secrete proinflammatory cytokines in response to C pneumoniae infection. Methods and Results — Lipid loading of RAW 264.7 cells and mouse peritoneal macrophages with either oxidized or acetylated LDL significantly inhibits the growth of C pneumoniae. Modified forms of LDL are not directly toxic to C pneumoniae and do not inhibit either the initial binding or internalization of C pneumoniae by macrophages. Lipid loading does not reduce infection of macrophages with Chlamydia trachomatis . Treatment of lipid-loaded macrophages with live, heat-killed, or UV-inactivated C pneumoniae stimulates secretion of cytokines. C pneumoniae also induces expression of the mRNA for tumor necrosis factor-α in foam cells despite inhibition of nuclear factor-κB binding to DNA by prior treatment with oxidized LDL. Conclusions — Foam cell formation is not conducive to growth of C pneumoniae but does not inhibit the C pneumoniae –induced secretion of proinflammatory cytokines.
Type of Medium:
Online Resource
ISSN:
0009-7322
,
1524-4539
DOI:
10.1161/01.CIR.0000015062.41860.5B
Language:
English
Publisher:
Ovid Technologies (Wolters Kluwer Health)
Publication Date:
2002
detail.hit.zdb_id:
1466401-X
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