Foam Cell Formation Inhibits Growth of Chlamydia pneumoniae but Does Not Attenuate Chlamydia pneumoniae –Induced Secretion of Proinflammatory Cytokines

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.