Published Online
on April 1, 2002

A more recent version of this article appeared on April 23, 2002

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Submitted on October 26, 2001
Revised on January 7, 2002
Accepted on February 5, 2002

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

Erwin Blessing MD, Cho-chou Kuo MD, PhD, Tsun-Mei Lin MD, Lee Ann Campbell PhD, Florian Bea MD, Brian Chesebro , and Michael E. Rosenfeld PhD^*

From the Department of Pathobiology (E.B., C.-c.K., T.-M.L., L.A.C., F.B., B.C., M.E.R.) and the Interdisciplinary Graduate Program in Nutritional Sciences (F.B., M.E.R.), University of Washington, Seattle.

^* To whom correspondence should be addressed. E-mail: ssmjm{at}u.washington.edu.

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- in foam cells despite inhibition of nuclear factor-B 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.

Key words: atherosclerosis • lipids • leukocytes • inflammation • infection

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