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(Circulation. 2002;105:1976.)
© 2002 American Heart Association, Inc.

Basic Science Reports

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; 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.

Correspondence to Michael Rosenfeld, PhD, Department of Pathobiology and Interdisciplinary Graduate Program in Nutritional Science, Box 353410, University of Washington, Seattle, WA 98195. 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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