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Originally published In Press as doi:10.1074/jbc.M204810200 on September 4, 2002

J. Biol. Chem., Vol. 277, Issue 46, 44147-44154, November 15, 2002
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Prostaglandin E2 Suppresses Chemokine Production in Human Macrophages through the EP4 Receptor*

Kiyoshi TakayamaDagger , Guillermo García-Cardeña§, Galina K. SukhovaDagger , Jason Comander§, Michael A. Gimbrone Jr.§, and Peter LibbyDagger §

From the Dagger  Leducq Center for Cardiovascular Research, Department of Medicine, and the § Center for Excellence in Vascular Biology, Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115

Pro-inflammatory pathways participate in the pathogenesis of atherosclerosis. However, the role of endogenous anti-inflammatory pathways in atheroma has received much less attention. Therefore, using cDNA microarrays, we screened for genes regulated by prostaglandin E2 (PGE2), a potential endogenous anti-inflammatory mediator, in lipopolysaccharide (LPS)-treated human macrophages (MPhi ). PGE2 (50 nM) attenuated LPS-induced mRNA and protein expression of chemokines including monocyte chemoattractant protein-1, interleukin-8, macrophage inflammatory protein-1alpha and -1beta , and interferon-inducible protein-10. PGE2 also inhibited the tumor necrosis factor-alpha -, interferon-gamma -, and interleukin-1beta -mediated expression of these chemokines. In contrast to the case of MPhi , PGE2 did not suppress chemokine expression in human endothelial and smooth muscle cells (SMC) treated with LPS and pro-inflammatory cytokines. To assess the potential paracrine effect of endogenous PGE2 on macrophage-derived chemokine production, we co-cultured MPhi with SMC in the presence of LPS. In these co-cultures, cyclooxygenase-2-dependent PGE2 production exceeded that in the mono-cultures, and MIP-1beta declined significantly compared with MPhi cultured without SMC. We further documented prominent expression of the PGE2 receptor EP4 in MPhi in both culture and human atheroma. Moreover, a selective EP4 antagonist completely reversed PGE2-mediated suppression of chemokine production. Thus, endogenous PGE2 may modulate inflammation during atherogenesis and other inflammatory diseases by suppressing macrophage-derived chemokine production via the EP4 receptor.

* This work was supported by the Leducq Foundation and by National Institutes of Health NHLBI Grant HL-34636 (to P. L.). This work was presented in part at the Scientific Sessions of the American Heart Association, Anaheim, CA, November 11-14, 2001, and published in abstract form (Circulation (2001) 17, II-318).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed: Cardiovascular Division, Dept. of Medicine, Brigham and Women's Hospital, Harvard Medical School, 221 Longwood Ave., Eugene Braunwald Research Center, Rm. 307, Boston, MA 02115. Tel.: 617-732-6628; Fax: 617-732-6961; E-mail: plibby@rics.bwh.harvard.edu.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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