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A more recent version of this article appeared on March 10, 2006
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M510579200v1
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Papers In Press, published online ahead of print December 27, 2005
J. Biol. Chem, 10.1074/jbc.M510579200
Submitted on September 27, 2005
Revised on December 23, 2005
Accepted on December 27, 2005

Cholesterol-induced apoptotic macrophages elicit an inflammatory response in phagocytes that is partially attenuated by the Mer receptor

Yankun Li, Marie-Christine Gerbod-Giannone, Heather Seitz, Dongying Cui, Edward Thorp, Alan R. Tall, Glenn K. Matsushima, and Ira Tabas

Dept. of Medicine, Columbia University, New York, NY 10032

Corresponding Author: iat1{at}columbia.edu

Macrophage apoptosis and the ability of phagocytes to clear these apoptotic cells are important processes in advanced atherosclerosis. Phagocytic clearance not only disposes of dead cells but usually elicits an anti-inflammatory response. To study this process in a model of advanced lesional macrophage death, macrophages rendered apoptotic by free cholesterol loading (FC-AMs) were incubated briefly with fresh macrophages ("phagocytes"). FC-AMs were promptly ingested by the phagocytes, which was dependent upon actin polymerization and the phagocyte Mer receptor. Surprisingly, this brief exposure to FC-AMs triggered a modest pro-inflammatory response in the phagocytes: TNF-alpha and IL-1beta were induced, while the levels of TGF-beta and IL-10 were not increased. This response required cell contact between the FC-AMs and phagocytes but not FC-AM ingestion. TNF-alpha and IL-1beta induction required one or more proteins on the FC-AM surface and was dependent on signaling through Erk1/2 mitogen-activated protein kinase and NF-kappa B in the phagocytes. TNF-alpha production was markedly greater when Mer-defective phagocytes were used, indicating that Mer attenuated the inflammatory response. Interestingly, a more typical anti-inflammatory response was elicited when phagocytes were exposed to macrophages rendered apoptotic by oxidized LDL or UV radiation. Thus, the pro-inflammatory milieu of advanced atherosclerotic lesions may be promoted, or at least not dampened, by contact between FC-induced apoptotic macrophages and neighboring phagocytes prior to apoptotic cell ingestion.


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