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Hindawi Publishing Corporation PPAR Research Volume 2007, Article ID 52546, 8 pages doi:10.1155/2007/52546 Research Article Stimulatory Effects of Peroxisome Proliferator-Activated Receptor-γ on Fcγ Receptor-Mediated Phagocytosis by Alveolar Macrophages David M. Aronoff,1 Carlos H. Serezani,2 Jennifer K. Carstens,1 Teresa Marshall,2 Srinivasa R. Gangireddy,2 Marc Peters-Golden,2 and Raju C. Reddy2 1 Division of Infectious Diseases, Department of Internal Medicine, University of Michigan Health System, Ann Arbor 48109, MI, USA 2 Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Health System, Ann Arbor 48109, MI, USA Correspondence should be addressed to Raju C. Reddy, rajuc@ Received 16 March 2007; Accepted 31 July 2007 Recommended by Jesse Roman Alveolar macrophages abundantly express PPAR-γ, with both natural and synthetic agonists maintaining the cell in a quiescent state hyporesponsive to antigen stimulation. Conversely, agonists upregulate expression and function of the cell-surface receptor CD36, which mediates phagocytosis of lipids, apoptotic neutrophils, and other unopsonized materials. These effects led us to in- vestigate the actions of PPAR-γ agonists on the Fcγ receptor, which mediates phagocytosis of particles opsonized by binding of immunoglobulin G antibodies. We found that troglitazone, rosiglitazone, and 15-deoxy-Δ12,14-prostaglandin J2 increase the ability of alveolar, but not peritoneal, macrophages to carry out phagocytosis mediated by the Fcγ receptor. Receptor expression was not altered but activation of the downstream signaling proteins Syk, ERK-1, and ERK-2 was observed. Although it was previously known that PPAR-γ ligands stimulate phagocytosis of unopsonized materials, this is th