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Am J Physiol Lung Cell Mol Physiol 287: L497-L502, 2004. First published May 14, 2004; doi:10.1152/ajplung.00010.2004
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TRANSLATIONAL PHYSIOLOGY

Leptin augments alveolar macrophage leukotriene synthesis by increasing phospholipase activity and enhancing group IVC iPLA2 (cPLA2{gamma}) protein expression

Peter Mancuso,1 Claudio Canetti,2 Andrew Gottschalk,1 Patricia K. Tithof,3 and Marc Peters-Golden2

Departments of 1Environmental Health Sciences and 2Internal Medicine, Division of Pulmonary and Critical Care Medicine, University of Michigan, Ann Arbor, Michigan 48109-2029; and 3Department of Pathobiology, College of Veterinary Medicine, University of Tennessee, Knoxville, Tennessee 37996-4543

Submitted 14 January 2004 ; accepted in final form 9 May 2004

Leptin is a hormone secreted by adipocytes in correlation with total body fat mass. In addition to regulating energy homeostasis, leptin modulates immune functions such as macrophage phagocytosis and cytokine synthesis. Previously, we reported defective leukotriene synthesis in macrophages from leptin-deficient mice that could be restored with exogenous leptin. In the present study, we utilized macrophages from normal rodents to explore the mechanism by which leptin could enhance cellular leukotriene synthesis. Leptin pretreatment of either rat alveolar or murine peritoneal macrophages for 16 h dose dependently increased the synthesis of leukotriene B4 and cysteinyl leukotrienes in response to calcium ionophore or the particulate zymosan. Leptin also enhanced calcium ionophore-stimulated release of free arachidonic acid. Calcium-dependent and -independent arachidonoyl-selective phospholipase activities in macrophage lysates were likewise increased following leptin treatment. Immunoblot analysis of leptin-treated cells revealed that group IVC iPLA2 (cPLA2{gamma}) protein expression increased ~80%. These data demonstrate for the first time that phospholipase A2 activity and cPLA2{gamma} protein levels in alveolar macrophages represent targets for upregulation by leptin and provide previously unrecognized mechanisms by which this hormone can promote inflammatory responses.

monocyte/macrophage; lung; lipid mediators; inflammation; cytosolic phospholipase A2


Address for reprint requests and other correspondence: P. Mancuso, Dept. of Environmental Health Sciences, Univ. of Michigan, 1420 Washington Hts., SPH II, Ann Arbor, MI 48109-2029 (E-mail: pmancuso{at}umich.edu)




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