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This version published online on May 19, 2005
Endocrinology, doi:10.1210/en.2005-0406
A more recent version of this article appeared on August 1, 2005
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Submitted on April 7, 2005
Accepted on May 11, 2005

Leptin and Adiponectin Stimulate the Release of Pro-Inflammatory Cytokines and Prostaglandins from Human Placenta and Maternal Adipose Tissue via NF-{kappa}B, PPAR-{gamma} and ERK 1/2

Martha Lappas*, Michael Permezel, and Gregory E Rice

Department of Obstetrics and Gynaecology, University of Melbourne and Mercy Perinatal Research Centre, Mercy Hospital for Women, East Melbourne, Victoria, Australia 3002; Translational Proteomics, Baker Medical Research Institute, Baker Heart Research Institute, Melbourne, Victoria, Australia 3004

* To whom correspondence should be addressed. E-mail: mlappas{at}unimelb.edu.au.

Beyond their effects on central metabolic functions, leptin, resistin and adiponectin have profound effects on a number of other physiologic processes, including immune function and inflammation. Although leptin, resistin and adiponectin are produced in human placenta and adipose tissue, their immuno-regulatory actions in these tissues are not known. Therefore, the aim of this study was to determine the effect of leptin, resistin and adiponectin on the release of pro-inflammatory mediators in human placenta and subcutaneous adipose tissue. Samples were obtained from normal pregnancies at the time of Caesarean section. Tissue explants (n = 5) were incubated in the absence (basal control) or presence of a leptin (1, 10 and 100 ng/ml), resistin (1, 10, and 100 ng/ml) and adiponectin (0.1 and 0.5 µg/ml). After 6 h incubation, the medium was collected and the release of IL-1{beta}, IL-6, TNF-{alpha}, PGF2{alpha} and PGE2 was quantified by ELISA. There was no effect of resistin on pro-inflammatory cytokine or prostaglandin release; however leptin at 100 ng/ml and adiponectin at 0.1 and/or 0.5 µg/ml significantly increased the release of IL-1{beta}, IL-6, TNF-{alpha}, and PGE2 from human placenta and adipose tissue. Although both leptin and adiponectin significantly increased PGF2{alpha} release from human placenta, there was no effect of these hormones on PGF2{alpha} release from adipose tissue. Furthermore, this leptin- and adiponectin-induced pro-inflammatory response could be abrogated by treatment with the anti-inflammatory ERK1/2 MAPK inhibitor U0126, the PPAR-{gamma} ligand troglitazone and the NF-{kappa}B inhibitor BAY 11-7082. Collectively, these data indicate that leptin and adiponectin activate pro-inflammatory cytokine release and phospholipid metabolism in human placenta and adipose tissue, and anti-inflammatory agents can abrogate leptin- and adiponectin-induced inflammation.




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