The inflammatory state of the rat placenta increases in late gestation and is further enhanced by glucocorticoids in the labyrinth zone

Introduction: Inflammation plays central roles in key aspects of successful reproduction: ovulation, implantation and parturition. In this study we characterised the inflammatory profile of the rat placenta in late gestation with and without maternal glucocorticoid (dexamethasone) treatment. Methods: Placentas (n = 6/group) were collected from untreated (Con) rats at days 16 and 22 (term = day 23) and from dexamethasone-treated (Dex) rats at day 22. mRNA and protein expression was determined for enzymes of prostaglandin synthesis and metabolism (Ptgs-1, Ptgs-2, 15-Pgdh), pro-inflammatory cytokines (Tnf-alpha, Il-1 beta, Il-6), and the macrophage marker Emr-1 in the junctional (JZ) and labyrinth (LZ) zones of the placenta. Results: Tnf-alpha, Il-1 beta and Il-6 mRNAs all increased (2- to 4-fold) in both placental zones between days 16 and 22 (P < 0.01). Ptgs-2 mRNA (30-fold; P < 0.01) and PTGS-2 protein (2.4-fold; P < 0.05) similarly increased in LZ. In contrast, 15-Pdgh expression increased in JZ but decreased in 12; these changes were accompanied by decreased levels of PGE(2) in the JZ and a trend towards increased LZ levels. Dex treatment inhibited fetal and placental growth, but had minimal effects on expression of Ptgs-1, Ptgs-2 or 15-Pdgh. Nevertheless, Dex treatment increased 12 PGE(2) levels (5-fold, P < 0.01) at the end of gestation. Dex treatment increased Tnf-alpha mRNA expression in 12 (40%; P < 0.05), but modestly suppressed cytokine protein expression in JZ. Conclusions: These data demonstrate that the inflammatory state of the LZ increases near term coincident with the known increase in local glucocorticoid levels. This suggests the classic anti-inflammatory actions of glucocorticoids do not occur in the placental LZ. (C) 2013 Elsevier Ltd. All rights reserved.