P 14 Deficiency of regulatory profile in pregnant women with early-onset preeclampsia

Abstract

Introduction Preeclampsia (PE) is a pregnancy specific syndrome characterized by a systemic inflammatory response. An imbalance between Th17 and regulatory T cell detected in this pathology seems to be dependent on the deficiency of regulatory factors capable of modulating this inflammation. Vitamin D generates an immune tolerogenic status through its regulatory activities on the inflammatory response. Objectives The present study aimed to evaluate the plasma levels of vitamin D, cytokines and to analyze the profile of CD4+ T cells subsets as well as the expression of vitamin D receptor (VDR) in peripheral blood mononuclear cells from pregnant women with PE. Methods Twenty women with early-onset PE, 20 women with late-onset PE and 20 normotensive (NT) pregnant women were studied. Plasma concentrations of vitamin D was evaluated by chemiluminescence and the levels of IL-10, IL-17 and TNF-a were determined by ELISA. Gene expression of VDR, transcription factors RORc (Th17) and FoxP3 (Treg) were evaluated by qPCR. Results were analyzed by non-parametric tests at 5% significance level. Results Plasma concentration of vitamin D was significantly lower in early-onset PE group compared to late-onset PE and NT groups, while the levels of TNF-α and IL-17 were significantly higher in early-onset PE group. On the other hand, IL-10 levels were significantly lower in both PE groups than in NT group. Gene expression of VDR was significantly decreased in early-onset PE group compared to NT group, while higher expression of mRNA RORc and lower expression of mRNA FoxP3 were observed in preeclamptic women. Positive correlation between vitamin D vs VDR and VDR vs FoxP3 was observed in PE (r = 0.44, p  Conclusion In preeclamptic women there is a decrease in regulatory status, suggesting a deficient immunomodulatory role of vitamin D that result in higher inflammatory profile, more evident in the early-onset PE. This imbalance in maternal tolerance indicate that vitamin D may participate in the pathogenesis of the disease.