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Clinical and Developmental Immunology
Volume 2012, Article ID 639342, 9 pages
Research Article

Macrophage Migration Inhibitory Factor in Fetoplacental Tissues from Preeclamptic Pregnancies with or without Fetal Growth Restriction

1Department of Obstetrics and Gynecology, University of Turin, Sant’Anna Hospital, Via Ventimiglia 3, 10126 Torino, Italy
2Department of Physiology, University of Siena, Via Aldo Moro 4 53100 Siena, Italy
3Department of Molecular Pathology and Innovative Therapies, Marche Polytechnic University, Via Tronto 10/a 60020 Ancona, Italy

Received 24 May 2011; Revised 2 August 2011; Accepted 3 August 2011

Academic Editor: Gilbert Faure

Copyright © 2012 Simona Cardaropoli et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The proinflammatory cytokine MIF (macrophage migration inhibitory factor) is involved in physiological and pathological processes in pregnancy. MIF maternal serum levels are increased in preeclampsia (PE). We hypothesize that pregnancy tissues are the source of MIF overexpression in PE. MIF protein was studied in maternal sera, placental tissues, fetal membranes, and umbilical cord of 8 control and 20 PE pregnancies: 10 with normal fetal growth (PE-AGA) and 10 with fetal growth restriction (PE-FGR). MIF levels were significantly higher in PE-AGA membranes than in controls and PE-FGR. In PE-FGR, MIF cord concentrations were higher than in PE-AGA while MIF placental levels were lower than in controls. MIF maternal serum levels were higher in PE, compared to controls, and the difference was mainly due to PE-FGR samples. These data support MIF involvement in PE pathogenesis and suggest that different pregnancy tissues contribute to MIF production in PE with and without fetoplacental compromise.