Role of the Macrophage Migration Inhibitory Factor in the Pathophysiology of Pre-Eclampsia.

Affiliation

Todros T(1), Paulesu L(2), Cardaropoli S(3), Rolfo A(1), Masturzo B(4), Ermini L(2), Romagnoli R(2), Ietta F(2).
Author information:
(1)Department of Surgical Sciences, University of Turin, Via Ventimiglia 3, 10126 Turin, Italy.
(2)Department of Life Sciences, University of Siena, 53100 Siena, Italy.
(3)Department of Public Health and Pediatrics, University of Turin, 10126 Turin, Italy.
(4)Città della Salute e della Scienza, 10126 Turin, Italy.

Abstract

Proinflammatory cytokines are produced in pregnancy in response to the invading pathogens and/or nonmicrobial causes such as damage-associated molecules and embryonic semi-allogenic antigens. While inflammation is essential for a successful pregnancy, an excessive inflammatory response is implicated in several pathologies including pre-eclampsia (PE). This review focuses on the proinflammatory cytokine macrophage migration inhibitory factor (MIF), a critical regulator of the innate immune response and a major player of processes allowing normal placental development. PE is a severe pregnancy-related syndrome characterized by exaggerated inflammatory response and generalized endothelial damage. In some cases, usually of early onset, it originates from a maldevelopment of the placenta, and is associated with intrauterine growth restriction (IUGR) (placental PE). In other cases, usually of late onset, pre-pregnancy maternal diseases represent risk factors for the development of the disease (maternal PE). Available data suggest that low MIF production in early pregnancy could contribute to the abnormal placentation. The resulting placental hypoxia in later pregnancy could produce high release of MIF in maternal serum typical of placental PE. More studies are needed to understand the role of MIF, if any, in maternal PE.