title: Preeclampsia, a pregnancy-specific disease, is associated with fetal monocyte activation.
abstract: The maternal syndrome of preeclampsia is an exclusively pregnancy-related illness involving multiple organs and severe forms may be complicated by HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome. Recently, it has been proposed that both normal pregnancy and preeclampsia are associated with a systemic activation of the nonspecific maternal immune system and that, in particular, monocytes have a central role in the adjustment of maternal immune functions in pregnancy. Here we have investigated the role of the fetal nonadaptive immune system in normal term delivery, uncontrollable preterm labor, and preeclampsia. We demonstrate that spontaneous delivery at term as well as preterm occurrence of preeclampsia or HELLP syndrome are accompanied by an increased intracellular production of IL-6 in fetal monocytes, indicating strong activation of this cell type. In contrast, we show that elective cesarean delivery at term in the absence of labor or preterm delivery due to uncontrollable labor are not accompanied by an increased production of IL-6 in these cells. These results suggest that increased IL-6 synthesis in fetal monocytes may be a process occurring in association with normal spontaneous term delivery and that this process obviously occurs in early pregnancy in case of preeclampsia. Therefore, we propose that the activation of fetal monocytes as effectors of the innate immunity may be involved in mechanisms inducing spontaneous term delivery and that the occurrence of preeclampsia may be based on dysfunctions of probably both the maternal and the fetal innate immune system.
authors.affiliation: Department of Obstetrics and Gynecology, J.-W. Goethe-University of Frankfurt, Frankfurt/Main, Germany.
authors.forename: A
authors.initials: A
authors.lastname: Steinborn
authors.forename: C
authors.initials: C
authors.lastname: Sohn
authors.forename: C
authors.initials: C
authors.lastname: Sayehli
authors.forename: A
authors.initials: A
authors.lastname: Niederhut
authors.forename: E
authors.initials: E
authors.lastname: Schmitt
authors.forename: M
authors.initials: M
authors.lastname: Kaufmann
mesh_terms: D005260:Female; D005312:Fetal Blood / Q000378:metabolism; D005333:Fetus / Q000276:immunology*; D017359:HELLP Syndrome / Q000209:etiology; D015395:Histocompatibility Antigens Class I / Q000276:immunology; D000949:Histocompatibility Antigens Class II / Q000276:immunology; D006801:Humans; D015850:Interleukin-6 / Q000096:biosynthesis; D018950:Lipopolysaccharide Receptors / Q000032:analysis; D009000:Monocytes / Q000502:physiology*; D011225:Pre-Eclampsia / Q000276:immunology*; D011247:Pregnancy
chemical_list: D015395:Histocompatibility Antigens Class I; D000949:Histocompatibility Antigens Class II; D015850:Interleukin-6; D018950:Lipopolysaccharide Receptors