title: Decidual macrophages are significantly increased in spontaneous miscarriages and over-express FasL: a potential role for macrophages in trophoblast apoptosis.
abstract: Decidual macrophages (DM) are the second most abundant population in the fetal-maternal interface. Their role has been so far identified as being local immuno-modulators favoring the maternal tolerance to the fetus. Herein we investigated tissue samples from 11 cases of spontaneous miscarriages and from 9 cases of elective terminations of pregnancy. Using immunohistochemistry and dual immunofluorescence we have demonstrated that in spontaneous miscarriages the DM are significantly increased. Additionally, we noted a significant up-regulation of macrophage FasL expression. Our results further support a dual role for DM during pregnancy and miscarriages. We hypothesize that the baseline DM population in normal pregnancy is in line with an M2 phenotype supporting the ongoing gestation. In contrast, during spontaneous miscarriages, the increased FasL-expressing population could be a part of an M1 phenotype participating in Fas/FasL-related apoptosis. Our results highlight a new aspect of macrophage biology in pregnancy physiology and pathophysiology. Further studies with larger samples are needed to verify the current results and evaluate their clinical impact.
authors.affiliation: Department of Obstetrics and Gynecology, Innenstadt Campus, Ludwig-Maximilians University of Munich, Munich D-80377, Germany.
authors.forename: Sabine
authors.initials: S
authors.lastname: Guenther
authors.affiliation: Department of Obstetrics and Gynecology, Innenstadt Campus, Ludwig-Maximilians University of Munich, Munich D-80377, Germany.
authors.forename: Thomas
authors.initials: T
authors.lastname: Vrekoussis
authors.affiliation: Department of Obstetrics and Gynecology, Innenstadt Campus, Ludwig-Maximilians University of Munich, Munich D-80377, Germany.
authors.forename: Sabine
authors.initials: S
authors.lastname: Heublein
authors.affiliation: Department of Legal Medicine, Ludwig-Maximilians University of Munich, Munich D-80377, Germany.
authors.forename: Birgit
authors.initials: B
authors.lastname: Bayer
authors.affiliation: Department of Internal Medicine, Pharmacological ward, Ludwig-Maximilians University of Munich, Munich D-80377, Germany.
authors.forename: David
authors.initials: D
authors.lastname: Anz
authors.affiliation: Department of Obstetrics and Gynecology, Innenstadt Campus, Ludwig-Maximilians University of Munich, Munich D-80377, Germany.
authors.forename: Julia
authors.initials: J
authors.lastname: Knabl
authors.affiliation: Department of Obstetrics and Gynecology, Medical School, University of Ioannina, Ioannina 45110, Greece.
authors.forename: Iordanis
authors.initials: I
authors.lastname: Navrozoglou
authors.affiliation: Department of Obstetrics and Gynecology, Innenstadt Campus, Ludwig-Maximilians University of Munich, Munich D-80377, Germany.
authors.forename: Darius
authors.initials: D
authors.lastname: Dian
authors.affiliation: Department of Obstetrics and Gynecology, Innenstadt Campus, Ludwig-Maximilians University of Munich, Munich D-80377, Germany.|Department of Obstetrics and Gynecology, Grosshadern Campus, Ludwig-Maximilians University of Munich, Munich D-80377, Germany.
authors.forename: Klaus
authors.initials: K
authors.lastname: Friese
authors.affiliation: Department of Obstetrics and Gynecology, Medical School, University of Crete, Heraklion 71409, Greece.
authors.forename: Antonis
authors.initials: A
authors.lastname: Makrigiannakis
authors.affiliation: Department of Obstetrics and Gynecology, Innenstadt Campus, Ludwig-Maximilians University of Munich, Munich D-80377, Germany.
authors.forename: Udo
authors.identifier: 0000-0003-2623-3235
authors.initials: U
authors.lastname: Jeschke
mesh_terms: D000022:Abortion, Spontaneous / Q000378:metabolism* / Q000473:pathology; D000328:Adult; D017209:Apoptosis; D003656:Decidua / Q000378:metabolism* / Q000473:pathology; D053222:Fas Ligand Protein / Q000096:biosynthesis*; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D008264:Macrophages / Q000378:metabolism* / Q000473:pathology; D011247:Pregnancy; D014327:Trophoblasts / Q000378:metabolism* / Q000473:pathology
chemical_list: C505661:FASLG protein, human; D053222:Fas Ligand Protein