PMID- 24631282 OWN - NLM STAT- MEDLINE DCOM- 20141203 LR - 20140414 IS - 1532-3102 (Electronic) IS - 0143-4004 (Linking) VI - 35 IP - 5 DP - 2014 May TI - Intercellular adhesion molecule-1 expression in massive chronic intervillositis: implications for the invasion of maternal cells into fetal tissues. PG - 311-7 LID - S0143-4004(14)00080-0 [pii] LID - 10.1016/j.placenta.2014.02.006 [doi] AB - INTRODUCTION: Massive chronic intervillositis (MCI), also known as chronic intervillositis of unknown etiology, is a placental lesion associated with massive infiltration of mononuclear cells in the intervillous space, poor perinatal outcome, and high rate of recurrence. Our previous demonstration of increased syncytiotrophoblast (st) intercellular adhesion molecule-1 (ICAM-1) expression in villitis lesions and the finding of extensive monocyte/macrophagic cells in the maternal intervillous space in MCI, led us to further investigate stICAM-1 in MCI. MATERIALS AND METHODS: A cross-sectional study of placentas from the third trimester of pregnancy (34-41 weeks gestation) was conducted to determine stICAM-1 in MCI (n = 7). MCI stICAM-1 expression was compared to stICAM-1 in villitis (n = 7) and in normal villi from placentas with (n = 7) and without (n = 7) villitis. Maternal cells within villi in MCI were identified in placentas mismatched for maternal/fetal human leukocyte antigen (HLA)-DRw52. Villitis was diagnosed with hematoxylin and eosin staining and antibody to CD3 in serial sections, and ICAM-1 in syncytiotrophoblasts was confirmed with antibodies to ICAM-1 and cytokeratin. RESULTS: Placentas with MCI had higher stICAM-1 (79.8%) than placentas with villitis (27.1%), normal villi from placentas with villitis (11.5%), and normal villi from placentas without villitis (0.3%). Maternal cells were identified within villi of placentas (n = 5) mismatched (mothers positive, fetuses negative) for HLA-DRw52. CONCLUSIONS: Placentas with MCI have more stICAM-1 than placentas with or without villitis lacking MCI. The finding that MCI and villitis have prominent stICAM-1 and maternal cells in the villi suggests that MCI and villitis could have a similar pathophysiologic mechanism. CI - Copyright (c) 2014 Elsevier Ltd. All rights reserved. FAU - Labarrere, C A AU - Labarrere CA AD - CBL Partners for Life, Indianapolis, IN, United States; Indiana University School of Medicine, Indianapolis, IN, United States; Indiana University Health Methodist Research Institute, Indianapolis, IN, United States. Electronic address: clabarrere@sbcglobal.net. FAU - Bammerlin, E AU - Bammerlin E AD - Indiana University Health Methodist Research Institute, Indianapolis, IN, United States. FAU - Hardin, J W AU - Hardin JW AD - Epidemiology and Biostatistics, Columbia, SC, United States. FAU - Dicarlo, H L AU - Dicarlo HL AD - Indiana University Health Methodist Research Institute, Indianapolis, IN, United States; Westside Regional Medical Center, Fort Lauderdale, FL, United States. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20140228 PL - Netherlands TA - Placenta JT - Placenta JID - 8006349 RN - 126547-89-5 (Intercellular Adhesion Molecule-1) SB - IM MH - Adult MH - Chorionic Villi/*metabolism MH - Cross-Sectional Studies MH - Female MH - Fetus/*metabolism/pathology MH - Humans MH - Immunohistochemistry MH - Intercellular Adhesion Molecule-1/*metabolism MH - Placenta/*metabolism/pathology MH - Placenta Diseases/*metabolism/pathology MH - Pregnancy MH - Young Adult OTO - NOTNLM OT - Chorionic villi OT - ICAM-1 OT - Massive chronic intervillositis OT - Placenta OT - Syncytiotrophoblast OT - Villitis EDAT- 2014/03/19 06:00 MHDA- 2014/12/15 06:00 CRDT- 2014/03/18 06:00 PHST- 2013/12/23 00:00 [received] PHST- 2014/02/10 00:00 [revised] PHST- 2014/02/19 00:00 [accepted] PHST- 2014/03/18 06:00 [entrez] PHST- 2014/03/19 06:00 [pubmed] PHST- 2014/12/15 06:00 [medline] AID - S0143-4004(14)00080-0 [pii] AID - 10.1016/j.placenta.2014.02.006 [doi] PST - ppublish SO - Placenta. 2014 May;35(5):311-7. doi: 10.1016/j.placenta.2014.02.006. Epub 2014 Feb 28.