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Syncytiotrophoblast Intercellular Adhesion Molecule‐1 Expression in Massive Chronic Intervillositis
Author(s) -
Labarrere Carlos A,
Ortiz Miguel A,
Sosa Marcelo J,
Campana Gonzalo L,
Wernicke Mario,
Baldridge Lee Ann,
Terry Colin,
DiCarlo Hector
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a227-c
Subject(s) - syncytiotrophoblast , chorionic villi , placenta , pathology , cytotrophoblast , immunohistochemistry , intervillous space , medicine , h&e stain , fetus , andrology , biology , pregnancy , genetics
We determined syncytiotrophoblast (ST) intercellular adhesion molecule‐1 (ICAM‐1) expression in massive chronic intervillositis (MCI), and compared with ICAM‐1 expression in villitis, and normal chorionic villi from placentas (34–41 weeks gestation) with or without villitis. A cross‐sectional study was conducted to determine ST ICAM‐1 expression in MCI (n=7), villitis (n=7) and in normal villi from placentas with or without (n=7) villitis. Maternal cells within chorionic villi in MCI were identified in placentas mismatched for the maternal/fetal human leukocyte antigen (HLA)‐DRw52. Villitis was diagnosed with antibody to CD3 and hematoxylin and eosin staining of serial sections, and ICAM‐1 reactivity in ST was confirmed with antibodies to ICAM‐1 and cytokeratin. MCI had higher ST ICAM‐1 expression than villitis (79.8 vs. 27.1 percent villi, p=0.009) and normal chorionic villi from placentas with (79.8 vs. 11.5 percent villi, p=0.009) or without (79.8 vs. 0.3 percent villi, p=0.009) villitis. Maternal cells were identified within the villous fetal compartment in the capillaries and stroma of placentas (n=5) mismatched (mothers positive, fetuses negative) for HLA‐DRw52. Placentas with MCI have significantly more ST ICAM‐1 expression than placentas with or without villitis. The finding that MCI and villitis lesions have prominent ST ICAM‐1 expression compared with normal villi from placentas with or without villitis suggest that MCI and villitis could have a similar pathophysiologic mechanism.