Expression of intercellular adhesion molecule-1 messenger ribonucleic acid and protein in human term placental cells and its modulation by pro-inflammatory cytokines (interleukin-1beta and tumor necrosis factor alpha)

• Published in: Biology of reproduction 1998-04, Vol.58 (4), p.1003-1008
• Main Authors: GAFFURI, B, VIGANO, P, NOZZA, A, GORNATI, G, DI BLASIO, A. M, VIGNALI, M
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; Cell Differentiation; Cells, Cultured; Embryology: invertebrates and vertebrates. Teratology; Female; Fetal membranes; Fundamental and applied biological sciences. Psychology; Gene Expression; General aspects. Development. Fetal membranes; Humans; Intercellular Adhesion Molecule-1 - genetics; Intercellular Adhesion Molecule-1 - metabolism; Interleukin-1 - pharmacology; Placenta - metabolism; Polymerase Chain Reaction; Pregnancy; RNA, Messenger - analysis; RNA, Messenger - metabolism; RNA-Directed DNA Polymerase; Trophoblasts - metabolism; Tumor Necrosis Factor-alpha - pharmacology
• ISSN: 0006-3363; 1529-7268
• DOI: 10.1095/biolreprod58.4.1003

Intercellular adhesion molecule-1 (ICAM-1) is a ligand for the integrins lymphocyte function-associated antigen-1 (LFA-1) and complement receptor-3 (Mac-1), making it an important participant in many immune and inflammatory processes. Previous studies suggested that lack or reduced expression of ICAM-1 on trophoblast might partially explain its resistance to lysis by cytotoxic effectors. However, whether or not the adhesion molecule is expressed on placental cells is still a matter of debate. In this study, we determined ICAM-1 expression at mRNA, surface, and soluble protein levels on human trophoblasts throughout their functional differentiation in culture from cytotrophoblasts into syncytiotrophoblasts. Placental cells were obtained from 6 term placentas derived from normal pregnancies. ICAM-1 mRNA was detected by reverse transcription-polymerase chain reaction using two oligonucleotide primers specific for the human ICAM-1 gene. A single major DNA band of the expected size (943 base pairs) was obtained in both cytotrophoblasts and syncytiotrophoblasts. Flow cytometric analysis demonstrated expression of surface ICAM-1 protein on 45.5+/-3.5% of cytotrophoblasts. No changes were observed during differentiation in culture. Levels of the soluble form of ICAM-1 (sICAM-1) released by placental cells were undetectable when assessed by a specific ELISA. Finally, we investigated the effect of pro-inflammatory cytokines on placental ICAM-1 expression. Treatment of cultured trophoblasts for 24 h with interleukin-1beta (1 ng/ml) or tumor necrosis factor alpha (1 ng/ml) increased surface expression of ICAM-1 without inducing sICAM-1 shedding. However, on placental cells, the two cytokines exerted stimulatory effects lower than those detected on endometrial cells used as positive control. These observations document that the ICAM-1 gene is expressed in both cytotrophoblasts and syncytiotrophoblasts, suggesting that the molecule may be of value for some immune-mediated processes. On the other hand, the low sensitivity of trophoblasts to cytokine-mediated induction of ICAM-1 expression might represent a functional mechanism contributing to maternal tolerance for fetal graft.