M Winkler1, B Kemp, S Hauptmann, W Rath. 1. Department of Obstetrics and Gynecology, Technical University (RWTH), Aachen, Germany.
Abstract
OBJECTIVE: To determine whether 17 beta-estradiol, progesterone, and prostaglandin (PG) E2, alone or in combination with cytokines, influence the adhesiveness of vascular endothelium and thus play a role in the first stage of leukocyte infiltration of the uterine cervix during parturition. METHODS: Cultured umbilical vein endothelial cells obtained from 11 women after vaginal delivery at term were incubated with 17 beta-estradiol, progesterone, PGE2, tumor necrosis factor alpha (TNF-alpha), and interleukin-8, (IL-8), alone and in combination. The expression of endothelial leukocyte adhesion molecule-1, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 was investigated by immunofluorescence and flow cytometry. The Kolmogorov-Smirnov test was used for statistical analysis. RESULTS: We found that 17 beta-estradiol augmented the TNF-alpha-induced expression of endothelial leukocyte adhesion molecule-1, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 by 107, 9, and 39%, respectively. Alone, 17 beta-estradiol induced the expression of only intercellular adhesion molecule-1 (24%), as did PGE2 (13%). Neither progesterone nor IL-8 induced expression of any of these adhesion molecules. CONCLUSIONS: Unlike progesterone, 17 beta-estradiol and PGE2 stimulate the expression of adhesion molecules in vitro and may, therefore, promote adhesion of granulocytes to capillary endothelium.
OBJECTIVE: To determine whether 17 beta-estradiol, progesterone, and prostaglandin (PG) E2, alone or in combination with cytokines, influence the adhesiveness of vascular endothelium and thus play a role in the first stage of leukocyte infiltration of the uterine cervix during parturition. METHODS: Cultured umbilical vein endothelial cells obtained from 11 women after vaginal delivery at term were incubated with 17 beta-estradiol, progesterone, PGE2, tumor necrosis factor alpha (TNF-alpha), and interleukin-8, (IL-8), alone and in combination. The expression of endothelial leukocyte adhesion molecule-1, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 was investigated by immunofluorescence and flow cytometry. The Kolmogorov-Smirnov test was used for statistical analysis. RESULTS: We found that 17 beta-estradiol augmented the TNF-alpha-induced expression of endothelial leukocyte adhesion molecule-1, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 by 107, 9, and 39%, respectively. Alone, 17 beta-estradiol induced the expression of only intercellular adhesion molecule-1 (24%), as did PGE2 (13%). Neither progesterone nor IL-8 induced expression of any of these adhesion molecules. CONCLUSIONS: Unlike progesterone, 17 beta-estradiol and PGE2 stimulate the expression of adhesion molecules in vitro and may, therefore, promote adhesion of granulocytes to capillary endothelium.
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