Parturition: steroids, prostaglandin E2, and expression of adhesion molecules by endothelial cells

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.

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.

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.

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.