Estrogen and Progesterone Modulate Monocyte Cell Cycle Progression and Apoptosis
Article first published online: 17 MAR 2003
American Journal of Reproductive Immunology
Volume 49, Issue 3, pages 129–138, March 2003
How to Cite
Thongngarm, T., Jenkins, J. K., Ndebele, K. and McMurray, R. W. (2003), Estrogen and Progesterone Modulate Monocyte Cell Cycle Progression and Apoptosis. American Journal of Reproductive Immunology, 49: 129–138. doi: 10.1034/j.1600-0897.2003.00015.x
- Issue published online: 17 MAR 2003
- Article first published online: 17 MAR 2003
- Submitted March 05, 2002; revised May 05, 2002; accepted May 10, 2002
- cell cycle;
PROBLEM: Pregnancy is characterized by dramatic immunologic changes most commonly characterized as suppression of cell-mediated immunity. Mechanisms of this immunosuppression are obscure but may be caused by increases in pregnancy-associated sex steroids such as 17-β-estradiol or progesterone.
METHOD OF STUDY: Using five myelomonocytic cell lines in various stages of differentiation, the effects of 17-β-estradiol and progesterone on cell cycling, apoptosis, and bcl-2 expression in randomly cycling cells before and after lipopolysaccharide (LPS) activation were examined.
RESULTS: Lipopolysaccharide alone inhibited cell cycle progression in THP-1 monocyte-like cells and U-937 histiocyte-like cells. Estrogen alone produced cell cycle arrest in all myelomonocytic cells except HL-60 pro-myelocyte-like cells. Progesterone had effects predominantly on pro-myelocytic-like HL-60 cells, inducing apoptosis. Estrogen and progesterone both decreased levels of bcl-2 in KG-1α, HL-60, and THP-1 cells. LPS partially antagonized both estrogen-induced THP-1 apoptosis and its suppression of bcl-2 protein.
CONCLUSIONS: Sex steroid-induced effects on cell cycle transition and apoptosis are potential mechanisms by which pregnancy-induced cell-mediated immune suppression may occur. Further investigation should provide a better understanding of pregnancy-induced immune changes and, perhaps, sex-based differences in monocyte function and immunologic responses.