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Updated: Aug 2, 2026
09:41
Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
Published on: October 17, 2017
Estrogen and progesterone modulate monocyte cell cycle progression and apoptosis
T Thongngarm1, J K Jenkins, K Ndebele
1Division of Rheumatology, G.V. (Sonny) Montgomery VAMC, University of Mississippi Medical Center, Jackson, MS 39216, USA.
Summary
Pregnancy hormones like estrogen and progesterone can suppress immune cell function by affecting cell cycling and programmed cell death (apoptosis). These sex steroids may explain pregnancy-induced immune changes.
Area of Science:
- Immunology
- Endocrinology
- Cell Biology
Background:
- Pregnancy involves significant immune system alterations, often manifesting as suppressed cell-mediated immunity.
- The precise mechanisms behind this immunosuppression are not fully understood but may involve elevated sex steroids such as 17-beta-estradiol and progesterone.
Purpose of the Study:
- To investigate the effects of 17-beta-estradiol and progesterone on myelomonocytic cell lines.
- To examine the impact of these sex steroids on cell cycling, apoptosis, and bcl-2 expression.
Main Methods:
- Utilized five myelomonocytic cell lines at different differentiation stages.
- Assessed the influence of 17-beta-estradiol and progesterone on cell cycling, apoptosis, and bcl-2 expression.
- Examined effects both before and after lipopolysaccharide (LPS) activation.
Main Results:
- Lipopolysaccharide (LPS) inhibited cell cycle progression in THP-1 and U-937 cells.
- Estrogen caused cell cycle arrest in most myelomonocytic cells, while progesterone induced apoptosis in HL-60 cells.
- Both estrogen and progesterone reduced bcl-2 levels in KG-1alpha, HL-60, and THP-1 cells, with LPS partially counteracting some effects.
Conclusions:
- Sex steroid-induced alterations in cell cycle and apoptosis present a potential mechanism for pregnancy-associated immune suppression.
- Further research is needed to elucidate pregnancy-induced immune changes and potential sex-based differences in monocyte function.
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