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Modulation of IL10 and Its Receptor Subunits in Normal and Progesterone-Prolonged Gestation in the Mouse
Ingrid Liff1,2, Sharareh Adeli3, Ilona Telefus Goldfarb3
1Division of Maternal-Fetal Medicine and the Vincent Center for Reproductive Biology, Department of Obstetrics & Gynecology, Massachusetts General Hospital, Boston, MA, USA. iliff@tuftsmedicalcenter.org.
Reproductive Sciences (Thousand Oaks, Calif.)
|February 5, 2020
Summary
Progesterone (P4) maintains elevated interleukin 10 (IL10) and IL10 receptor alpha (IL10Rα) levels, prolonging gestation. This suggests P4 utilizes the IL10 pathway to modulate the immune system and delay parturition.
Area of Science:
- Reproductive immunology
- Endocrinology
- Molecular biology
Background:
- Parturition involves complex hormonal and immunological changes.
- Interleukin 10 (IL10) is an immunomodulatory cytokine implicated in pregnancy maintenance.
- Progesterone (P4) is crucial for sustaining pregnancy.
Purpose of the Study:
- To investigate the relationship between progesterone (P4) and interleukin 10 (IL10) signaling in parturition.
- To determine if P4 influences IL10 and its receptor subunits (IL10Rα, IL10Rβ) expression during gestation.
- To explore the role of P4 in regulating the timing of labor onset.
Main Methods:
- Comparing IL10, IL10Rα, and IL10Rβ levels in gestational tissues of control and P4-treated pregnant mice.
- Utilizing ELISA assays to quantify cytokine and receptor subunit levels.
- Administering RU486 to assess the P4 receptor's contribution to IL10 pathway modulation.
Main Results:
- P4 treatment prevented premature parturition and maintained elevated IL10 levels.
- P4 administration increased IL10Rα expression, reversing the typical decrease at term.
- RU486 treatment significantly decreased IL10Rβ levels, without affecting IL10 or IL10Rα.
Conclusions:
- Progesterone (P4) plays a role in prolonging gestation, at least partly through the IL10 signaling pathway.
- P4 appears to modulate the immune environment via IL10 to delay labor onset.
- These findings elucidate a novel immunomodulatory mechanism for P4 in pregnancy maintenance.
