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CME Credit Offered
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Poster Session 1

(229) Decidual Cell-Mediated Paracrine Inhibition of IL1b Signaling in Extravillous Trophoblasts Contributes to Pregnancy Maintenance

Thursday, January 30, 2025
10:30 AM – 12:30 PM  
Objective: Decidual cells (DCs) and extravillous trophoblasts (EVTs) interact at the maternal-fetal interface to establish an anti-inflammatory state and maintain pregnancy. Dysregulation of these interactions causes inflammation and initiates labor. Interleukin 1 receptor 1 (IL1R1) binds IL1b and IL1R antagonist (IL1RN) similarly to cause inflammation or anti-inflammation, respectively. We previously found higher IL1R1 and lower IL1RN levels in DCs from in-labor vs. non-in-labor term samples, suggesting a shift in these levels that activates inflammation, initiating labor. We hypothesize a similar shift of IL1R1 and IL1RN expression in EVTs in labor; though prior to, DCs prevent said shift via paracrine mediators to maintain pregnancy.

Study Design: Paraffin sections from gestational age-matched term non-in-labor (n=7) vs. in-labor (n=6) placentas were immunostained for IL1R1 and IL1RN and analyzed by HSCORE. DC cultures (n=3) from 1st trimester (FTDC) and term (TDC) were primed for 7d with 10-8M estradiol + 10-7M medroxyprogesterone acetate and condition media supernatants (CMS) collected and used to treat human trophoblast cultures (n=3) of term placentas. IL1R1 and IL1RN mRNA levels were analyzed by qPCR. Statistical analysis used a t-test with p< 0.05 considered significant.

Results: Analysis revealed that EVTs from in-labor vs. non-in-labor decidua basalis had: 1) higher IL1R1 levels (Mean±SEM 184.1±10.1 vs. 120.1±15.6, p=0.007); 2) lower IL1RN levels (121.3±13.1 vs. 186.5±10.1; p=0.002); and 3) ~two-fold higher IL1R1/IL1RN ratio (0.73±0.1 vs. 1.58±0.2; p=0.002). CMS from TDCs caused 2.28-fold higher IL1R1 (p=0.001) and 6.6-fold IL1RN (p=0.03) levels in trophoblast cultures vs. untreated controls with similar results from FTDC CMS.

Conclusion: Our in-situ results indicate that EVTs undergo a shift to lower IL1RN and higher IL1R1 levels, activating IL1b signaling in the transition to labor. In contrast, in vitro results support the thesis that paracrine signals from DCs preferentially induce IL1RN (7-fold) over IL1R1 (2-fold) expression in EVTs to block IL1b signaling across gestation to maintain pregnancy.