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Updated: May 12, 2026
Isolation of Primary Human Decidual Cells from the Fetal Membranes of Term Placentae
Published on: April 30, 2018
Prolactin and proinflammatory cytokine expression at the fetomaternal interface in first trimester miscarriage
Emanuele Garzia1, Roberta Clauser, Luca Persani
1Unit of Obstetrics and Gynecology, Department of Health Sciences, San Paolo Hospital Medical School, University of Milano, Milan, Italy. emgarzi@tin.it
Objective:
To investigate the expression of prolactin (PRL), PRL-receptor (PRL-R), and the TH1 cytokines interleukin-2 (IL-2), tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ) at the maternofetal interface.
Design:
Case-control study.
Setting:
University hospital unit of gynecology and obstetrics and research laboratories.
Patient(S):
Women undergoing suction curettage for spontaneous miscarriage (study group) and voluntary termination of pregnancy (control group) in the first trimester.
Intervention(S):
Samples of decidua and villi collected and histologically examined at the time of suction curettage.
Main Outcome Measure(S):
Evaluation of all villous samples for karyotype with only euploid cases included; detection of transcripts of PRL, PRL-R, TNF-α, IFN-γ, and IL-2 by qualitative reverse-transcriptase-polymerase chain reaction (RT-PCR); investigation of pattern and site of expression by immunohistochemistry.
Result(S):
In both groups, PRL-R and IFN-γ were broadly expressed. The expression of PRL was impaired or absent in the villi of the study group compared with controls. Expression of TNF-α was reduced, although not statistically significantly, in both decidual and villous samples of the study group. Immunohistochemical analysis showed the lack of IL-2 expression in decidual specimens of the control group versus the full expression shown in the study group.
Conclusion(S):
Our results highlight the correspondence between PRL expression and vital pregnancy and the involvement of the TH1 cytokines with different specific roles at the implantation site. Prolactin and IL-2 may reciprocally influence expression.
