Prolactin and proinflammatory cytokine expression at the fetomaternal interface in first trimester miscarriage
Impaired prolactin (PRL) expression in samples from miscarriages and the particular expression of the proinflammatory cytokines suggest the pivotal role of PRL in vital pregnancies, reciprocally affected by interleukin-2 expression.
Emanuele Garzia, M.D., Roberta Clauser, M.D., Luca Persani, M.D., Ph.D., Stefano Borgato, M.D., Gaetano Bulfamante, M.D., Laura Avagliano, M.D., Federica Quadrelli, M.D., Anna Maria Marconi, M.D.
Volume 100, Issue 1, Pages 108-115.e2, July 2013
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.
University hospital unit of gynecology and obstetrics and research laboratories.
Women undergoing suction curettage for spontaneous miscarriage (study group) and voluntary termination of pregnancy (control group) in the first trimester.
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.
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.
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.