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The Production of Interleukin-11 and Decidualization Are Compromised in Endometrial Stromal Cells Derived from Patients with Infertility

Nuffield Department of Obstetrics and Gynecology, University of Oxford, John Radcliffe Hospital (N.K., P.K., J.H.H., J.E.M., D.H.B., H.J.M.), Oxford OX3 9DU, United Kingdom; Department of Obstetrics and Gynecology, Hanyang University College of Medicine (J.H.H.), Seoul, Korea; and Cancer Research UK Growth Factor Group, University of Birmingham School of Biosciences (J.K.H.), Birmingham B15 2TT, United Kingdom

Address all correspondence and requests for reprints to: Dr. Helen J. Mardon, Nuffield Department of Obstetrics and Gynecology, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, United Kingdom. E-mail: helen.mardon{at}obs-gyn.ox.ac.uk.

IL-11 signaling is critical for decidualization of the endometrial stroma in early pregnancy in the mouse. In this study, we investigate the function of IL-11 signaling in cAMP-induced decidualization of human endometrial stromal cells. We show that treatment of endometrial stromal cells with 8-bromo-cAMP (8-Br-cAMP) results in an increase in the levels of secreted IL-11, whereas levels of cell surface IL-11 receptor are similar with or without 8-Br-cAMP treatment. The production of IL-11 correlates with the production of molecular markers of decidualization, prolactin and IGF-binding protein-1. The expression of these markers is inhibited when IL-11 signaling is specifically blocked in decidualizing endometrial stromal cells by the IL-11 antagonist W147A. We demonstrate that 8-Br-cAMP-induced endometrial stromal cells derived from patients with primary infertility produce lower levels of prolactin, IGF-binding protein-1, and IL-11 than cells derived from fertile women. Our results suggest that IL-11 expression is critically important during decidualization in the human endometrium, and that aberrant regulation of endometrial IL-11 production may be associated with some types of infertility.

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