Researchers at Warwick Medical School have discovered that recurrent pregnancy loss can be due to a dysfunctional monthly fertility window. The study, led by Professor Jan Brosens and Professor Siobhan Quenby of the Division of Reproductive Health, sheds new light on the mechanisms that determine the timing and duration of the fertility window and how that may increase the chances of miscarriage.
The release of the cytokine IL-33 and the activation of its receptor (ST2) in cells in the uterus induces an inflammatory response that controls the stage that we are familiar with as the two to three days of peak fertility.
Work at the Clinical Sciences Research Laboratories at University Hospital, Coventry, showed clearly that in patients with a record of recurrent pregnancy loss, this inflammatory response was prolonged. When the fertility window remains open too long, embryos implant out-of-phase into an environment that cannot support the pregnancy, which leads to miscarriage.
Professor Quenby explained what this discovery means for those who suffer from persistent pregnancy loss, “The study fundamentally changes our understanding of the issue with far reaching clinical implications. The IL-33/ST2 pathway is already considered to be a major target for therapeutic interventions across Alzheimer's, cardiovascular disease, obesity, asthma and other autoimmune disorders. We believe that targeting the same pathway in the uterus may help to prevent miscarriage by regulating the fertility window.
“It’s an exciting discovery that we hope will mean new developments for a group of women for who there isn’t currently any help.”
Notes for editors:
“Disordered IL-33/ST2 Activation in Dicdualizing Stromal Cells Prolongs Uterine Receptivity in Women with Recurrent Pregnancy” will be published in PLOS ONE Journal.