Abstract
Endometriosis is a complex, inflammatory disease that affects 6-10% of reproductive-aged women. Almost half of the women with endometriosis experience infertility. Despite the excessive prevalence, the pathogenesis of endometriosis and its associated infertility is unknown and a cure is not available. While many theories have been suggested to link endometriosis and infertility, a consensus among investigators has not emerged. In this extensive review of the literature as well as research from our laboratory, we provide potential insights into the role of immune dysfunction in endometriosis associated infertility. We discuss the implication of the peritoneal inflammatory microenvironment on various factors that contribute to infertility such as hormonal imbalance, oxidative stress and how these could further lead to poor oocyte, sperm and embryo quality, impaired receptivity of the endometrium and implantation failure.
Highlights
Endometriosis is a chronic, inflammatory, estrogendependent disease that is characterized by the growth of endometrial tissue outside of the uterine cavity
Pro-inflammatory cytokines, chemokines and receptors including CXCL1, CX3CL1, CXCL9, CXCL10, IL-32, CXCR2, IL-7R and adhesion molecules including ICAM3 and SELL had a higher expression in the eutopic endometrium of infertile, endometriosis patients compared to fertile controls [34]
Heublein et al demonstrated that TNF-α down regulates the expression of G-protein coupled estrogen receptor (GPER) in endometrial stromal cells isolated from women with endometriosis and the presence of GPER has been suggested to act as a selector that is important for folliculogenesis and follicle maturation [61]
Summary
Endometriosis is a chronic, inflammatory, estrogendependent disease that is characterized by the growth of endometrial tissue outside of the uterine cavity. We discuss the implication of the peritoneal inflammatory microenvironment on various factors that contribute to infertility such as hormonal imbalance, oxidative stress and how these could further lead to poor oocyte, sperm and embryo quality, impaired receptivity of the endometrium and implantation failure. Pro-inflammatory cytokines, chemokines and receptors including CXCL1, CX3CL1, CXCL9, CXCL10, IL-32, CXCR2, IL-7R and adhesion molecules including ICAM3 and SELL had a higher expression in the eutopic endometrium of infertile, endometriosis patients compared to fertile controls [34].
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