Effects of endometrial stromal cells and peritoneal fluid on fertility associated with endometriosis

Endometriosis is one cause of infertility. The disease causes severe non-bacterial inflammation and adhesion in the ovarian tubes and/or referred reproductive organs, but a number of types of unexplained infertility without severe organic disorders also exist. In the present study, we investigated the effects of endometrial stromal cells (SC) and peritoneal fluid (PF) in endometriosis on the fertilization and embryonic development rates using mouse ova and embryos. In addition, we prepared endometriosis artificially in rats and investigated the effects of peritoneal perfusate on the fertilization and embryonic development rates. We also investigated the in vitro fertilization rate in these rats. The mouse ova, sperm, and two-cell embryos were cultured on SC isolated surgically from patients with uterine myoma (M) or endometriosis (E), and 24 hours later, the fertilization and embryonic development rates were investigated. To this co-culture system, PF from M or E patients was added, at varying concentrations, and the fertilization and embryonic development rates were investigated. Then, rats with experimental endometriosis were prepared. After confirmation of the presence of lesions, peritoneal perfusate was added, at varying concentrations, to the co-culture system, and the fertilization and embryonic development rates were investigated. In addition, the in vitro fertilization rate was investigated in these rats. Both the fertilization rate and the embryonic development rate were significantly lower for the co-culture system in the E group. In the PF addition system, PF decreased the fertilization and embryonic development rates at lower concentrations in the E group. In rats with artificial endometriosis, peritoneal perfusate from rats with lesions significantly decreased the fertilization and embryonic development rates at lower concentrations. The in vitro fertilization rate was significantly lower in rats with lesions. The above results strongly suggested that inhibitions of fertilization and embryonic development induced by SC and PF, and altered quality of the ovum itself, might be responsible for infertility in endometriosis.