Gut dysbiosis and immunological profile in endometriosis

Abstract Ectopic growth of normal cells or debris originating from endometrium, the inner layer of female reproductive tube leads to endometriosis. The main symptoms are dyspareunia, dysmenorrhea, and sometimes chronic pelvic pain. Unfortunately, it has no cure or treatment, only symptoms relief medication or surgical removal. Endometriosis causes estrogen imbalance leading to intestinal bacterial estrobolome dysregulation and subsequent change in immune response. Our study aims to investigate the linkage between gut dysbiosis and immunological response in endometriotic mice. Balb/c mice were ovariectomized (OVX) 7 days before intraperitoneal transplantation of 2mm2 endometrial tissue from OVX donors to OVX- or intact ovary recipients. Colonic content was collected 2 weeks post transplantation for 16s rRNA pyrosequencing. Peritoneal exudate was collected and stained to determine the phenotype of infiltrating cells by flow cytometry. Results revealed a significant increase in the number of exudate cells, natural killer (NK) cells and myeloid derived suppressor cells (MDSCs) in endometriotic mice. Phylogenetic taxonomy showed an increase in the biomass of the bacteria in endometriotic OVX mice in comparison with endometriotic nonovariectomized mice. However, the abundance of Phylum Tenericutes, Order Clostridiales, Dehalobacterium sp. and Anaeroplasma sp. were decreased. Collectively, endometriosis changed estrogen metabolism and gut microbiota which resulted in the immune modulation. (Supported by NIH P01AT003961, R01AT006888, R01MH094755, P20GM103641, R01AI129788 and R01AI123947 to PN and MN, and MoHESR to AKM).